Microbiology

TOPNOTCH MEDICAL BOARD PREP MICROBIOLOGY MAIN HANDOUT BY PACIFICO ERIC E.
CALDERON, MD, MBEth

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This handout is only valid for the September 2021 PLE batch. This will be rendered obsolete for the next batch since we update our handouts regularly.
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The handouts, videos and other review materials, provided by Topnotch Medical Board
GENERALITIES
Preparation Incorporated are duly protected by RA 8293 otherwise known as the WHAT ARE MICROORGANISMS?
Intellectual Property Code of the Philippines, and shall only be for the sole use of the person: • These are minute (yes, they are small!) organisms that are too
a) whose name appear on the handout or review material, b) person subscribed to Topnotch
Medical Board Preparation Incorporated Program or c) is the recipient of this electronic little to be seen by the unaided eye – individually!
communication. No part of the handout, video or other review material may be reproduced,
shared, sold and distributed through any printed form, audio or video recording, electronic
To set the mood for studying microbiology and parasitology, it would be
medium or machine-readable form, in whole or in part without the written consent of prudent to recall fundamental concepts resonant of your undergraduate
Topnotch Medical Board Preparation Incorporated. Any violation and or infringement, years. This introductory video can be helpful.
whether intended or otherwise shall be subject to legal action and prosecution to the full
extent guaranteed by law. Some concepts might be familiar to you already, particularly if you have
a highly technical background in biology. Otherwise, I encourage you to
dig deep into the basics. Here, feel free you to jot down notes.
DISCLOSURE Dr. Calderon
The handouts/review materials must be treated with utmost confidentiality. It shall be the MICROBIAL GROUPS
responsibility of the person, whose name appears therein, that the handouts/review
materials are not photocopied or in any way reproduced, shared or lent to any person or • Microorganisms – classified as such because they are ‘true’
disposed in any manner. Any handout/review material found in the possession of another organisms because they have ‘cells’
person whose name does not appear therein shall be prima facie evidence of violation of RA o Bacteria
8293. Topnotch review materials are updated every six (6) months based on the current
trends and feedback. Please buy all recommended review books and other materials listed o Protozoa
below. o Microscopic algae (the medically important one cause red tide
THIS HANDOUT IS NOT FOR SALE!
poisoning – which produces saxitoxin – Na channel blocker)
o Fungi (it is interesting to note how medical mycology
INSTRUCTIONS flourished as a science upon the emergence of HIV)
To scan QR codes on iPhone and iPad
1. Launch the Camera app on your IOS device
2. Point it at the QR code you want to scan • Acellular infectious agents – not true organisms because they
3. Look for the notification banner at the top lack cells (refer to my explanation below)
of the screen and tap
To scan QR codes on Android
o Viruses
1. Install QR code reader from Play Store o Viroids
2. Launch QR code app on your device o Prions
3. Point it at the QR code you want to scan
4. Tap browse website These biological ‘entities’ are technically NOT considered ‘living things’
(i.e. organisms) because they lack the basic unit of life, the cell. However,
Approach to Topnotch Microbiology they gain biological activity when they parasitize a host cell. When
• You may opt to purchase the following learning material: external to cells, generally they are mere molecules.
o Review of Medical Microbiology & Immunology: A Guide Remember that to be considered an organism – biologically speaking –
to Clinical Infectious Diseases, 15e the agent should satisfy this tenet of the cell theory: All living organisms
are composed of one or more cells (see below).
o Philippine Textbook of Medical Parasitology
o BRS Microbiology THE CELL THEORY
These will serve as your major references; they are excellent 1. All living organisms are composed of one or more cells.
2. The cell is the basic unit of structure and organization in organisms.
resources that can support your success in this subject.
– So, viruses, viroids, and prions are not considered as ‘living things’.
• This lecture mainly uses Jawetz, Melnick, & Adelberg’s Medical 3. Cells arise from pre-existing cells. – This means that cells must come
Microbiology, Philippine Textbook of Medical Parasitology, and only from cells through reproductive division (e.g. binary fission,
BRS Microbiology and is supplemented by other sources (e.g. mitosis, meiosis). Life does not come from merely mixing molecules.
Dr. Calderon
CDC, WHO, Microbiology Made Ridiculously Simple).
• Mobile genetic elements
• For some pointers that needs to be further elucidated, I refer you
o Bacteriophages
to Jawetz, Melnick, & Adelberg's Medical Microbiology, 28e.
o Plasmids
o Transposons
MICROBIOLOGY Mobile genetic elements (MGEs) are a type of genetic material move
around within a genome. They can also be transferred from one species
By Pacifico Eric E. Calderon, MD or replicon to another.
Edited by: Frinz Moey C. Rubio, MD & Tiffany Grace C. Uy, MD MGEs are found in all organisms and play an integral role in genetics
because, as segments of DNA, they facilitate the movement of genetic
TOPIC PAGE information between chromosomes. In this way, they contribute to
1. Generalities 2 genetic diversity.
2. Parasitology 16 Why is genetic diversity important? Well, this is meant to ensure survival
3. Mycology 40 of organisms (e.g. antimicrobial resistance, toxin production).
4. Bacteriology 48 Dr. Calderon
5. Virology 72 • Animal parasites

o Nematodes (roundworms)
This handout is only valid for the September 2021 PLE batch. o Trematodes (flukes)
This will be rendered obsolete for the next batch o Cestodes (tapeworms)
since we update our handouts regularly.
Welcome to Microbiology review! Here are some pointers for a

I. PROKARYOTES
more productive review experience.
INTRODUCTION
TO MICROBIOLOGY
https://qrs.ly/33cjshj
Mastering Biology Pearson
TOPNOTCH MEDICAL BOARD PREP MICROBIOLOGY MAIN HANDOUT BY PACIFICO ERIC E. CALDERON, MD, MBEth Page 1 of 88
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TOPNOTCH MEDICAL BOARD PREP MICROBIOLOGY MAIN HANDOUT BY PACIFICO ERIC E. CALDERON, MD, MBEth
✔GUIDE QUESTION
Substance X, an antibiotic isolated from nature, is found to inhibit the
PROKARYOTES in vitro growth of both Escherichia coli and Staphylococcus aureus, but
Refer to the table below not of Candida albicans. Further experiments reveal that the substance
https://qrs.ly/c1cjshn is capable of inhibiting protein synthesis by binding to the 30s
ribosomal subunit. The activity of substance X is similar to that of what
antimicrobial?
PROKARYOTES EUKARYOTES A. Ampicillin
DNA within a nuclear B. Tetracycline
NO YES
membrane? C. Clindamycin
Mitotic division? NO YES D. Levofloxacin
DNA associated with
NO YES
histones? GUIDE QUESTION 1
Chromosome number? 1 >1
https://qrs.ly/ekcjsi5
Membrane-bound
NO YES
organelles?
60S + 40S =
Size of ribosome? 50S + 30S = 70S II. EUKARYOTES
80s
Cell wall containing
YES NO
peptidoglycan?
Even though prokaryotes do not have a nucleus, they DO contain genetic
information. Prokaryotes generally have single circular chromosomes
where they store their genetic information. The AREA that contains this
genetic material is called the NUCELOID.
Dr. Calderon
As a mnemonic in remembering the size of the ribosomes

Prokaryotes = ODD first digit (i.e. 30s, 50s, 70s)
Eukaryotes = EVEN first digit (i.e. 40s, 60s, 80s)
Dr. Rubio
Prokaryotic ribosomes: 50 + 30 = 70
S stands for Svedberg unit
EUKARYOTES
Refer to the table above.
https://qrs.ly/r3cjsid
© Topnotch Medical Board Prep Eukaryotes can be unicellular (e.g. protozoa, some microscopic algae that
SVEDBERG UNIT case red tide poisoning). Many people think that eukaryotes are all
• Non-SI unit for sedimentation rate multicellular, but this is not the case. While prokaryotes are always
• Sedimentation rate is the rate at which particles of a given size unicellular organisms, eukaryotes can be either unicellular or
and shape travel downwards under centrifugal force multicellular.
Dr. Calderon
• The Svedberg is technically a measure of time, and is defined as
exactly 10-13 s (100 femtosecs) – So, the smaller the subunit, the ✔GUIDE QUESTION
Which of the following organisms lack membrane sterols?
faster the sedimentation rate (therefore, less time)!
A. Yeasts
B. Mycoplasmas
C. Protozoa
D. Staphylococci
Generally, bacteria do not have sterols in their membranes; but
mycoplasmas are an exception. In fact, they are the only bacteria
WITH sterols.
The other groups have sterols, as follows:
Protozoa and animals – cholesterol
Fungi – ergosterol
By now, remember that ergosterol is found in fungi. This
molecule is a common target in antifungal therapy, e.g.
ketoconazole inhibits ergosterol synthesis, amphotericin directly
targets membrane sterols.
Dr. Calderon
Which group of infectious agents does not require DNA as genetic
material?
A. Retroviruses
B. Prions
C. Bacteria
D. Viroid
The questions asks which one does not require.
© Topnotch Medical Board Prep Even if prions are composed of proteins only, they still require
This figure is useful for correlation to antimicrobial pharmacology. Note genetic material to direct their synthesis. Remember: DNA makes
the groups of drugs that target the 30S and 50S ribosomal subunits: RNA makes protein. This is the central dogma!
• 30s – Aminoglycosides, Tetracyclines The PRNP gene provides instructions for making a protein called
• 50s – Chloramphenicol, macrolides (e.g. Erythromycin), Lincosamides prion protein (PrP), which is active in the brain and several other
(e.g. clindamycin), Linezolid, Streptogramins (e.g. dalfopristin / tissues.
Dr. Calderon
quinupristin)
Dr. Calderon
Which of the following infectious agents lack nucleic acids?
A. Viruses
MNEMONIC B. Bacteria
BUYS AT 30, CELLS for 50! C. Viroid
AT – aminoglycosides, tetracyclines D. Prions
CELLS – chloramphenicol, erythromycin, linezolid, Prions lack nucleic acids. They are made of PRroteIns Only
(proteinaceous infectious particle). In reference to the preceding
lincosamides (clindamycin), streptogramin
question, however, it will still require DNA and RNA to direct its
See my highlights in the list above. This is corny but can be helpful! synthesis, but its final product will be purely protein, that is, it is
You can also refer to the pharmacology notes.. composed of amino acids.
Dr. Calderon
The rest of the infectious agents contain nucleic acids, either DNA
or RNA or both.
Dr. Calderon
PROTOZOA AND
CHARACTERISTIC VIRUSES BACTERIA FUNGI
HELMINTHS
Cells No Yes Yes Yes
Approximate diameter
0.02 – 0.2 1–5 3 – 10 (yeasts) 15 – 25 (trophozoites)
(µm)
Nucleic acid Either DNA or RNA Both DNA and RNA Both DNA and RNA Both DNA and RNA
Eukaryotic
(unicellular – protozoa)
Type of nucleus None Prokaryotic Eukaryotic
(multicellular –
helminths)
Ribosomes Absent (30S + 50S = 70S) (40S + 60S = 80S) 80S
Mitochondria Absent Absent Present Present
Protein capsid and Rigid wall containing Rigid wall containing
Nature of outer surface Flexible membrane
lipoprotein envelope peptidoglycan chitin
Motility None Some None Most
Not binary fission (refer
Method of replication Binary fission Mitosis via budding Mitosis
to viral genetics)
TRANSPOSONS PRIONS
• a.k.a. “transposable” elements • Noncellular infectious proteins
• Mobile genetic elements • Naked proteins that have the same amino acid sequence as
• DNA pieces that move readily from one site to another either certain normal human cell surface proteins but have folded
within or between the DNA of bacteria, plasmids, and differently
bacteriophages • These are misfolded proteins with the ability to transmit their
• “Jumping genes” misfolded shape onto normal variants of the same protein. They
• “Cut and paste” or “copy and paste” characterize several fatal and transmissible neurodegenerative
• Code for drug-resistant enzymes, toxins, or metabolic enzymes diseases in humans and many other animals
• Cause mutations in genes into which they insert (via a mutation) • Pathology: dysfunction due to protein misfolding
or alter the expression of nearby genes (e.g. causing the
activation or repression of antibiotic resistance genes).
• Two methods of transposition (see figure below):
o cut-and-paste (direct transposition)
o copy-and-paste (replicative transposition)
Mayo Foundation of Medical Education and Research

CORRELATION BIOCHEMISTRY
‘Normal’ prion proteins (PrPc) have alpha helices (they are
normally expressed in neurons to aid in proper neuronal
functioning). ‘Abnormal prion proteins (PrPsc) have more
beta-pleated sheets, which are more resistant to proteases and
chemicals.
• ‘Pathological’ prions suffer from a misfolding, where the beta
sheets are produced.
• This misfolding makes pathological prions resistant to
https://www.golifescience.com/transposons-mobile-dna/ proteases, many chemicals, and normal autoclaving. Hence, they
are resistant to fundamental microbial control, making them the
‘most stubborn’ among all infectious agents (most difficult to
control!)
• Associated with spongiform encephalopathies, e.g. Creutzfeldt-
Jakob disease, kuru, fatal familial insomnia
PATHOGENESIS OF PRION INFECTION
Sateesh, Mysore. (2014). Innovation, Future and Sustainable Approach in Modern Biotechnology.
SPONGIFORM ENCEPHALOPATHIES Curious about kuru? Check out this video:

• Appearance of the vacuolated neurons, as well as their loss of
function and the lack of an immune response or inflammation KURU
https://qrs.ly/6lbou80
Dr. Calderon
ANIMAL PRION DISEASES

• Scrapie (sheep, goats, mice, hamsters)
• Transmissible mink encephalopathy (mink)
• Bovine spongiform encephalopathy (BSE)
https://neuropathology-web.org/chapter5/chapter5ePrions.html
o Also known as mad cow disease
• Chronic wasting disease (mule, deer, elk)
HUMAN PRION DISEASES
• Creutzfeldt-Jakob disease (CJD) TRANSMISSION
• Variant CJD (vCJD) • Sporadic
• Gerstmann-Sträussler-Scheinker (GSS syndrome) • Infection
• Fatal familial insomnia (FFI) o use of bovine growth hormone (from dead cows)
• Sporadic fatal insomnia o transplantation of contaminated tissues (cornea)
o use of contaminated medical devices (brain electrodes)
o ingestion of infected tissue (cannibalism: ‘kuru’)
PRION DISEASES • Inherited syndrome
https://qrs.ly/yvbou7u
SUSCEPTIBLE POPULATION
• women and children of the Fore tribe in the jungles of New
Classic or Guinea
Sporadic Kuru Variant CJD • neurosurgeons and brain surgery patients
CJD • transplant surgeons and transplant patients
Associated
with SPECTRUM OF DISEASE
Etiology Sporadic Cannibalism consumption
• progressive, neurodegenerative disease
of meat from
o loss of muscle control
cows with BSE
o shivering, myoclonic jerks and tremors
Diagnosis Histopathology o loss of coordination
Higher Cortical Dysfunction and Dementia o rapidly progressive dementia
↓ o death
Clinical
Cerebellar manifestations
Presentation
Dysdiadochokinesia, ataxia, myoclonic jerks, TREATMENT AND PREVENTION
etc. • no treatment available
* - bovine spongiform encephalopathy (a.k.a. mad cow disease) • cessation of ritual cannibalism
• elimination of animal products from livestock feed
• Kuru = to shake
• disinfection of neurosurgical tools and electrodes
o Fatal neurodegenerative prion protein (PrP) disease in man
o 5% hypochlorite solution or 1.0 M sodium hydroxide or
o Cerebellar syndrome autoclaved at 15 psi for 1 hour
o With characteristics and relentless progression of neurological
symptoms through well-defined clinical stages Standard autoclave conditions. To be effective, the autoclave must
reach and maintain a temperature of 121° C for around 15-20 minutes
o Initially, cognition is fairly well-preserved,
by using saturated steam under at least 15 psi of pressure. So, for prion
o Disease presentation is sufficiently distinctive to be easily control, the autoclaving time is extended to 1 hour!
recognized by patients, their relatives, and the local Dr. Calderon
community
✔GUIDE QUESTION
Prions are not normal and may cause disease because they exhibit a problem with which of the following?
A. Folding of segments of polypeptide into geometrically ordered units
B. Amino acid sequence in a polypeptide chain
C. Protein assembly into the mature polypeptide and its component domains
D. Number and types of polypeptide units of oligomeric proteins and their spatial arrangement
Prion anomaly occurs because of the ‘straightening’ of alpha helices into beta sheets. This phenomenon falls within the concept of secondary protein structures.
Dr. Calderon
Let us recall biochemistry!
• Primary - Amino acid sequence in a polypeptide chain

• Secondary – Folding of segments of polypeptide into geometrically ordered units
• Tertiary – Protein assembly into the mature polypeptide and its component domains
• Quaternary – number and types of polypeptide units of oligomeric proteins and their spatial arrangement
Dr. Calderon
✔GUIDE QUESTION ✔GUIDE QUESTION
PrP knockout mice, which are engineered not to express the PrP gene, Combining drugs such as ampicillin and sulbactam circumvents which
show no obvious pathological phenotype. However, these mice have mechanism of bacterial resistance?
been shown to have abnormalities in all of the following, EXCEPT which A. Enzymatic inactivation
one? B. Transpeptidase mutation
A. Synaptic transmission C. Reprogramming of peptidoglycan precursors
B. Immunity D. Mutation of DNA topoisomerases
C. Circadian rhythm
D. Sleep
Since normal cellular prions (PrPc), sometimes called prion-like
proteins (to differentiate them from the infectious prions), are
involved in proper neurologic functioning, taking them out of the
picture, e.g. through genetic knockout, can lead to neurologic
impairment. By convention, immunity is, of course, not considered a
neurologic function.
Let’s recall!
What are the standard autoclave conditions?
Temperature: _______oC
Pressure: _______ psi
Time: _______ mins
Dr. Calderon
III. BACTERIAL STRUCTURE

BACTERIAL SHAPE AND SIZE
• three shapes:
o cocci (spheres) © Topnotch Medical Board Prep
o bacilli (rods) Ampicillin is a beta-lactam drug that belongs to the penicillin group
of antibacterial agents. It can be susceptible to hydrolysis by bacterial
o spirochetes (spirals)
beta-lactamases (a.k.a. penicillinases). The addition of beta-
§ Leptospira lactamase inhibitors (e.g. sulbactam, clavulanic acid, tazobactam)
§ Treponema can ‘protect’ the antibiotic from enzymatic hydrolysis and subsequent
§ Borreliella (new name of Borrelia since 2019) inactivation.
• cocci arranged in three patterns: Dr. Calderon
Lysozymes are enzymes that kill bacteria by cleaving which part of the
o pairs (diplococci)
cell wall?
o chains (streptococci) A. Pentaglycine bridges
o clusters (staphylococci) B. Multiple layers of peptidoglycan “net”
o sarcina (eight-membered cocci formation) C. β 1→ 4 glycosidic bond between NAG and NAM
D. Tetrapeptide side chains
✔GUIDE QUESTION Lysozymes destroy bacterial peptidoglycan by cleaving the β 1→4
A 27 G1P1 consults because of a painful and erythematous right breast. glycosidic linkage between NAG and NAM. They are found in the
Since the birth of her child three weeks ago, she has been breastfeeding secretions (tears) of the lacrimal glands of animals and in nasal
exclusively. On PE, there are visible small fissures around the nipple. mucus, gastric secretions, and egg white.
The breast feels warm. Purulent discharge from the nipple is noted.
Culture of the discharge isolates Gram-positive bacteria. What is the Antibacterial mechanisms of lysozyme
most likely cellular morphology of the organism? 1. Hydrolysis of the β-1,4 glycosidic bond between the NAM of 1
A. Rod monomer and the NAG of the adjacent monomer → hydrolysis
B. Spherical, arranged in chains of peptidoglycan leads to cell wall instability and bacterial cell
C. Spherical, arranged in grapelike clusters death
D. Spiral 2. Formation of pores by lysozyme (red cylinders) on the bacterial
cell membrane → a mechanism involving its cationic nature;
independent of peptidoglycan hydrolysis
GUIDE QUESTION 2 Dr. Calderon
A 27 G1P1 consults because of a painful and erythematous right breast.
https://qrs.ly/pfcjsmt Since the birth of her child three weeks ago, she has been breastfeeding
exclusively. On PE, there are visible small fissures around the nipple.
The breast feels warm. Purulent discharge from the nipple is noted.
Culture of the discharge isolates Gram-positive bacteria. What is the
BACTERIAL CELL WALL most likely cellular morphology of the organism?
• All bacteria have a cell wall composed of peptidoglycan except A. Rod
Mycoplasma – Mycoplasma do not have cells walls! B. Spherical, arranged in chains
C. Spherical, arranged in grapelike clusters
• Peptidoglycan = sugar backbone (glycan) + peptide side chains
D. Spiral
(peptido) cross-linked by transpeptidase
Peptidoglycan structure GUIDE QUESTION 3

https://qrs.ly/zzcjsny
GRAM-POSITIVE VS GRAM-NEGATIVE
COMPONENT GRAM (+) CELLS GRAM (-) CELLS
• Thicker; • Thinner;
Peptidoglycan
• multilayer • thinner layer
Teichoic acids • Yes • No
Lipopolysaccharide • No • Yes
Periplasmic space • No • Yes
Benjamin Cummings, an imprint of Addison Wesley Longman, Inc.
• Porin proteins – Facilitate passage of small, hydrophilic

molecules into the cell.
• In the outer membrane of gram-negative bacteria → channels
allow the entry of essential substances such as sugars, amino
acids, vitamins, and metals as well as many antimicrobial drugs
such as Penicillins.
Gram stain, also called Gram's method, is a method of staining used to
distinguish and classify bacterial species into two large groups: gram-
positive bacteria and gram-negative bacteria.
COLOR CHANGES DURING GRAM STAIN
In Gram staining, the bacteria are first washed in a purple stain, crystal
violet, followed by iodine. The iodine and crystal violet form large
complexes which bind to the cell and turn it purple.
The cells are then washed with alcohol. Here, alcohol strips the outer
lipid layers away from the cell.
The Gram-positive cell looses (yes, “lumuluwag”) some of its large chunky
peptidoglycan cell wall, but maintains enough of it to retain the purple
color.
The Gram-negative cell has its outer membrane and thin peptidoglycan
layer completely stripped away, leaving it colorless (decolorized).
The cells are then exposed to a second stain, safranin. This turns the
colorless Gram-negative cells pink, but it is not strong enough to alter the
deep purple color of Gram-positive cells.
Dr. Calderon
GRAM-NEGATIVE CELL WALLS

• outer membrane of gram-negative bacteria contains endotoxin
(lipopolysaccharide - LPS)
COMPONENT
FUNCTION
OF LPS
Active component of LPS
Lipid A Induces TNF and IL-1
Structure: beta-hydroxymyristic acid
Core Contributes to stability of the outer
oligosaccharide membrane
O polysaccharide Antigen structure
• All gram-positive bacteria have NO endotoxin EXCEPT Listeria
monocytogenes
✔GUIDE QUESTION
© Topnotch Medical Board Prep
Which component of the Gram-negative cell wall reduces its
susceptibility to lysozymes? ✔GUIDE QUESTION
A. Teichoic acids Which of the following is the OLDEST acid-fast staining method, which
B. Beta-lactamases in the periplasm requires heating the specimen during the procedure?
C. M protein A. Fluorochrome C. Kinyoun
D. Outer membrane B. Ziehl-Neelsen D. Auramine-rhodamine
The peptidoglycan layer in Gram-negative cells is ‘sandwiched’ between
two membranes: an outer membrane and the plasma membrane (as an
inner membrane). The outer membrane serves as a physical barrier that
‘protects’ the peptidoglycan immediately underneath from insult. Note
that lysozymes result to cleavage of peptidoglycan glycosidic bonds: β
1→4 glycosidic bond between NAG and NAM.
Dr. Calderon
It is extremely difficult to stain mycobacteria by ordinary

methods. This is because of the high lipid content of their cell
walls. The phenolic compound carbol fuchsin is used as the
primary stain because it is lipid soluble and penetrates the waxy
cell wall.
Staining by carbol fuchsin is further enhanced by steam heating
(acting as a mordant); this process melts the wax and allow the
stain to move into the cell.
STAINING TECHNIQUES Acid then is used to decolorize nonacid-fast cells; acid-fast cells
GRAM STAINING are unaffected by this decolorization attempt. The ability of the
bacteria to resist decolorization with acid confers ‘acid-
STEP PROCEDURES REAGENT fastness’ to the bacterium.
1 Primary Stain CRYSTAL VIOLET
After decolorization, the smear is then counterstained with
2 Mordant IODINE malachite green or methylene blue which stains the
3 Decolorizing Agent ALCOHOL/ACETONE background material, providing a contrast color against which
4 Counterstain SAFRANIN the red AFB can be seen.
The Kinyoun staining procedure is often referred to as cold
MEMORY AID GRAM STAINING carbolfuchsin because NO HEAT is applied during the staining
V–I–A–S process, unlike in the Ziehl-Neelsen procedure.
Violet Alcohol/Acetone Remember:
Iodine Safranin Ziehl-Neelsen – uses heat. It’s zizzling!
Kinyoun – is kold.
Dr. Calderon
BACTERIA NOT SEEN IN GRAM STAIN OTHER STAINING TECHNIQUES
ALTERNATIVE NAME REMARKS
NAME REASON
APPROACH • Rickettsia, Chlamydia, Trypanosomes,
• Too mycolic acid Giemsa stain
Plasmodium, Borrelia, Helicobacter pylori
(lipid) in cell wall • Stains glycogen, mucopolysaccharides
Mycobacteriae ACID-FAST STAIN Periodic acid-
so dye cannot • Used to diagnose Whipple disease
penetrate Schiff (PAS)
(Tropheryma whipplei)
DARKFIELD stain
Spirochetes • Too thin to see • PAS the sugar (glycogen)
MICROSCOPY • Uses negative staining technique
Mycoplasma (wherein it does not stain the microbe,
spp. • No cell wall India Ink stain but instead, it stains the background to
NONE (SEROLOGIES)
Ureaplasma • Very small make the microbe more visible)
sp. • Cryptococcus neoformans
• Poor uptake of Mucicarmine • Directly stains the thick polysaccharide
Legionella
red counterstain SILVER STAIN stain capsule of Cryptococcus neoformans red
spp.
• Intracellular
• Coccidioides, Pneumocystis jirovecii,
• Intracellular Silver stain
Legionella, Helicobacter pylori
• Lacks classic • Used to identify bacteria, viruses, P
GIEMSA STAIN →
Chlamydiae peptidoglycan Fluorescent jirovecii, Giardia lamblia,
INCLUSION BODIES
becomes of ↓ antibody stain Cryptosporidium
muramic acid
• FTA-ABS for syphilis
GIEMSA/ TISSUE
Rickettsiae • Intracellular Tannic acid
STAINS • To visualize flagella of bacteria
stain
Bartonella,
Feulgen stain • To visualize the nucleoid of bacteria
Anaplasma, • Intracellular TISSUE STAINS
Malachite
Ehrlichia • To visualize the spores of bacteria
green stain
MEMORY AID BACTERIA NOT SEEN IN GRAM STAIN
ESSENTIAL COMPONENTS OF BACTERIA
These Little Microbes May Unfortunately Lack Real Color But
The term ‘essential’ refers to structures the bacterium CANNOT LIVE
Are Everywhere
WITHOUT. So, if you take it out of the picture, the bacterium will not
Treponema Leptospira thrive (e.g. cell wall, ribosomes). GENETICALLY speaking, if the
Mycobacteria Mycoplasma bacterium requires something that is essential, then it must be acquired
Ureaplasma Legionella from parental cells, i.e. from parent to offspring during cell division. That
Rickettsiae Chlamydia is why an essential structure is said to be genetically inherited in a vertical
Bartonella Anaplasma direction (downward: from parent to offspring). So, if a structure is
Ehrlichia essential, it is inherited from the parents via the CHROMOSOME itself,
UNLIKE non-essential structures that are inherited via OTHER genetic
means (e.g. conjugation, transduction, transformation → discussed below
and in bacterial genetics).
Dr. Calderon
Cell Wall As described previously

✔GUIDE QUESTION
Cytoplasmic Lipoprotein bilayer Site of oxidative and
Gram-positive bacteria were inoculated under the skin of experimental
animals and then the infection is treated with antibiotics. Bacteria
membrane without sterols ETC enzymes
isolated from the injection site several days later assume a spherical RNA and protein in
configuration when placed in an isotonic solution and disintegrate Ribosome 50S and 30S Protein synthesis
when placed in a hypotonic solution. Which antibiotic was most likely subunits
used in this experiment? Nucleoid DNA Genetic material
A. Cefalexin C. Azithromycin Participates in cell
B. Ciprofloxacin D. Co-trimoxazole Invagination of
Mesosome division and
Bacterial morphology (shape) is determined by the cell wall. The plasma membrane
secretion
bacteria described in this case lost their cell walls after antibiotic Space between Contains many
treatment, characterized by lack of osmotic instability (e.g.
plasma membrane hydrolytic enzymes,
changes in shape and integrity under varying tonicity). This is Periplasm
most likely caused a loss of the cell wall. The bacteria were and outer including b-
probably treated with a cell wall inhibitor (recall MOA of membrane lactamases
antibacterials). Choices B and C are protein synthesis inhibitors
and are unlikely to directly affect cell wall synthesis, while choice NON-ESSENTIAL COMPONENTS OF BACTERIA
D is an inhibitor of folate synthesis (necessary for DNA
replication). Non-essential components, as the term implies, are accessory structures,
Dr. Calderon i.e. nice to have. A bacterium can possess them or not.
Pathogenicity-wise, if a bacterium possesses a non-essential component,
it is MORE VIRULENT (e.g. capsule inhibits phagocytosis, hence, an
GUIDE QUESTION 4 infection can spread easily; a spore can survive inclement environmental
conditions, hence, prolonging its existence). That said, it is possible for a
https://qrs.ly/41ck66w
bacterium from the same species (say, bacterium A) to lack a non-
essential component, and for bacterium B to have it. If that component is
a capsule, then bacterium A is non-encapsulated and bacterium B is
A 24/M presents to his primary care physician with complaints of
encapsulated. Between A and B, B is more virulent because it possesses
burning with urination. Three days later, the patient also has fever, skin
the capsule!
flushing, and altered level of consciousness. PE: BP 60/40, HR 120/min.
Genetics-wise, non-essential components are optionally transferred from
If blood cultures are positive for Klebsiella pneumoniae, which of the
bacterium to another, hence, it obtains it from ‘friends’ via horizontal
following bacterial factors is most likely responsible for this patient’s
transfer (sideward: from a friend to itself). So, we can say that a non-
current condition?
essential component is acquired from outside the parent-child
A. Capsule C. Peptidoglycan
relationship. These genetic processes are what we will discuss in
B. Lipid A D. Flagellar antigen
bacterial genetics. So, if a structure is non-essential, it is inherited from
Lipid A, a component of LPS in Gram-negative outer membrane, is the friends via the MOBILE GENETIC ELEMENTS (plasmids, phages,
sufficient to cause endothelial cell injury by promoting the recombinant DNA), UNLIKE essential structures that are inherited from
expression of tissue factor and proinflammatory cytokines, parents.
leading to apoptosis of these cells. In a blood stream infection, Therefore, basically, if a structure is:
presence of lipid A can lead to endotoxin shock (the clinical picture • ESSENTIAL – it is acquired from CHROMOSOMES via binary fission
described in this vignette).
Dr. Calderon
• NON-ESSENTIAL – it is acquired from GENETIC MOBILE ELEMENTS CAPSULES
via special genetic transfers (e.g. conjugation, transduction,
transformation) • All bacterial capsules are composed of polysaccharide EXCEPT
Dr. Calderon Bacillus anthracis (polypeptide of D-glutamate)
Protects against • Spore: formed by gram-positive rods, especially Bacillus and
Capsule Polysaccharide Clostridium spp
phagocytosis
Attachment (ordinary
Pilus or
Glycoprotein pili)
fimbria
conjugation (sex pili)
Mediates adherence
Glycocalyx Polysaccharide
to surfaces → biofilms
Flagellum Protein Motility
Keratin-like coat, Resistance to heat,
Spore
dipicolinic acid and chemicals
Genes for antibiotic
Plasmid DNA
resistance and toxins
Glycogen, lipids, Site of nutrients in
Granule
polyphosphates cytoplasm
SPORULATION IN BACTERIA
©Topnotch Medical Board Prep

✔GUIDE QUESTION Significance of Plasmids
A herd of cattle dies of anthrax. Anthrax is caused by the bacterium • Antibiotic resistance
Bacillus anthracis, a spore-forming organism. To break the chain of • Resistance to heavy metals
transmission, which of the following is probably the BEST way to
• Resistance to UV light
handle the carcasses of the cattle?
A. Burying six feet below the ground • Pili (fimbriae)
B. Market sale and proper food preparation • Exotoxins and several enterotoxins.
C. Incineration of the carcasses • Bacteriocins – toxic proteins produced by certain bacteria that
D. Treating the mass grave with antibiotic spray prior to burial are lethal for other bacteria.
The preferred method of disposal of an anthrax carcass is
incineration. Remember that Bacillus anthracis is a spore-former,
and the spore confers protection and resistance to environmental
stressors. It may also deter scavengers that would otherwise open
up the carcass and thereby increase the contamination, and flies
that might spread the disease.
PLASMIDS
• Extrachromosomal, double-stranded,
circular DNA capable of replicating
independently of the bacterial
chromosome.
• Can sometimes be integrated into the bacterial chromosome →
called episomes CONJUGATION between a plasmid bearing donor and a plasmid-less
recipient. Here the ‘donor’ creates a conjugation pilus to build a cytosolic
bridge with the donor. The plasmid is then replicated and ‘transferred’ to
the recipient through the rolling circle method of replication. The
recipient then becomes competent to also act as a donor.
Dr. Calderon
✔GUIDE QUESTION IV. BACTERIAL GROWTH

As part of an orientation seminar, a medical resident received • Bacterial growth is a coordinated process of increase in
orientation on proper hand washing protocol while in the hospital and
treating patients. Which of the following microbial characteristics
individual cell mass and size and duplication of the chromosome,
necessitate the use of soap-based products over the alcohol rubs/gels followed by cell division
commonly found in every patient room in the hospital? • Bacterial reproduction occurs via binary fission
A. Aerobic growth D. Naked DNA virus proteins
B. Cell wall teichoic acid E. Spore-forming BACTERIAL GROWTH CYCLE
C. LPS
Hand hygiene is a critical action recommended for preventing and
controlling the transmission of pathogens within healthcare settings to
ensure that patients remain safe and that their risks of acquiring infection
are minimized
The method employed in ensuring that hand hygiene is effective falls into
one of two categories:
Hand rubbing with an alcohol-based hand rub
Hand rubbing is the gold standard technique to perform hand hygiene on
all occasions except for those described for handwashing with soap and
water, i.e. hand rubbing is the action recommended for health-care
workers for the routine, day-to-day decontamination of hands. Review of Medical Microbiology and Immunology, 15th edition
Handwashing with soap and water: PHASE REMARKS

Handwashing still plays a key role in hand hygiene and should be • Phase during which vigorous
employed when hands are visibly dirty or visibly soiled with blood or other metabolic activity occurs, but cells
PHASE I: LAG
body fluids; after using the toilet; and when exposure to potential spore-
PHASE do not divide
forming pathogens is strongly suspected or proven, including during
outbreaks of diarrhea. See A in figure above • Can last for minutes up to hours
• Zero growth rate
At this point, it is crucial for you to learn how to differentiate the following
terms used in microbial control: PHASE II: LOG OR • When rapid cell division occurs
METHOD DEFINITION EXAMPLE EXPONENTIAL • b-lactam antibiotics are most
• Autoclaving PHASE efficacious during this phase
• Exposure to See B in figure above
• Destroys or eliminating
ethylene oxide gas • Occurs when nutrition depletion or
ALL forms of microbial
Sterilization
life, including bacterial
(for surgical toxic products cause growth to slow
instruments) PHASE III: until the number of new cells
spores STATIONARY
• Filtration (for most produced balances the number of
IV solutions) PHASE cells that die
• Eliminates many or all See C in figure above
• Application of • When bacterial spores are formed
pathogenic
microorganisms, except
rubbing alcohol – • Zero growth rate
Disinfection to inanimate • Marked by a decline in the number of
bacterial spores, on PHASE IV:
objects
inanimate objects DEATH PHASE viable bacteria
• Refers to the application
• Preoperative skin
See D in figure above • Negative growth rate
of chemicals on the
Antisepsis prep
surface of the skin and
mucous membranes
• Hand rubbing EFFECT OF BACTERICIDAL
• Reducing microbial & BACTERIOSTATIC ANTIMICROBIALS
contamination to an
• Heating cutlery
Sanitization acceptable “safe” level
(e.g. at KFC!)
(terminology used in
food safety)
Degerming
or Cleaning • Physical removal of
• Handwashing with
(a simpler microorganisms by
soap and running
terminology using such things as
water
used by the soaps or detergents
CDC)
Rubbing alcohol, for example, can be both a disinfectant and
antiseptic, depending on where you use it (inanimate or living).
Now, is handwashing a form of sterilization if it also removes
spores? No. It is a method of degerming, or cleaning, a form of
physical removal of the organisms. So here, the idea is, if you can't
kill it (with alcogel), just remove it. This speaks of the superiority of
meticulous handwashing in many medical and public health
scenarios.
Dr. Calderon
Alcohol-based hand sanitizers may be effective against the following
organisms, except which one? V. BACTERIAL OXYGEN METABOLISM
A. Staphylococcus aureus C. HPV 16
AEROBIC AND ANAEROBIC GROWTH
B. Clostridium difficile D. Candida albicans
• oxygen metabolic generates toxic products such as superoxide
There is concern because alcohol-based hand rubs are known to be and hydrogen peroxide
less effective on soiled hands generally and, specifically, when there
is C. difficile infection. This is because of the hand rubs’ inability to
• superoxide dismutase, peroxidase and catalase are needed to
kill the C. difficile spores that at times can be present. Alcohol is survive in aerobic environments
likely to eliminate all these microorganisms (A, C, and D), except
clostridial spores. ENZYMATIC DETOXIFICATION
Dr. Calderon
AEROBIC METABOLISM • Nocardia, Bacillus cereus, Neisseria,

Pseudomonas, Bordetella, Legionella,
• Obligate Aerobes Obligate Aerobes
Brucella, Mycobacterium, Leptospira,
o completely dependent on oxygen for ATP-generation
Mycoplasma pneumoniae
• Microaerophiles
o use fermentation but can tolerate low amounts of oxygen • Streptococcus, spirochetes (Borreliella,
because they have SOD Microaerophiles Treponema), Campylobacter,
Helicobacter
• Staphylococcus, Bacillus anthracis,
ANAEROBIC METABOLISM Facultative
Corynebacterium, Listeria,
• Facultative Anaerobes Anaerobes
Mycoplasmas (in general)
o utilize oxygen if it is present, but can use fermentation in its Aerotolerant • Propionibacterium (Cutibacterium),
absence Anaerobes Lactobacillus
• Aerotolerant Anaerobes Obligate
o exclusively anaerobic but insensitive to the presence of oxygen • Actinomyces, Bacteroides, Clostridium
anaerobes
• Obligate Anaerobes
o cannot grow in the presence of oxygen because they lack SOD, MEMORY AID BACTERIAL OXYGEN METABOLISM
peroxidase and catalase OBLIGATE AEROBES
Nosy and Nagging Pests Must Breathe Lots of oxygen.
OXYGEN REQUIREMENT Nocardia
Neisseria
Pseudomonas
Mycobacteria
Bordetella/Brucella/B. cereus
Legionella
OBLIGATE ANAEROBES
Anaerobes Can’t Breathe Fresh Air
Clostridium
Bacteroides
Fusobacterium
BACTERIAL OXYGEN METABOLISM Actinomyces
ENVIRONMENT EFFECT OF
GROUP
Aerobic Anaerobic OXYGEN
Obligate aerobe Growth No Growth Required
VI. BACTERIAL GENETICS
*Required but DNA TRANSFER BETWEEN BACTERIAL CELLS
No at low levels Transfer Type of Cells
Microaerophile Growth* Process
Growth (< 0.2 atm) Procedure Involved
only DNA transferred from
Not required Conjugation one bacterium to Prokaryotic
Facultative for growth but another
Growth Growth DNA transferred by a
anaerobe utilized when
available Transduction bacteriophage from Prokaryotic
Aerotolerant Not required one cell to another
Growth Growth Purified DNA taken up Prokaryotic
anaerobe and not utilized Transformation
Obligate No by a cell or eukaryotic
Growth Toxic
anaerobe Growth
TRANSDUCTION
TRANSDUCTION AND
ITS ASSOCIATED EXOTOXIN
https://qrs.ly/k2ck66y
TRANSFORMATION
MEMORY AID PROPHAGE-CODED BACTERIA
Lysogenized strains of ABCDE
shigA – like toxin: EHEC
Botulinum
Cholera
Diphtheria
Erythrogenic toxin
These toxins are produced by bacteria that have been infected by toxin-
coding phages. Hence, lysogenized strains of these bacteria may actually
produce toxins and cause disease. For example, if E. coli is lysogenized to
contain the shiga-like toxin gene, then it gains more virulence, e.g. bloody
diarrhea with hemolytic uremic syndrome. Ordinarily, E. coli can cause
CONJUGATION watery diarrhea; but bloody E. coli diarrhea must be a different
Figure 2.6. High-Yield Microbiology and Infectious Diseases. 2nd ed. Baltimore, MD: Lippincott Williams & Wilkins: 2007 pathogenic strain. This strain of lysogenized E. coli is called E. coli
O157:H7, or enterohemorrhagic E. coli. In more recent text, this strain is
known as the shiga-toxin producing E. coli (STEC).
VIRAL REPLICATION: Dr. Calderon
LYTIC VS LYSOGENIC
https://qrs.ly/g3bou8e VII. NORMAL FLORA
• Refer to microbes that are permanent residents of the body
• Normal flora are low-virulence organisms in their usual
anatomic site
Resident • Microbes regularly found in a given
microbiota area of the body at a given time
• Nonpathogenic or potentially
Transient pathogenic microbes that inhabit the
microbiota skin or mucous membranes for hours,
days, weeks
• Colonization resistance occurs when normal flora occupy
receptor sites preventing pathogens from binding
Skin • Staphylococcus epidermidis
Nose • Staphylococcus aureus
Mouth • Viridans Streptococci
Dental plaque • Streptococcus mutans
GRIFFITH EXPERIMENT – TRANSFORMATION • Bacteroides, Escherichia coli
(Journal of Hygiene 27 (2): 113–159, 1928.)
Colon • Bifidobacteria – dominant intestinal
microbiota in among breastfed children
• Lactobacillus vaginalis
Vagina • Escherichia coli
• Streptococcus agalactiae
VIII. INFECTION BIOLOGY

MECHANISMS OF BACTERIAL DISEASE
• production of toxins (both exotoxins and endotoxins)
• induction of inflammation
MODES OF TRANSMISSION
• Human to Human
o direct (sexual, transvaginal), fecal-oral, inhalation,
transplacental, blood-borne
• Nonhuman to Human
o soil, water, direct animal source, vector-borne, animal excreta,
fomites
BACTERIAL ADHERENCE
• pili mediate attachment of bacteria
• glycocalyx mediates strong adherence to surface of human
cells → allows adhesion to prosthetic devices
• surface proteins called curli mediate binding to endothelium
and to extracellular proteins such as fibronectin
MEMORY AID
Salma Hayek and her curli hair (Salmonella)
ENZYMES IN BACTERIAL INVASION
• hyaluronidase (a.k.a. spreading factor)
o spread through subcutaneous tissue
• coagulase
o accelerates formation of a fibrin clot coating the organisms
with a layer of fibrin
• immunoglobulin A (IgA) protease
o cleaves IgA → allows adherence to mucous membranes
o seen in SHiN organisms – S pneumoniae, H influenzae type b,
Neisseriae (gonococci and meningococci)
• leucocidin
o destroys both neutrophilic leukocytes and macrophages (e.g.
Panton-Valentine leucocidin or PVL)
✔GUIDE QUESTION EXOTOXINS
Which of the following may be considered primarily responsible for the • polypeptides secreted by certain bacteria that alter specific cell
development of cellulitis from a small furuncle?
functions resulting in the symptoms of disease
A. Lipases
B. Hyaluronidases • have an A–B subunit structure:
C. Panton-Valentine leucocidins o A subunit is the active (toxic) subunit
D. Hemolysins o B subunit is the binding subunit
Since hyaluronate is a major constituent of the ground substance of
most connective tissues (the skin in particular), hyaluronidase may be ✔GUIDE QUESTIONS
crucial for the spreading of pathogens from an initial site of infection. There is a specific bacterial product that produces temporary relief of
his esophageal symptoms in achalasia. Which agent produces this
Hyaluronidase, therefore, is also known as the ‘spreading factor.’ e.g. bacterial product?
A pimple today becomes cellulitis tomorrow! A. PrPres
Dr. Calderon
B. Clostridium tetani
C. Rhabdovirus
D. Clostridium botulinum
GUIDE QUESTION 5
The item describes botulinum toxin, a toxin produced by
https://qrs.ly/cock67l
lysogenized strains of Clostridium botulinum. Injection of
botulinum toxin into muscles causes temporary paralysis of the
specific muscle, which lasts for months to over one year. In
A 42/M complains of penile discharge and intermittent fevers. A
gastroenterology, botulinum toxin is used primarily to treat
urethral smear shows Gram-negative diplococci within leukocytes.
achalasia. The toxin acts by binding presynaptically to high-
What virulence factor mediates the initiation of this infection?
affinity recognition sites on the cholinergic nerve terminals and
A. Membrane attack complex
decreasing the release of acetylcholine, causing a neuromuscular
B. Pili
blocking effect. This mechanism laid the foundation for the
C. LPS
development of the toxin as a therapeutic tool.
D. Polysaccharide capsule Dr. Calderon
When an exotoxin binds to a receptor, it activates T-cells by binding
SIMULTANEOUSLY to a T-cell receptor and MHC II molecule on an
GUIDE QUESTION 6 antigen-presenting cell WITHOUT requiring an antigen. It activates
https://qrs.ly/mgck67v large number of T cells to cause a cytokine storm. What is the nature of
this exotoxin?
A. Superantigen
VIRULENCE FACTORS B. Protein synthesis inhibitor
C. ADP-ribosylator
• Polysaccharide Capsule D. Protease
o protect against phagocytosis
o anti-capsular antibodies allow more effective phagocytosis to Superantigens are microbial peptides that can polyclonally
activate a large fraction of T cells (up to 20%). They escape
occur (OPSONIZATION)
normal antigen processing by antigen presenting cells (APCs) and
• Cell Wall Proteins can directly bind to T cell receptor (TCR). This binding of TCR with
o M protein of S. pyogenes (group A Streptococcus) of MHC-II by superantigen results into polyclonal activation of T cells
antiphagocytic (via molecular mimicry – it can cause the which can ultimately result in life-threatening autoimmune
autoimmune response seen in acute rheumatic fever) responses, even deaths.
o Protein A of S. aureus binds to Fc region of IgG → prevents Examples of bacterial superantigens and their roles:
opsonization and phagocytosis • Staphylococcal enterotoxins: Food poisoning
• Staphylococcal toxic shock toxin (TSST-1): Toxic shock
TOXIN PRODUCTION syndrome
PROPERTY EXOTOXIN ENDOTOXIN • Staphylococcal exfoliating toxins (exfoliatin): Staphylococcal
Source G(+) and G(-) bacteria G(-) bacteria scalded skin syndrome
• Streptococcal pyrogenic exotoxins (exotoxin A and exotoxin B):
No (released from
Secreted Shock
Yes outer membrane Dr. Calderon
from cell
ONLY during lysis)
Chemistry Polypeptide Lipopolysaccharide
Location of Plasmid or Bacterial
genes bacteriophage chromosome
Toxicity High Low
Antigenicity High Low
Vaccines Toxoids No vaccine
Destroyed rapidly at
60°C
Stable at 100°C for
Heat stability (except
1 hr
staphylococcal
enterotoxin)
Mechanism See below ↑TNF, IL1, IL6
Disease Tetanus, botulism Meningococcemia
BIOLOGICAL EFFECT TOXIN NAME ORGANISM GENE LOCATION MECHANISM
Streptolysin 0 Streptococcus pyogenes Bacterial chromosome Forms membrane pore
a toxin Clostridium perfringens Bacterial chromosome Degrades phospholipids →
Alter cellular
and plasmid myonecrosis
components
Type III cytotoxin Pseudomonas aeruginosa Phage Alters actin cytoskeleton
Type III cytotoxin Salmonella sp. Bacterial chromosome
Exfoliative toxins A, B Staphylococcus aureus Phage Release of cytokines
TSST-1 Staphylococcus aureus Bacterial chromosome Release of cytokines
Superantigens
Enterotoxin Staphylococcus aureus Phage Release of cytokines
Erythrogenic toxins A,C Streptococcus pyogenes Phage Release of cytokines
Diphtheria toxin Corynebacterium diphtheriae Phage ADP ribosylates EF 2
Exotoxin A Pseudomonas aeruginosa Bacterial chromosome ADP ribosylates EF 2
Inhibition of protein
Shiga toxin Shigella dysenteriae Plasmid Inactivates 60S ribosome
synthesis
Vero toxin (Shiga-like) Enterohemorrhagic E. coli Bacterial chromosome Inactivates 60S ribosome
or phage
Cholera toxin Vibrio cholerae Bacterial chromosome Turns on adenylate cyclase
activity
Heat labile toxin Enterotoxigenic E. coli Plasmid Turns on adenylate cyclase
Increased synthesis of activity
cAMP Anthrax toxin Bacillus anthracis Plasmid Mimics adenylate cyclase
activity
Pertussis toxin Bordetella pertussis Bacterial chromosome Turns off adenylate cyclase
activity
Increased synthesis of Heat stable toxin Enterotoxigenic E. coli Plasmid Turns on guanylate cyclase
cGMP activity
Tetanus toxin Clostridium tetani Plasmid Inhibits inhibitory
neurotransmitter release
from Renshaw cells
Altered nerve
(GABA/glycinergic cells)
transmission
Botulinum toxin Clostridium botulinum Phage Inhibits acetylcholine release
from stimulatory neurons
(Ach)
BRS Microbiology and Immunology (Board Review Series)
ENDOTOXINS IX. DIAGNOSTIC MICROBIOLOGY

• Lipopolysaccharides (LPS) located in the outer membrane of ✔GUIDE QUESTION
gram-negative bacteria A 45/F consulted her physician for painless enlarging anterior neck
• Lipid A is the toxic component of LPS masses accompanied by fever, chills, weight loss and malaise. Fine
o induces the overproduction of cytokines, such as TNF & IL-1 needle aspiration was done to rule out a malignancy. If the physician
o activates the complement cascade suspects TB lymphadenitis, which of the following should he request to
RAPIDLY identify the mycobacterial species?
o activates the coagulation cascade, resulting in disseminated A. PCR
intravascular coagulation B. Culture on blood agar plate
MEMORY AID ENDOTOXIN C. Ziehl-Neelsen staining
D. Culture on Lowenstein-Jensen medium
eNdotoxin is an integral part of gram-Negative cell walls.
The PCR (polymerase chain reaction) method enables direct
detection of infectious or parasite agents through enzymatic
amplification of a part of their genome. This specific method can
target and detect very weak quantities of pathogens in different
types of samples. The question asks for a rapid, specific (key word:
species) method, hence, PCR fits these criteria so well. Acid-fast
staining (choice C) is rapid but not specific, while culture (choice
D) takes weeks because the organism is grows slowly.
MICROBIOLOGIC EXAMINATION
• Culture
• Microbial Identification: Colony and cellular morphology;
growth characteristics under various conditions, utilization of
carbohydrates and other substrates; enzymatic activity,
immunoassays, and genetic probes
• Serodiagnosis: A high or rising titer of specific IgG antibodies or
the presence of specific IgM antibodies may suggest or confirm a
diagnosis
Endotoxin is a component of Gram-negative bacteria and plays an • Antimicrobial Susceptibility: Microorganisms, particularly
important role in the pathogenesis of septic shock when it is recognized
bacteria, are tested in vitro to determine whether they are
by immune cells.
Dr. Calderon susceptible to antimicrobial agents
GENERALITIES ON BACTERIAL STRUCTURE

MICROBIAL CULTURE
All bacteria have cell walls composed Mycoplasma • Culture – propagation of microorganisms in media conducive to
of peptidoglycan EXCEPT pneumoniae their growth
All gram-positive bacteria have NO Listeria • Culture medium – a nutritive substance in which cultures of
endotoxin EXCEPT monocytogenes microorganisms are grown
All bacterial capsules are composed Bacillus anthracis o May be a gel or liquid medium
of polysaccharide EXCEPT (poly-D-glutamate) Here is a link to a video that launches a parade of culture media. You
Staphylococcal might want to jot down notes. My comments about individual culture
All exotoxins are heat-labile EXCEPT media are embedded in the discussion of specific organisms in the
enterotoxin
bacteriology section of this handout.
INTRODUCTION TO
MICROBIOLOGICAL
CULTURE MEDIA
https://qrs.ly/l2bou95
Dr. Calderon
SPECIALIZED MEDIA FOR BACTERIAL GROWTH ✔GUIDE QUESTION
Bacteria Agar An 18-year-old male presents with urinary tract infection. You suspect
Clostridium perfringens Egg Yolk Agar he has an E coli infection. What is the gold standard for diagnosis?
A. Urethral swab and Gram stain
Corynebacterium Cystine-Tellurite Agar,
B. Urine dipstick test
diphtheriae Loeffler Agar C. Culture on eosin-methylene blue (EMB) agar
group D streptococci Bile Esculin Agar D. Urinalysis
N. meningitidis,
The gold standard test for the detection of E coli is culture, which has
N. gonorrhoeae from Chocolate Agar high sensitivity and specificity. This also applies to MOST bacterial
sterile sites agents. Remember in culture media, you are able to isolate the
N. gonorrhoeae from organism. Moreover, the isolated colony can be checked under the
Thayer-Martin Agar
nonsterile sites microscope for direct identification of the bacterial agent. More or
Chocolate + Factors X (Heme) less, if you can see the organism DIRECTLY, it is the GOLD
Haemophilus influenzae STANDARD.
And V (NAD) Dr. Rubio
Staphylococcus aureus Mannitol Salt Agar A 39/M consults because of chronic cough of one month. Sputum
Eosin Methylene Blue Agar culture reveals colonies first observed after two weeks of incubation.
Escherichia coli
(+) green metallic sheen The colonies appear rough, dry, and buff colored. What is the most
OTHER MEDIA FOR BACTERIAL GROWTH (JAWETZ) likely organism?
A. Mycobacterium tuberculosis
Agar Bacteria Isolated
B. Mycoplasma pneumoniae
Löwenstein-Jensen, C. Streptococcus pneumoniae
Mycobacterium tuberculosis
Middlebrook D. Haemophilus influenzae
Vibrio cholerae (yellow
Thiosulfate Citrate Bile colonies)
Salts Sucrose (TCBS) Vibrio parahaemolyticus GUIDE QUESTION 7
(green colonies) https://qrs.ly/jqck681
Bordet-Gengou /
Bordetella pertussis
Regan-Lowe agar
Buffered charcoal-yeast
Legionella pneumophila
extract
MOLECULAR TESTS
Skirrow’s medium Campylobacter
Stuart’s medium Helicobacter pylori • nucleic acid amplification tests, nucleic acid probes, and nucleic
Barbour-Stoenner-Kelly acid sequence analysis
Borrelia burgdorferi • highly specific, quite sensitive and much faster than culture
(BSK)
Eaton Mycoplasma pneumoniae • especially useful for those bacteria that are difficult to culture
such as Chlamydia and Mycobacterium species
Cetrimide Pseudomonas aeruginosa
Xylose-Lysine-
Salmonella, Shigella ✔GUIDE QUESTION
Deoxycholate (XLD)
Which of the following molecular techniques represents a variation of
Ellinghausen-McCullough- the polymerase chain reaction, involving the use of an enzyme to
Johnson-Harris (EMJH) / Leptospira interrogans convert viral RNA or messenger RNA to DNA prior to amplification?
Fletcher’s A. Reverse transcriptase PCR
Cary-Blair Vibrio B. Real-time PCR
Cefsulodin-Irgasan- C. Branched-chain
Yersinia D. DNA assay Southern blot
Novobiocin (CIN)
X. PARADE OF ANTIMICROBIALS
I am placing this section here to bridge micro to some principles of pharmacology. This section is not intended to replace the antimicrobials section of your
pharmacology handout. Meanwhile, please note that it is important for you to be equipped with your knowledge of pharmacology of antibiotics when taking the
micro exam (day 1) – even if the actual pharma exam is scheduled the following week. Do not be surprised if the micro exam will be pharma-intense, e.g. antibiotic,
mechanisms of resistance.
Anecdote: The Boards once asked almost 50-60% antimicrobials questions in a micro exam.
Dr. Calderon
MECHANISMS OF ACTION
SITES OF ACTION OF ANTIMICROBIALS

Figure 37.1. Brenner GM, Stevens CW. Pharmacology. 5TH ed. Philadelphia: Elsevier; 2018.
BLOOD-BRAIN BARRIER PENETRABILITY --- MEMORIZE! Drug Mechanism of Resistance
Excellent with or without Good only with Hydrolysis, mutant penicillin-
Beta-lactams
inflammation inflammation binding protein (PBP)
• Sulfonamides • Penicillins Tetracycline Active efflux from cell
• Chloramphenicol • Cephalosporins: cefuroxime Aminoglycosides Inactivation by enzymes
• Trimethoprim (2nd gen); 3rd gen Overproduction of the target site
Sulfonamides
• Metronidazole parenteral (except of the drug
• Rifampicin Cefoperazone); 4th gen Fluoroquinolones Mutant DNA gyrase
• Isoniazid • Imipenem + Cilastatin Chloramphenicol Reduced uptake into cell
• Fluconazole • Meropenem Vancomycin Reprogramming of D-ala-D-ala
• Flucytosine • Aztreonam Quinupristin Ribosomal methylation
• Ciprofloxacin Macrolides,
RNA methylation, drug efflux
• Vancomycin Erythromycin
Minimal or not good even No passage even with
with inflammation inflammation ✔GUIDE QUESTION
• Aminoglycosides • Polymyxins When combined with the beta-lactamase inhibitor tazobactam, this
• Tetracyclines • 1st and 2nd gen penicillin possesses the broadest antibacterial spectrum among its
kind. Which antibacterial is described?
• Lincosamides cephalosporins
A. Ampicillin C. Piperacillin
• Macrolides • Amphotericin B B. Amoxicillin D. Ticarcillin
MECHANISMS OF ANTIMICROBIAL RESISTANCE
Piperacillin is broad-spectrum β-lactam antibiotic of the
ureidopenicillin class. Piperacillin and other ureidopenicillins
have a polar side chain that allows penetration into gram-
negative bacteria and reduces susceptibility to cleavage by gram-
negative beta-lactamases. These properties confer activity
against Pseudomonas aeruginosa. Piperacillin, therefore, is
sometimes referred to as an ‘anti-pseudomonal penicillin’.
Piperacillin is most commonly used in combination with the beta-
lactamase inhibitor Tazobactam (Piperacillin-Tazobactam),
which enhances piperacillin's effectiveness by inhibiting many
beta lactamases to which it is susceptible.
✔GUIDE QUESTION Which antibacterial agent (or combination of antibacterial agents) is

A 28-year-old Caucasian male with cystic fibrosis developed generally anti-pseudomonal?
Pseudomonas aeruginosa pneumonia. Sensitivity studies showed A. Amoxicillin + clavulanic acid
resistance to levofloxacin. Which of the following drug resistance B. Aztreonam
mechanisms is most likely responsible for this? C. Trimethoprim-sulfamethoxazole
A. Production of ESBL D. Vancomycin
B. Alteration of gyrases Pseudomonal infections are increasingly resistant to certain
C. Production of acetyltransferases antibiotics, and the organism may acquire resistance during
D. Decreased ribosomal binding therapy. Two agents from different classes should be used when
Two mechanisms of quinolone resistance have been established to the risk of antibiotic resistance is high (e.g. in severe sepsis,
date: alterations in the targets of quinolones, and decreased septicemia, and inpatient neutropenia).
accumulation due to impermeability of the membrane and/or an
overexpression of efflux pump systems.
Pseudomonas infection can be treated with a combination of an Enterobius causes autoinfection via the mechanism known as
antipseudomonal beta-lactam (e.g. penicillin or cephalosporin) retroinfection. The adult forms of this nematode reside in the cecum of
and an aminoglycoside. Carbapenems (e.g. imipenem, the large intestine. After undergoing sexual intercourse, the male dies
meropenem) with antipseudomonal quinolones may be used in while the female travels through the colon up to the perianal folds to
conjunction with an aminoglycoside. deposit its eggs. This explains the pruritus ani symptoms of this
condition and the presence of D-shaped eggs at the perianal folds.
Antibiotics that have activity against P. aeruginosa include:
Normally, fecal-oral transmission will cause the start over of the life cycle.
• Aminoglycosides (Gentamicin, Amikacin, Tobramycin, but not
But some eggs will hatch at the perianal folds. Then, the larvae will enter
Kanamycin)
the anus and travel to the colon to develop into adult worms causing
• Quinolones (Ciprofloxacin, Levofloxacin, but not Moxifloxacin)
autoinfection.
• Cephalosporins (Ceftazidime, Cefepime, Cefoperazone, Dr. Rubio
Cefpirome, Ceftobiprole, but not Cefuroxime, Cefotaxime, or • Hyperinfection or Superinfection
Ceftriaxone) o Infected individual is further infected with same species
• Antipseudomonal Penicillins: Carboxypenicillins (Carbenicillin
leading to massive infection (e.g. Strongyloides, Capillaria,
and Ticarcillin), and Ureidopenicillins (Mezlocillin, Azlocillin,
and Piperacillin). P. aeruginosa is intrinsically resistant to all Ascaris)
other Penicillins.
• Carbapenems (Meropenem, Imipenem, Doripenem, but not MODES OF TRANSMISSION
Ertapenem) • Ingestion of contaminated food and water
• Polymyxins (Polymyxin B and Colistin) • Skin penetration
• Monobactams (Aztreonam) • Arthropod vectors
Note: Memorize this list. • Congenital transmission
• Inhalation of airborne eggs (seen only in Enterobius sp)
• Sexual intercourse
MEDICAL PARASITOLOGY
REFERENCES:
Medical Parasitology in the Philippines by Vicente Belizario and Winifreda de Leon, 2015, Published: University of the
Philippines Press
ARTHROPODS
CDC DPDx, 2019 (https://www.cdc.gov/dpdx/az.html)
WHO Fact Sheets, 2020 (https://www.who.int/news-room/fact-sheets)
I am placing arthropods first as a nudge so you won’t forget studying
them!
GENERAL CONSIDERATIONS Dr. Calderon
For Parasitology, the website www.cdc.gov can be *very* helpful! If you ✔GUIDE QUESTION
want clearer views of the life cycle diagrams and explicit annotations, A 38/M college professor complains of intense itchy, painful, red
then this is the site to visit. I have decided to lead you to this resource for streaks between his fingers and in the groin area. The patient reports
some more useful and practical information, although I think you can that the itchiness seems to be worse at night. He lives in an in-campus
treat this step as optional. housing for University staff. Several of his housemates have presented
Dr. Calderon with similar problems over the last couple of weeks.
INTRODUCTION TO
PARASITOLOGY
https://qrs.ly/hzck6a0
TYPES OF PARASITES What is the most likely etiology?

LOCATION A. Microsporum C. Ixodes
B. Sarcoptes D. Pediculus
• Lives inside the body of the host
Endoparasite The most likely diagnosis here is scabies. Human scabies is caused
• Presence in host connotes INFECTION
by cutaneous infestation of Sarcoptes scabiei var. hominis, the
• Lives outside the body of the host
Ectoparasite ‘human itch mite’. The mite burrows into the upper layer of the
• Presence in host connotes INFESTATION skin where it thrives and lays eggs.
HOST RELATIONSHIP The most common symptoms of scabies
Obligate • Need a host at some stage of their life cycle are pruritus and acneiform rashes.
Parasite to complete development and propagation The scabies mite usually is spread by
Facultative • May exist in a free-living state but becomes direct, prolonged skin-to-skin contact
Parasite parasitic when the need arises with a person who has scabies. Its
distribution in the finger webs, wrist,
axillae, areolae, umbilicus, lower
TYPES OF HOSTS abdomen, genitalia, and buttocks is
Definitive or commonly referred as the circle of
• Parasite attains sexual maturity Hebra.
Final Host Dr. Calderon
Intermediate The physician requests for mineral oil prep of the skin scrapings. What
• Harbors the asexual or larval stage
Host is the most likely microscopic finding?
• Parasite does not develop further to later A. Mites
Paratenic Host B. Amastigotes and lymphocytes
stages but remains alive and is able to
C. Lice
infect another susceptible host D. Hyphae with conidia
• Allow life cycle to continue and become
Reservoir Host Scabies is usually diagnosed based on the usual appearance and
additional sources of human infection
distribution of the rash and the presence of burrows.
A good example of your paratenic hosts are wild pigs. Usually, Whenever possible, scabies should be confirmed by identifying the
mammals will develop paragonimiasis when they eat the metacercariae mite or mite eggs or fecal matter (scybala). This is done by careful;
of Paragonimus westermani found in crayfish and freshwater crabs removal of the mite from the end of its burrow (using a needle tip)
(Sundathelphusa philippina). However, in wild pigs, the ingested or to microscopically examine skin scrapings for mites, eggs, or
metacercariae does not develop into adult worms. Instead, they reinfect scybala. However, it is possible that a person is still infested even
the muscles of wild pigs as metacercariae AGAIN! Thus, when man eats if mites, eggs, or scybala cannot be found. There are occasions
the metacercariae-infected muscles, these will excyst in the intestine and when that an otherwise healthy may harbor between 10 and 15
invade the lungs to cause paragonimiasis in humans. In conclusion, mites.
paratenic hosts are actually troublesome when initiating ecological Dr. Calderon
efforts in controlling the spread of parasitic organisms. What is the treatment for this infection?
Dr. Rubio
A. Nifurtimox
SPECIAL TYPES OF INFECTION B. Clotrimazole
• Autoinfection C. Betamethasone
o Infected individual becomes his own direct source of infection D. Permethrin
(e.g. Enterobius, Strongyloides, Capillaria) Scabicide lotion or cream should be applied to all areas of the
body - from the neck down to the feet and toes.
Also, when treating young children and infants, scabicide lotion or
cream also should be applied to their entire head and neck. This is
because scabies can affect their face, scalp, neck, and the rest of BEDBUGS
their body. The medication is left on for the recommended time https://qrs.ly/18bp7r6
before washing it off. Note, however, that only permethrin or
sulfur ointment may be used in infants.
Dr. Calderon
Anticipatory guidance points to consider:
• Wearing of clean clothing Drugs and MOA
• Examining and treating close personal and sexual contacts → Permethrin: neuronal membrane depolarization via Na+
those who have had direct prolonged skin-to-skin contact with channels
a person with scabies within one month Malathion: acetylcholinesterase inhibitor
• Concurrent treatment of all persons infested → to prevent Lindane: blocks GABA channels → neurotoxicity
reinfestation Dr. Calderon
Dr. Calderon
ARTHROPODS OF MEDICAL IMPORTANCE
AS INDIRECT CAUSES OF INJURY (VECTORS OF DISEASE)
Below is the table containing the common vectors of microbial diseases of
SCABIES medical and public health importance. I hope this will be helpful for your
https://qrs.ly/onbp7pa quick review of the different vectors of the various diseases
Dr. Rubio
Carried Disease –
Organism Scientific Name
Pathogen
ARTHROPODS OF MEDICAL IMPORTANCE Epidemic typhus – R
AS DIRECT CAUSES OF INJURY Human body
Pediculus prowazekii
Scientific humanus Trench fever – B quintana
Organism Disease Features louse
Name corporis Relapsing fever – B
Pediculus Causes pediculosis of the recurrentis
humanus scalp and hair (kuto) Plaque – Yersinia pestis
Oriental rat Xenopyslla
capitis (+) nits (eggs) are seen on Endemic typhus – R typhi
flea cheopis
Hymenolepis diminuta
(head louse) hair shafts
Dengue virus
Pediculus Causes pediculosis of the
Yellow fever Yellow fever virus
Lice humanus body Aedes
mosquito Chikungunya virus
corporis (+) nits (eggs) are seen on Zika virus
(body louse) hair shafts Culex
Causes pediculosis of the - Japanese encephalitis
Pthirus pubis tritaeniorhynchus
groin Anopheles
(pubic or crab
Most infectious sexually- - minimus Malaria – Plasmodium sp.
louse)
transmitted agent (Lentz) flavirostris
Causes cimicosis Confused Tribolium
Bedbugs Cimex Hymenolepis nana
(+) linear pruritic lesions beetle confusum
Pulex irritans Causes pulicosis Cat flea
Ctenocephalides
Flea felis
(human flea) (+) zigzag pruritic lesions Dipylidium caninum
Sarcoptes Causes scabies (a.k.a seven- Ctenocephalides
Dog flea
scabiei var. year itch) canis
Mites hominis (+) burrows between digits Assassin /
Panstrongylus American trypanosomiasis /
Mite infection associated Kissing /
Demodex Rhodnius Chagas disease –
with facial makeup materials Reduviid
Triatoma Trypanosoma cruzi
bugs
Can cause ascending
Ticks Dermacentor West African sleeping
paralysis sickness – Trypanosoma
Causes Myiasis brucei gambiense
Maggots of Sarcophaga, Tsetse fly Glossina
(+) maggots emerging from East African sleeping
flies Calliphora
sites of bites sickness – Trypanosoma
Mites and ticks are NOT insects! They are arachnids. They possess brucei rhodesiense
eight (8) legs (vs the six-legged morphology of insects). Phlebotomus,
Sandfly Leishmania sp.
Dr. Rubio Lutzomyia
River blindness –
Blackfly Simulium
Onchocerca volvulus
PEDICULOSIS Deer fly or
African eye worm disease
https://qrs.ly/pabp7pb Mango fly or Chrysops
(loiasis) – Loa loa
Horse fly
Freshwater Sundathelphusa Paragonimus westermani
crab philippina (contains metacercariae)
Oncomelania Schistosoma japonicum
Freshwater
hupensis (origin of the free-living
snail
quadrasi cercaria)
PARASITES OF MEDICAL IMPORTANCE
© Topnotch Medical Board Prep
PROTOZOA I. ENTAMOEBA HISTOLYTICA

PROTOZOAN INFECTIONS PARASITE BIOLOGY
• Protozoans are classified as unicellular eukaryotic organisms • Pseudopod-forming non-flagellated protozoa
• Common in underdeveloped tropical and subtropical countries • Most invasive parasite among Entamoeba
o Poor sanitary conditions and hygienic practices
o Inadequate control of the vectors INFECTIVE DIAGNOSTIC
TRANSMISSION
TREATMENT OF PROTOZOAN INFECTIONS STAGE STAGE
• Protozoal diseases are less easily treated than bacterial Trophozoites,
infections Fecal-oral route Mature cysts mature cysts,
• Many of the antiprotozoal drugs cause serious toxic effects in the immature cysts
host Cyst
• Most have not proved to be safe for pregnant patients • Infective form that is ingested: quadrinucleated cyst
• Smaller than Entamoeba coli cyst
OVERVIEW – PROTOZOA
• Has four nuclei (vs 8 nuclei of Entamoeba coli)
Type and
Species Disease • Excysts to trophozoite form in the intestines
Location
• Predominates in non-diarrheal formed stools
Entamoeba histolytica Amebiasis
Giardia lamblia Giardiasis Trophozoite
Intestinal tract
Cryptosporidium • Motile, invasive form: able to colonize and invade the large
Cryptosporidiosis
parvum bowels
Urogenital Trichomonas • Nucleus has a small central nucleolus and fine chromatin
Trichomoniasis
tract vaginalis granules along the border of the nuclear membrane
Plasmodium spp. Malaria • Found in diarrheal stools and within the intestinal and
Toxoplasma gondii Toxoplasmosis extraintestinal lesions
Blood and
Trypanosoma cruzi Chagas disease • Characteristically contain ingested red blood cells
tissue
Trypanosoma brucei Sleeping sickness (erythrophagocytosis) → hematophagous
Leishmania spp. Leishmaniasis
CORRELATION INTERNAL MEDICINE / PEDIATRICS • Ameboma
Presence of trophozoites in fecalysis is NOT an indication for o Mass-like lesion in abdomen associated with dysentery
initiating treatment for amebiasis. REMEMBER: there are also o Granulomatous lesion that may form in the cecal or
commensal ameba present in the GI tract that also form rectosigmoid areas
trophozoites. A clinical indication would be the presence of • Amebic liver abscess (ALA)
erythrophagocytosis – since this is a sign that there is o Most common extraintestinal form
pathogenic ameba in the GI tract (E histolytica) o Usually in the posterosuperior aspect of the right lobe. This
is according to majority of references. But according to
Schwartz, it is the superior-anterior aspect.
o Anchovy sauce-like aspirate
• Secondary amebic meningoencephalitis (SAM)
o Rare complication of amebiasis
o Trophozoites travel into the circulation → blood-brain barrier
→ CNS dysfunction
Primary amebic meningoencephalitis (PAM) – Naegleria fowleri
Secondary amebic meningoencephalitis (SAM) – Entamoeba
LIFE CYCLE OF ENTAMOEBA HISTOLYTICA histolytica
Dr. Rubio
DIAGNOSIS
• Stool O&P: Microscopic detection of trophozoites with ingested
RBC and cysts in stool specimens
o Cannot distinguish morphologically among the closely related
commensals E. dispar and E. moshkovskii
• Stool culture – Robinson’s and Inoki medium, Diamond medium

• PCR – allows differentiation of E. histolytica from the
nonpathogenic E. dispar and E. moshkovskii
• ALA – detection of antibodies in serum, ultrasound, CT, MRI
TREATMENT
• Tissue Amebicides
o Act on organisms in the bowel wall and the liver
o e.g. Metronidazole (DOC for invasive amebiasis), tinidazole,
chloroquine, emetines
Cysts and trophozoites are passed in feces (1). Cysts are typically found in • Luminal Amebicides
formed stool, whereas trophozoites are typically found in diarrheal stool. o Act only in the lumen of the bowel
Infection with Entamoeba histolytica (and E. dispar) occurs via ingestion of o e.g. Diloxanide furoate (DOC for asymptomatic cyst passers),
mature cysts (2) from fecally contaminated food, water, or hands. Exposure iodoquinol, paromomycin
to infectious cysts and trophozoites in fecal matter during sexual contact may
also occur. Excystation (3) occurs in the small intestine and trophozoites (4)
are released, which migrate to the large intestine. Trophozoites may remain DISEASE FORM DRUG(s) OF CHOICE
confined to the intestinal lumen (A: noninvasive infection) with individuals Asymptomatic
Luminal agent (diloxanide furoate,
continuing to pass cysts in their stool (asymptomatic carriers). Trophozoites intestinal
iodoquinol, paromomycin)
can invade the intestinal mucosa (B: intestinal disease), or blood vessels, colonization
reaching extraintestinal sites such as the liver, brain, and lungs (C: Amebic colitis Metronidazole or Tinidazole
extraintestinal disease). Trophozoites multiply by binary fission and produce (dysentery) plus Luminal agent*
cysts (5), and both stages are passed in the feces (1). Cysts can survive days
to weeks in the external environment and remain infectious in the
Metronidazole or Tinidazole
environment due to the protection conferred by their walls. Trophozoites followed by Luminal agent*
passed in the stool are rapidly destroyed once outside the body, and if Amebic liver Percutaneous or surgical drainage if:
ingested would not survive exposure to the gastric environment. (Source: CDC) abscess • Abscess is 5 cm or greater diameter
• if they are in the left lobe
PATHOGENESIS: VIRULENCE FACTORS • no clinical response to medical therapy
• Gal/GalNAc Lectin mediates adherence
Just remember two drugs here: METRONIDAZOLE and DILOXANIDE
• Amebapores for penetration FUROATE.
• Cysteine proteases for cytopathic effect Dr. Calderon
SPECTRUM OF DISEASE: Amebiasis COMMENSAL AMOEBAE OF MINOR IMPORTANCE

• Cyst carrier state (NICE TO KNOW)
• Amebic colitis • Non-invasive and do not cause disease
o Dysentery without fever • Reproduce by binary fission
o Flask-shaped, narrow-necked colon ulcers • Cysts pass through the acidic stomach unscathed, protected by
o Most serious complication: perforation and SBP their cyst wall
According to Robbins and Cotran Pathologic Basis of Disease, once • Excystation occurs in the small intestine
the E histolytica reaches the lamina propria it will now perform “lateral
burrowing.” This explains the Erlenmeyer flask-like ulcers.
Dr. Rubio
•
• Morphologically similar to E. histolytica but
Entamoeba
their DNA and ribosomal RNA are
dispar
different
Entamoeba • Similar to E. histolytica but is much smaller
hartmanni and does not ingest RBC, sluggish
• Cosmopolitan in distribution, harmless
Entamoeba inhabitant of colon, trophozoite has no
coli ingested RBCs, has a larger cyst and greater
number of nuclei (8) than E. histolytica (4)
Entamoeba • Parasite of pigs and monkey, cyst is
polecki uninucleated G. duodenalis trophozoites in Kohn stain, resembling an “old man
• Has no cyst stage and does not inhabit the with eyeglasses” and cyst.
intestines, found in the mouth, moves
Entamoeba quickly and has numerous blunt LIFE CYCLE OF GIARDIA LAMBLIA
gingivalis pseudopodia, transmission is via kissing,
droplet spray or sharing utensils,
numerous food vacuoles with leukocytes
Endolimax
• Small size, sluggish movement
nana
Iodamoeba • No peripheral chromatin granules on the
butschlii nuclear membrane, large glycogen body
II. FREE LIVING AMEBA

• Free-living amebae are common in the environment as
trophozoites
ORGANISM DISEASE AND MANAGEMENT
• Can invade nasal mucosa of healthy
people swimming in warm fresh water
(hot springs)
Naegleria fowleri
• Trophozoites penetrate the cribriform
plate and migrate to the brain via the
olfactory nerves
• Causes Primary amebic
meningoencephalitis (PAM), a
nearly fatal disease, in healthy people
• Treatment: Pentamidine (DOC),
Amphotericin B + Clotrimazole
• Can cause sight-threatening Amebic
Acanthamoeba keratitis in healthy people in
castellanii. association with contact lens
o Forms dendriform epithelial pattern
on cornea
• Can cause Granulomatous amebic
encephalitis (GAE) in Cysts are resistant forms and are responsible for transmission of giardiasis.
immunocompromised patients Both cysts and trophozoites can be found in the feces (diagnostic stages) (1).
• DOC: Pentamidine, ketoconazole, or The cysts are hardy and can survive several months in cold water. Infection
flucytosine occurs by the ingestion of cysts in contaminated water, food, or by the fecal-
oral route (hands or fomites) (2). In the small intestine, excystation releases
trophozoites (each cyst produces two trophozoites) (3). Trophozoites
III. GIARDIA LAMBLIA/ DUODENALIS / multiply by longitudinal binary fission, remaining in the lumen of the
INTESTINALIS proximal small bowel where they can be free or attached to the mucosa by a
ventral sucking disk (4). Encystation occurs as the parasites transit toward
PARASITE BIOLOGY
the colon. The cyst is the stage found most commonly in non-diarrheal
• Flagellate that lives in the duodenum and upper small intestine feces (5). Because the cysts are infectious when passed in the stool or shortly
• Falling leaf motility afterward, person-to-person transmission is possible. While animals are
• Simple asexual life cycle infected with Giardia, their importance as a reservoir is unclear. (Source:
• Covered with variant surface proteins → antigenic variation CDC)
• Direct oral-anal sexual contact among MSM increases risk
PATHOGENESIS
INFECTIVE DIAGNOSTIC • Adhesive disc and lectin facilitate attachment to avoid
TRANSMISSION peristalsis
STAGE STAGE
Trophozoites, • Villous flattening, crypt hypertrophy and disruption of
Fecal-oral route Cysts cytoskeleton
cysts
• Ultimately leads to enterocyte apoptosis
Cyst • Trophozoite causes inflammation of the duodenal mucosa →
• Infective form: ingestion of cysts malabsorption of protein and fat
• Found in diarrheal and formed stools
SPECTRUM OF DISEASE: Giardiasis
Trophozoite • Risk factors
• Each cyst excysts to form 2 trophozoites o History of travel, history of drinking untreated surface water,
• Pear-shaped with two nuclei, four pairs of flagella, and a suction children at daycare
disk with which it attaches to the intestinal wall • Acute Infection
• Found only in diarrheal stools o Abdominal pain, diarrhea and excessive flatus, smelling like
rotten eggs (hydrogen sulfide)
• Chronic Infection
o Constipation, weight loss and steatorrhea
DIAGNOSIS SPECTRUM OF DISEASE: Trichomoniasis
• Stool O&P: Demonstration of trophozoites and/or cysts in stool • In females: watery, foul-smelling, yellow-greenish vaginal
specimens discharge accompanied by itching and burning; strawberry
• Direct fecal smear cervix
• Enterotest/duodenal string test: Swallowing a gelatin capsule • In males: frequently asymptomatic; occasionally, urethritis,
attached to a nylon string, one end attached to patient’s cheek → epididymitis, and prostatitis can occur.
trophozoites adhere to the string and can be visualized after
withdrawal DIAGNOSIS
• Saline preparation of vaginal fluid
TREATMENT • Gold standard used to be Culture (Diamond’s modified medium,
• Tinidazole single dose is agent of choice Feinberg and Whittington culture medium)
• Metronidazole (x 5-7 days) or Nitazoxanide (x 3 days) are • Current gold standard: NAATs
alternatives
IV. TRICHOMONAS VAGINALIS TREATMENT

PARASITE BIOLOGY • Single oral dose of 2 grams (four 500 mg tablets) of
Metronidazole
• The only established urogenital protozoan
• Treat sexual partner
• Exists only as a trophozoite
• Most prevalent non-viral sexually transmitted infection
• Pear-shaped, flagellated trophozoites V. LEISHMANIA SPP.
• The trophozoite is transmitted through coitus and no cyst form Leishmaniasis
is known • Transmitted by sandfly (Phlebotomus or Lutzomyia)
• 2 forms: amastigotes, promastigotes
INFECTIVE DIAGNOSTIC
TRANSMISSION
STAGE STAGE INFECTIVE DIAGNOSTIC
TRANSMISSION
Sexual intercourse Trophozoites Trophozoites STAGE STAGE
Transmitted by
Promastigote Amastigote
LIFE CYCLE OF TRICHOMONAS VAGINALIS sandflies
• Diagnosis:
o Microscopic demonstration from lesion and tissue scrapings,
aspirates, or biopsy
o Montenegro Skin test (Leishmanin skin test) – identify
exposure
• Conventional therapy:
o Sodium stibogluconate (Pentavalent antimonial; antimony
is a chemical element with the symbol Sb (from Latin: stibium)
and atomic number 51)
o Second-line agents: Amphotericin B, Pentamidine
• Post-kala azar dermal leishmaniasis (PKDL) – sequela of visceral
leishmaniasis
LEISHMANIASIS CUTANEOUS MUCO-CUTANEOUS VISCERAL

L. tropica
Causative Agent L. braziliensis L. donovani
L. mexicana
• Kala-azar
• Oriental sore • Espundia
• Oriental button
Local Name
• Nasal stuffiness, discharge,

• Papulonodular with ulceration, • Fever, weight loss,
epistaxis, nodule on septum/
Presentation surrounding induration and raised hepatosplenomegaly,
turbinate, septal ulceration
border pancytopenia
(“tapir nose”)
Diagnostic sample • Scrapings of ulcer base • Snips/ Scrapings • Splenic aspiration
VI. TRYPANOSOMA CRUZI • Xenodiagnosis

Remember two things about this disease:
o Allowing an uninfected, laboratory-raised reduviid bug to feed
on the patient
This is American trypanosomiasis or Chagas disease. Tom Cruz is an
American!
SPECTRUM OF DISEASE:
This is Chagas disease, not sleeping sickness! America does not sleep!
Chagas Disease (American Trypanosomiasis)
(Sleeping sickness if African trypanosomiasis.)
Dr. Calderon • Acute Chagas’ disease
PARASITE BIOLOGY o Focal or diffuse inflammation mainly affecting myocardium
• Blood and tissue protozoan o Unilateral palpebral swelling (Romaña sign)
• All 4 forms: amastigote (tissue), promastigote, epimastigote, o Nodule near bite, furuncle-like (chagoma)
trypomastigote (blood) o Fever, LAD and hepatosplenomegaly
• Transmitted by reduviid bug in their feces o Resolves in about 2 months
o When the feces touch mammalian conjunctivae, oral/nasal • Chronic disease
mucosa, skin abrasions o Cardiac (rhythm disturbances, cardiomyopathy, congestive
heart failure)
DIAGNOSTIC o GIT (megaesophagus, megacolon)
TRANSMISSION INFECTIVE STAGE
STAGE o Death is usually due to cardiac arrhythmias or congestive heart
Reduviid bug Metacyclic Trypomastigotes failure
(Triatoma) bite trypomastigotes in blood o Leading cause of CHF in Latin America
TREATMENT
• Nifurtimox
• Alternative: Benznidazole
• There is no effective drug against the chronic form.
Transmitted by the reduviid bug. Trypanosoma cruzi trypomastigotes. MEMORY AID CHAGAS DISEASE TREATMENT
Romaña sign of acute Chagas disease. BENZ, WITH A FUR COAT ON
Benznidazole
LIFE CYCLE OF TRYPANOSOMA CRUZI Nifurtimox
✔GUIDE QUESTION
Infection with which of the following is associated with the
development of megacolon?
A. Oxyuriasis
B. Trypanosomiasis
C. Amoebic colitis
D. Isosporiasis
Trypanosomiasis cruzi can lead to a dilated esophagus or colon,
leading to difficulties with eating or passing stool.
Dr. Calderon
VII. TRYPANOSOMA BRUCEI

PARASITE BIOLOGY
• Blood and tissue protozoan
• Only 2 forms: epimastigote, trypomastigote
• Remarkable antigenic variation of surface glycoproteins
• 2 members
An infected triatomine insect vector (or “kissing bug”) takes a blood meal and o Trypanosoma brucei gambiense (West) – Chronic
releases trypomastigotes in its feces near the site of the bite wound. o Trypanosoma brucei rhodesiense (East) – Acute
Trypomastigotes enter the host through the wound or through intact
E (east) R (rhodesiense)
mucosal membranes, such as the conjunctiva (1). Common triatomine vector
ER cases are usually ACUTE CASES! Moreover, East African
species for trypanosomiasis belong to the genera Triatoma, Rhodnius,
trypanosomiasis is MORE FATAL than West African trypanosomiasis
and Panstrongylus. Inside the host, the trypomastigotes invade cells near the Dr. Rubio
site of inoculation, where they differentiate into intracellular
amastigotes (2). The amastigotes multiply by binary fission (3) and INFECTIVE DIAGNOSTIC
TRANSMISSION
differentiate into trypomastigotes, and then are released into the circulation STAGE STAGE
as bloodstream trypomastigotes (4). Trypomastigotes infect cells from a Tsetse fly Metacyclic Trypomastigotes
variety of tissues and transform into intracellular amastigotes in new (Glossina) bite trypomastigotes in blood
infection sites. Clinical manifestations can result from this infective cycle. The
bloodstream trypomastigotes do not replicate (different from the African
trypanosomes). Replication resumes only when the parasites enter another
cell or are ingested by another vector. The “kissing bug” becomes infected by
feeding on human or animal blood that contains circulating parasites (5).
The ingested trypomastigotes transform into epimastigotes in the vector’s
midgut (6). The parasites multiply and differentiate in the midgut (7) and
differentiate into infective metacyclic trypomastigotes in the hindgut (8).
(Source: CDC)
Transmitted by tsetse fly bite. Trypanosoma brucei trypomastigotes.

PATHOGENESIS
• Myocardial, glial, and reticuloendothelial cells are frequent sites MEMORY AID SLEEPING SICKNESS
• Cardiac muscle is the most frequently and severely affected WaGER!
tissue West = Gambian
• Neuronal damage leads to cardiac arrhythmias and loss of tone East = Rhodesian
in the colon (megacolon) and esophagus (megaesophagus)
DIAGNOSIS
• Thick and thin blood smears with Giemsa stain – direct
visualization of parasites
• Stained BMA or muscle biopsy
• Culture of the organism on special medium
LIFE CYCLE OF TRYPANOSOMA BRUCEI DIAGNOSIS
• Thick and thick blood films stained with Giemsa
• Trypomastigotes in expressed fluid from chancre, lymph node
aspirate, and CSF
TREATMENT
FIRST-LINE ALTERNATIVE
DISEASE STAGE
DRUGS DRUGS
Suramin,
Early Pentamidine
eflornithine
West
Melarsoprol,
African CNS
Eflornithine eflornithine-
involvement
nifurtimox
Early Suramin Pentamidine
East
CNS
African Melarsoprol --
involvement
MEMORY AID TREATMENT OF SLEEPING SICKNESS
It SURe is nice to go to SLEEP. MELAtonin helps with SLEEP.
SURAmin-MELArsoprol is used for African SLEEPing sickness.
During a blood meal on the mammalian host, an infected tsetse fly
(genus Glossina) injects metacyclic trypomastigotes into skin tissue. The TO SUMMARIZE
parasites enter the lymphatic system and pass into the bloodstream (1). Trypanosoma brucei Trypanosoma brucei
Inside the host, they transform into bloodstream trypomastigotes (2), are gambiense rhodesiense
carried to other sites throughout the body, reach other body fluids (e.g.,
• Causes the disease along
lymph, spinal fluid), and continue the replication by binary fission (3). The • Found in the arid regions of
entire life cycle of African trypanosomes is represented by extracellular water courses in west
east Africa
stages. The tsetse fly becomes infected with bloodstream trypomastigotes Africa
when taking a blood meal on an infected mammalian host (4, 5). In the fly’s • Causes a more acute,
midgut, the parasites transform into procyclic trypomastigotes, multiply by • Runs a low-grade chronic rapidly progressive disease
binary fission (6), leave the midgut, and transform into epimastigotes (7). course over a few years that, if untreated, is usually
The epimastigotes reach the fly’s salivary glands and continue multiplication fatal within several months
by binary fission (8). The cycle in the fly takes approximately 3 weeks.
Rarely, T. b. gambiense may be acquired congenitally if the mother is
• Transmitted by Glossina • Transmitted by Glossina
infected during pregnancy. (Source: CDC) palpalis (or riverine morsitans (or savannah
tsetse) tsetse)
PATHOGENESIS • Treatment: • Treatment:
• Trypomastigotes spread from the skin → blood → lymph nodes Early stage: Pentamidine Early stage: Suramin
→ brain CNS involvement: CNS involvement:
• The typical somnolence (sleeping sickness) progresses to coma Eflornithine Melarsoprol
as a result of a demyelinating encephalitis (ascending reticular
activating system or ARAS, brainstem) VIII. PLASMODIUM
• In the acute form, a cyclical fever spike (approximately every 2 PARASITE BIOLOGY
weeks) occurs that is related to antigenic variation • Most important parasitic disease in man
• Rhodesian more rapid and fatal than gambian • Blood and tissue sporozoan
Microbes with ANTIGENIC VARIATION as a means to escape the • Asexual life cycle consists of schizogony and gametogony
immune response of the host: • Sexual life cycle involves sporogony
Giardia lamblia, Trypanosoma brucei, Borrelia recurrentis
Hepatitis C virus INFECTIVE DIAGNOSTIC
TRANSMISSION
Dr. Rubio STAGE STAGE
SPECTRUM OF DISEASE: Bite of infected
HUMAN AFRICAN TRYPANOSOMIASIS female mosquito Trophozoites,
• Early Phase (Hemolymphatic stage) (Anopheles Sporozoites schizont,
§ Indurated skin ulcer (trypanosomal chancre) flavirostris gametocytes
§ Intermittent weekly fever and LAD minimus)
§ Enlargement of the posterior cervical LN (Winterbottom
sign)
LIFE CYCLE OF PLASMODIUM
• Late Phase (Meninoencephalitic stage)

§ Encephalitis → excessive somnolence
§ Deep hyperesthesia (Kerandel sign)
§ Untreated disease is usually fatal as a result of pneumonia
§ Trypanosomes in CSF and plasma cells with cytoplasmic
immunoglobulin globules (Morula cells of Mott)
The malaria parasite life cycle involves two hosts. During a blood meal, a PATHOGENESIS
malaria-infected female Anopheles mosquito inoculates sporozoites into the
• Pathologic findings from the destruction of red blood cells
human host (1). Sporozoites infect liver cells (2) and mature into schizonts
(3), which rupture and release merozoites (4).
o Release of the merozoites and splenic sequestration of infected
cells
Note: in P. vivax and P. ovale, a dormant stage (hypnozoites) (hypnos=sleep,
o Enlarged spleen characteristic of malaria is due to congestion
zoon animal: sleeping animals) can persist in the liver (if untreated) and
cause relapses by invading the bloodstream weeks, or even years later.
of sinusoids with erythrocytes, coupled with hyperplasia of
lymphocytes and macrophages
After this initial replication in the liver (exo-erythrocytic schizogony (A)), the
• People with RBC defects (G6PD, sickle cell) are immune to
parasites undergo asexual multiplication in the erythrocytes (erythrocytic
schizogony (B)). malaria
• Partial immunity based on humoral antibodies that block
Merozoites infect red blood cells (5). The ring stage trophozoites mature into
schizonts, which rupture releasing merozoites (5). Some parasites
merozoites from invading the red cells occurs in infected
differentiate into sexual erythrocytic stages (gametocytes) (7) individuals (premunition)
§ Results to low level of parasitemia and low-grade
Blood stage parasites are responsible for the clinical manifestations of the
disease. The gametocytes, male (microgametocytes) and female
symptoms
(macrogametocytes), are ingested by an Anopheles mosquito during a blood
meal (8). SPECIAL CLINICAL OUTCOMES
The parasites’ multiplication in the mosquito is known as the sporogonic • Recrudescence
cycle (C). While in the mosquito’s stomach, the microgametes penetrate the o Recurrence of symptoms after a temporary abatement (2-4
macrogametes generating zygotes (9). The zygotes in turn become motile weeks)
and elongated (ookinetes) (10) which invade the midgut wall of the mosquito o When the infection persisted undetected in the blood, and then
where they develop into oocysts (11). The oocysts grow, rupture, and release becomes detected again
sporozoites (12), which make their way to the mosquito’s salivary glands. o Seen in P. falciparum, P. knowlesi and P. malariae
Inoculation of the sporozoites (1) into a new human host perpetuates the
malaria life cycle. (Source: CDC)
• Relapse
o Return of a disease after its apparent cessation (1-6 mos) due
to reactivation of hypnozoites
o Seen in P. ovale and P. vivax (with hypnozoite stage)
SPECIES DIFFERENTIATION
P. knowlesi P. falciparum P. vivax P. ovale P. malariae
Asexual cycle 24 hrs 48 hrs 48 hrs 48 hrs 72 hrs
Periodicity Quotidian Malignant tertian Benign tertian Benign tertian Benign quartan
RBC preference All ages All ages Young RBCs Young RBCs Old RBCs
Parasitemia Can be high Highest Low Low Lowest
Trophozoites
Merozoites 16 0 12 – 24 8 6- 12
Round Banana-shaped Large round Small round Compact
Gametocytes
Cerebral malaria No Yes No No No
Recrudescence Yes Yes No No Yes
Relapse No No Yes Yes No
Drug resistance Few Many Few Few Few
DIAGNOSIS
• Thin and thick smears with Giemsa or Wright’s stain
o Thick smear to screen for the presence of organisms
o Thin smear for species identification
• Highest yield when blood samples taken during fever or 2-3
hours after peak
• Malarial rapid diagnostic tests (HRP II, pLDH, aldolase)
• Maurer Dots
Gold standard for diagnosing Plasmodium is direct microscopy with
thin or thick smears. Remember: if you are able to directly observe the o Coarse granulations
etiologic agent it is the GOLD STANDARD. present in red blood
Dr. Rubio cells invaded by P.
MALARIAL DOTS falciparum
• Schuffner Dots
o Punctate granulations present in red blood cells invaded by P.
• Ziemann Dots
ovale and P. vivax
o Fine dots present in
red blood cells
invaded by P.
malariae
MEMORY AID MALARIAL DOTS ALTERNATIVE
CLINICAL SETTING DRUG THERAPY
Schuffner dots = P. Ovale & Vivax DRUG
SOVrang daming dots! Chloroquine-
Maurer dots = coMMa-shaped = P. falciparum sensitive P.
SCHUFFNER MAURER ZIEMANN falciparum and P. Chloroquine -
malariae
• Punctate • Coarse
• Fine dots infections
granulations granulations
P. vivax and P. Chloroquine +
• P. vivax
• P. falciparum • P. malariae ovale infections Primaquine
• P. ovale
Malarone
Infected RBC with 1-2 small chromatin dots → P. falciparum
Uncomplicated
(Atovaquone-
Infected RBC with presence of ring form stage only → P. falciparum infections with Quinine +
Proguanil)
Infected RBC with presence of band form stages → P. malariae chloroquine- Doxycycline or
OR Mefloquine OR
Dr. Calderon resistant P. Clindamycin
Co-Artemether +
falciparum
SPECTRUM OF DISEASE: Malaria Lumefantrine
Artesunate +
• Malaria Attack Cycle: starts with (1) shivering and chills,
Doxycycline / Artemether +
followed by a (2) high fever, followed by (3) sweating and a Severe or
Clindamycin OR Doxycycline /
return to normal temperature. uncomplicated
Mefloquine / Clindamycin OR
• Paroxysmal fever with malaise and bone pains infections with P.
Malarone OR Mefloquine /
• Hemolytic anemia, jaundice and splenomegaly falciparum
Quinidine Malarone
• Parasitic pneumonitis gluconate
• Cerebral malaria: diffuse symmetric encephalopathy
o Malarial or Dürck granulomas PROPHYLAXIS
• Acute renal failure (blackwater fever) DRUG PROPHYLACTIC USE
• Septic shock (algid malaria) Chloroquine Areas without resistant P. falciparum
Areas with chloroquine-resistant P.
Malarone
falciparum
Areas with chloroquine-resistant P.
Mefloquine
falciparum
Doxycycline Areas with multidrug-resistant P. falciparum
Terminal prophylaxis of P. vivax and P. ovale
Primaquine
infections; alternative for primary prevention
IX. BABESIA MICROTI

Babesiosis
• Transmitted by the bite of the Ixodes tick
CLASSICAL MALARIA PAROXYSMS (3 stages) • Clinical presentation:
• Shivering, peripheral vasoconstriction o Influenza-like symptoms, hepatosplenomegaly, hemolytic
Cold Stage • Children: vomiting and febrile convulsions anemia
• Lasts for 15 to 60 minutes o Asplenic patients are affected more severely
• Headache, palpitations, tachypnea, • Diagnosis: Giemsa- stained thin blood smears
epigastric discomfort, thirst, nausea, o Pathognomonic: Intraerythrocytic ring-shaped
Hot stage or vomiting, confusion, delirium trophozoites in tetrads in the form of a Maltese cross
Flush phase • Skin is hot and flushed o No exoerythrocytic phase
• May reach 41°C • Treatment:
• Lasts for 2 to 6 hours o Mild to moderate disease: Atovaquone + Azithromycin
Sweating o Severe disease: Quinidine + Clindamycin
• Defervescence, diaphoresis
Stage
AREAS OF HIGH AREAS OF CHLOROQUINE

ENDEMICITY RESISTANCE
• Palawan
• Palawan
• Kalinga- Apayao
• Davao del Norte
• Ifugao
• Compostela Valley
• Agusan del Sur
Transmitted by Ixodes tick. Maltese cross shown in Giemsa stain.
TREATMENT
• Tissue Schizonticides X. TOXOPLASMA GONDII
o Kill schizonts in the liver PARASITE BIOLOGY
o E.g. primaquine • Tissue protozoan (intracellular)
• Blood Schizonticides • Definitive host is the domestic cat (Felidae)
o Kill these parasitic forms only in the erythrocyte • Humans and other mammals are intermediate hosts
o E.g. chloroquine, quinine • Only stages present in humans: tachyzoites and bradyzoites
• Gametocides
o Kills gametocytes in human blood
o E.g. primaquine
• Sporonticides
o Prevent sporogony and multiplication in the mosquito
o E.g. proguanil, pyrimethamine
PHARMACOLOGY AND LIFE CYCLE -

MALARIA (ANTIMALARIALS,
PATHOPHYSIOLOGY, TREATMENT)
https://qrs.ly/fobp7st Toxoplasma gondii tachyzoites on left.
Tissue cysts filled with bradyzoites on right.
✔GUIDE QUESTION
INFECTIVE DIAGNOSTIC A male neonate is observed to have an enlarged abdomen and is
TRANSMISSION jaundiced. Cranial CT shows multiple calcified lesions in the brain. The
STAGE STAGE
mother relays that during the latter months of her pregnancy, she
• Ingestion of
experienced only mild symptoms including intermittent malaise,
undercooked meat, fatigue, and occasional myalgias. What kind of maternal exposures is
Cysts containing
contaminated food most likely causally linked to the infant's condition?
Oocyst, bradyzoites,
and water A. Consumption of unpasteurized goat cheese
tachyzoite, pseudocysts
• Transplacental B. Mosquito bite
bradyzoite containing C. Contact with feline fecal matter
• Organ
tachyzoites D. Recent visit to a daycare center
transplantation
• Blood transfusion
To diagnose acute and congenital infections, an immune-fluorescence GUIDE QUESTION 8
assay for IgM antibody is used. https://qrs.ly/7hck6ds
Microscopy of Giemsa-stained preparations demonstrates crescent-
shaped trophozoites during acute infections. Cysts may also be seen in
the tissue. CONGENITAL INFECTION SYNDROMES
Congenital infections are diagnosed by detecting T. gondii DNA in INFECTION SYNDROME
amniotic fluid using molecular methods, e.g. PCR. Hydrocephalus, diffuse
Dr. Calderon
PATHOGENESIS intracranial (cerebral)
T. gondii
calcification, chorioretinitis
• Two types of extraintestinal stages:
o Rapidly multiplying tachyzoites
Rubella PDA, sensorineural hearing loss, cataracts
§ Initial and acute stages
§ CMI limits spread Microcephalus, periventricular
o Slowly multiplying bradyzoites calcification
CMV
§ Important in tissue diagnosis
• Preferred diagnostic test: IgM antibody
HSV Vesicular lesions, keratoconjunctivitis
• Formation of tissue cysts most commonly in the skeletal muscle,
myocardium, brain, and retina T. saddle nose, mulberry molars, Hutchinson teeth,
pallidum saber shins, rhagades, Higoumenakis sign
LIFE CYCLE OF TOXOPLASMA GONDII VZV Limb abnormalities, cicatricial lesions
Parvovirus
Hydrops fetalis
B19
XI. CRYPTOSPORIDIUM PARVUM

PARASITE BIOLOGY
• Opportunistic intestinal protozoa
• Undergoes sporogony (produce oocysts), schizogony (produce
merozoites) and gametogony (produce gametocytes)
• Autoinfection in immunocompromised patients
TRANSMISSION
STAGE STAGE
Thick-walled Thick-walled
Fecal-oral route
oocysts oocysts
SPECTRUM OF DISEASE: Toxoplasmosis

• Immunocompetent
o Heterophil-negative mononucleosis
• Immunocompromised Cryptosporidium oocysts.
o Most common: encephalitis LIFE CYCLE OF CRYPTOSPORIDIUM PARVUM
§ Ring enhancing lesions
• Congenital Toxoplasmosis
o Abortion, stillbirth, or neonatal disease with hydrocephalus,
encephalitis, chorioretinitis and hepatosplenomegaly
§ Intracranial calcifications (found at the cerebral area)
Intracranial (intracerebral calcifications): Congenital toxoplasmosis
Periventricular calcifications: Congenital CMV infection
Dr. Rubio
DIAGNOSIS
• Examination of tissue imprints stained with Giemsa
• Sabin-Feldman methylene blue dye test
o Presence of Toxoplasma antibodies in the serum will prevent
the dye from entering the cytoplasm of live tachyzoites
o Positive for Toxoplasma Abs: trophozoites not stained
o Negative for Toxoplasma Abs: blue stained trophozoites
TREATMENT
• Sulfadiazine plus pyrimethamine
• For patients who cannot receive sulfa drugs, clindamycin can
be added to pyrimethamine.
• Prophylaxis for immunocompromised: trimethoprim –
sulfamethoxazole
PATHOGENESIS Wide-necked ulcers: Balantidium coli
• The oocysts excyst in the small intestine, where the trophozoites Narrow-necked ulcers: Entamoeba histolytica
(and other forms) attach to the gut wall. Dr. Rubio
• Presence of Salmonella in the intestines aggravate balantidiases

• Invasion does not occur.
• DOC: Tetracycline, metronidazole
• The jejunum is the site most heavily infested.
SPECTRUM OF DISEASE: Cryptosporidiosis

• Self-limited non-bloody diarrhea (2 to 3 weeks)
• Severe life-threatening diarrhea if CD4 < 200
o Due to autoinfection (thin-walled oocysts infect other
enterocytes)
• Acute and gangrenous cholecystitis
Balantidium coli trophozoite and cyst.
DIAGNOSIS
• Sheater’s sugar floatation, formalin ether concentration
technique (FECT) TOXIC ALGAE
• Kinyoun’s modified acid-fast stain: oocysts appear as red-pink DINOFLAGELLATES –
doughnut-shaped circular organisms in a blue background FLAGELLATED MARINE PROTISTS
TREATMENT HARMFUL ALGAL
• Nitazoxanide - DOC for immuno-competent patients BLOOM (HAB) –
• NO effective drug therapy for severely immunocompromised ASSOCIATED ILLNESS
patients, but paromomycin may be useful in reducing diarrhea. https://qrs.ly/k4bp8y6
HAART for HIV patients
• • Usually considered algae, dinoflagellates are
mostly marine plankton, but they also are
XII. CYCLOSPORA CAYETANENSIS
common in freshwater habitats.
& ISOSPORA BELLI • Algal blooms cause red tide
• Coccidial sporozoa • Most common in the Philippines is Pyrodinium
• Infective and diagnostic stage: oocysts bahamense var. compressum (in photo)
• Causes diarrhea in immunocompromised patients • Eating bivalve mollusks (mussels, clams,
• DOC: TMP-SMX oysters, and scallops) and fish obtained from red tide
SHELLFISH POISONING SYNDROMES

CLINICAL
SYNDROME TOXIN INCUBATION
PRESENTATION
Facial paresthesia,
Paralytic Saxitoxin total paralysis,
Cyclospora and Isospora cysts. respiratory failure
15 mins
Facial paresthesia,
XIII. BALANTIDIUM COLI Neurotoxic Brevetoxin slurred speech,
Balantidial Dysentery ataxia, diarrhea
• Largest protozoan and only ciliate pathogen of humans Diarrhea, nausea
Okadaic
Diarrhetic and vomiting,
• Infective stage: cysts acid
abdominal pain
• Pigs are the main reservoir → diarrhea among slaughter house 30 mins
Diarrhea, short-
worker Domoic
Amnesic term memory loss,
• Diagnosis is made by finding large ciliated trophozoites or large acid
seizures
cyst with a characteristic V-shaped nucleus in the stool
• Round-based, wide-necked intestinal ulcers
NEMATODES
OVERVIEW – NEMATODES
Location Species Disease Transmission Treatment

Ascaris Ascariasis Ingestion of eggs Albendazole
Ancylostoma and Necator Hookworm Larval penetration of skin Albendazole
Trichuris Whipworm Ingestion of eggs Mebendazole
Intestines
Enterobius Pinworm Ingestion of eggs Mebendazole
Strongyloides Strongyloidiasis Larval penetration of skin Ivermectin
Capillaria Capillariasis Eggs in undercooked fish Albendazole
Wuchereria and Brugia Filariasis Mosquito bite DEC
Tissue
Trichinella Trichinosis Larvae in undercooked meat Thiabendazole
GENERALITIES The larvae mature further in the lungs (10 to 14 days), penetrate the alveolar
walls, ascend the bronchial tree to the throat, and are swallowed (7). Upon
• Elongated, cylindrical (roundworms) reaching the small intestine, they develop into adult worms. Between 2 and 3
• With separate sexes, some parthenogenetic (e.g. Strongyloides) months are required from ingestion of the infective eggs to oviposition by the adult
Parthenogenesis is a form of reproduction in which an egg can develop female. Adult worms can live 1 to 2 years. (Source: CDC)
into an embryo without being fertilized by a sperm. FIRSTLY, it is important for you to note that it is the unembryonated egg
Dr. Rubio
exits the body. This egg could be unfertilized or fertilized as long as
there is no embryo yet. Then, the egg MUST go to the soil (e.g. garbage)
✔GUIDE QUESTION
so it can EMBRYONATE there. After an embryo has developed
A 10-year-old girl from Forbes Park, Makati has had abdominal pain
(embryonation, yeah!) then the egg now becomes infective. The idea is
and cramps for the past few days. Her examination produced normal
this: THE SOIL stage is essential.
findings except for nonspecific abdominal discomfort with a complete
blood count showing anemia and 22% eosinophilia. A stool specimen SECONDLY, note that the life cycle involves passing through the lungs, in
revealed the characteristic eggs of A. lumbricoides. Which is the most this order: from mouth → GI (where the larvae hatches and then PIERCES
appropriate treatment? through the tissues of the body and migrates to the lungs) → PULMONARY
A. Albendazole (now the larvae in the lungs cause inflammation and cough) → larvae
B. Praziquantel climb to PHARYNX → swallow back to GI. The idea is this: THE
C. Piperazine PULMONARY stage is important. Because of this phenomenon, we must
D. Bithionol consider a worm infection in a patient with chronic cough, e.g. Loeffler
syndrome).
Albendazole (400 mg single oral dose) is the treatment of choice
for ascariasis in stable patients older than 12 months with In this discussion, I want you to identify three worms with a LUNG
uncomplicated infection. MIGRATION phase (you may countercheck with the lifecycle diagrams):
Dr. Calderon • Ascaris
Which drug used in the treatment of intestinal nematodes is both • Hookworms
ovicidal and larvicidal? • Strongyloides
A. Praziquantel By virtue of passage through the lungs, these worms cause pulmonary
B. Mebendazole symptoms.
C. Iodoquinol Dr. Calderon
D. Albendazole DIAGNOSIS
Albendazole > mebendazole for ascaris • Direct fecal smear
Dr. Calderon
• Kato thick, Kato Katz
A barrel-shaped egg with bipolar plugs was found
on stool examination of a 2/M from Payatas. The
boy is infected with which parasite?
A. Giant roundworm
B. Whipworm
KATO-KATZ TECHNIQUE
C. Pinworm https://qrs.ly/5mbp8yk
D. Guinea worm
The standard method for demonstrating the presence of
whipworm is by identifying whipworm eggs in a stool sample.
Because eggs may be difficult to find in light infections, a
concentration technique is helpful.
Dr. Calderon
I. ASCARIS LUMBRICOIDES
PARASITE BIOLOGY • Ascaris egg, fertile but • Ascaris egg, infertile
• Most common and largest intestinal nematode unembryonated • Elongated, occasionally
• Giant roundworm • Round or ovoidal, with thick triangular, kidney shaped or
• Soil-transmitted helminth shell. Mammillated other bizarre forms. Shell
albuminous coat or covering often very thin. Internal
INFECTIVE on outer shell. Coat is material is a mass of
TRANSMISSION DIAGNOSTIC STAGE
STAGE sometimes lost and de- irregular globules and
Unembryonated egg, corticated eggs have a granules that fills shell.
Embryonated
Ingestion of eggs fertilized egg, colorless shell with gray or
egg black internal material. Eggs
unfertilized egg, adults
may be in 2, 4, or more cells,
LIFE CYCLE OF ASCARIS LUMBRICOIDES or contain a fully developed
larva
PATHOGENESIS
• Major damage occurs during larval migration
• Principal site of tissue reaction is the lungs, where inflammation
with an eosinophilic exudate occurs
• Heavy worm burden may contribute to malnutrition
• WANDERING WORMS: due to erratic behavior of adult
worms → hepatobiliary ascariasis, pancreatitis,
appendicitis
SPECTRUM OF DISEASE: Ascariasis

• Hypersensitivity pneumonitis (Loeffler syndrome)
Again, what worms have a lung migration phase?
__________________, _________________, ________________________
Dr. Calderon
• Acute intestinal obstruction

• Malabsorption syndromes
• Nutrient deficiencies
• Hepatobiliary ascariasis
Adult worms (1) in the lumen of the small intestine. A female may produce • Acute pancreatitis
approximately 200,000 eggs per day, which are passed with the feces (2).
Unfertilized eggs may be ingested but are not infective (because they need to pass • Acute appendicitis
through the soil to get ‘activated’, a process called ‘embryonation’. Larvae develop • Acute peritonitis, chronic granulomatous peritonitis
to infectivity within fertile eggs after 18 days to several weeks (3), depending on
the environmental conditions (optimum: moist, warm, shaded soil). After infective TREATMENT
eggs are swallowed (4), the larvae hatch (5), invade the intestinal mucosa, and
are carried via the portal, then systemic circulation to the lungs (6) . • Albendazole
II. NECATOR AND ANCYLOSTOMA

PARASITE BIOLOGY
• Soil-transmitted helminth
• Blood-sucking nematodes
• Hookworms
o Necator americanus (New World hookworm)
o Ancylostoma duodenale (Old World hookworm) Necator with semilunar cutting
• Differentiated based on character of buccal spears of filariform plates (Ne-cut-tor!)
larvae
Think ‘technology’!
INFECTIVE DIAGNOSTIC • Old world = teeth
TRANSMISSION
STAGE STAGE • New world = cutters
Larval penetration Between the 2 most common causes of hookworm infection in the
Filariform larvae Eggs in feces
of skin Philippines, Ancylostoma duodenale causes MORE BLEEDING than
Necator americanus because it has 2 PAIRS OF TEETH (vs the 1 pair of
LIFE CYCLE OF NECATOR AND ANCYLOSTOMA cutting plates seen in Necator americanus)
Dr. Rubio
PATHOGENESIS
• Major damage due to blood loss at site of attachment
o Blood consumed oozes in response to an anticoagulant made
by the worm
o Microcytic anemia caused by blood loss
SPECTRUM OF DISEASE: Hookworm Infection

• Acute disease
o Ground itch or dew itch at site of entry
o Eosinophilic pneumonia during transpulmonary passage
(Loeffler’s syndrome)
o Wakana syndrome: vague GI disturbances and eosinophilia
following peroral infection
• Chronic disease
o Microcytic, hypochromic anemia
o Hypoalbuminemia
Eggs are passed in the stool (1), and under favorable conditions (moisture, TREATMENT
warmth, shade), larvae hatch in 1 to 2 days and become free-living in
contaminated soil. These released rhabditiform larvae grow in the feces • Albendazole
and/or the soil (2), and after 5 to 10 days (and two molts) they become
filariform (third-stage) larvae that are infective (3). These infective larvae CUTANEOUS LARVA MIGRANS
can survive 3 to 4 weeks in favorable environmental conditions. On contact • Parasitic skin infection caused by animal hookworms:
with the human host, typically bare feet, the larvae penetrate the skin and o Ancylostoma braziliense (cat hookworm)
are carried through the blood vessels to the heart and then to the lungs. They
o Ancylostoma caninum (dog hookworm)
penetrate into the pulmonary alveoli, ascend the bronchial tree to the
pharynx, and are swallowed (4). The larvae reach the jejunum of the small • Pathophysiology: filariform larvae of animal hookworms
intestine, where they reside and mature into adults. Adult worms live in the CANNOT ENTER THE BLOOD CIRCULATION because humans
lumen of the small intestine, typically the distal jejunum, where they attach are not their primary host → stays in the skin → causes
to the intestinal wall with resultant blood loss by the host (5). Most adult inflammation and eventually dies over time
worms are eliminated in 1 to 2 years, but the longevity may reach several
years. (Source: CDC)
Here note that hookworms pass through the skin – so the infection can
have cutaneous manifestations (e.g. larvae migrans). From the skin, the
infective larvae try looking for a vein, and if successful, find themselves
joining the circulation in a journey to the lungs. Remember, they pass
through the lungs before they migrate to the pharynx and become
swallowed. So, by now, perhaps I have made it clear how they find their
way to the GI even if they pass through the skin.
Dr. Calderon
DIAGNOSIS
• Direct fecal smear
• Kato thick, Kato-katz technique Source: NEJM
• Harada-Mori culture: method of incubating fecal material on a Please take note that cutaneous larva migrans (CLM) is not seen in
filter paper strip in a test tube containing water (cover one-third human hookworms. It is a common confusion among medical students.
of the length of the paper strip) for the purpose of culturing and Dew itch or ground itch – skin lesion seen in human hookworm
recovering nematode larvae (Strongyloides stercoralis, infections. They represent the site of filariform larval penetration.
hookworm). Dr. Rubio
Hookworm egg Buccal spears of filariform III. TRICHURIS TRICHIURA

larvae PARASITE BIOLOGY
• Whipworm
• Soil-transmitted helminth
TRANSMISSION
STAGE STAGE
Unembryonated
Ingestion of eggs Embryonated egg
egg
Ancylostoma with teeth
DIAGNOSIS
Oval or ellipsoidal with a • Direct fecal smear
thin shell • Kato-katz technique: barrel/lemon/football-shaped eggs with
bipolar plugs
IV. ENTEROBIUS VERMICULARIS

PARASITE BIOLOGY
• Pinworm, seatworm
• Most common soil-transmitted helminth in developed
countries
• Life cycle is confined to humans
• Only intestinal nematode infection that cannot be controlled
through sanitary disposal of human feces because the eggs are
deposited in the perianal region
The egg of Trichuris has a Adult Trichuris removed
characteristic ‘barrel’ shape with during a colonoscopy INFECTIVE DIAGNOSTIC
two terminal polar plugs. The TRANSMISSION
STAGE STAGE
eggshell consists of three layers, Ingestion or Eggs on perianal
the outermost of which is stained Embryonated eggs
inhalation of eggs folds
dark brown by host bile pigment.
Rarely, eggs may become airborne and be inhaled and swallowed.
Note: It looks like a football or a
Chinese lantern. The migration of newly hatched larvae from the anal skin back into the
Dr. Calderon rectum (aka RETROinfection) may occur (unknown frequency).
PATHOGENESIS Dr. Calderon
DIAGNOSIS
• Burrow their hair-like anterior ends into the intestinal mucosa
via a pore-forming protein called TT47 • Graham scotch tape swab technique/perianal cellulose tape
swab
• Anemia strongly correlated to heavy intensity trichiuriasis
o D-shaped eggs
• Predispose to amebic dysentery (ulcers as site of invasion)
• Detection of adult worms or eggs on microscopic examinations
• Eggs are rarely found in the stools
LIFE CYCLE OF TRICHURIS TRICHIURA Ova of Enterobius.
Elongated, asymmetrical
with one side flattened,
other side convex (hence, D-
shaped). Smooth, thin
eggshell. Occasionally may
contain a fully developed
larva.
Diagnosis of pinworm can be made using these simple techniques:
• Searching for the worms in the perianal region 2 to 3 hours after the
infected person falls asleep
• Touching the perianal skin with transparent tape to collect possible
pinworm eggs around the anus first thing in the morning (perianal
swab)
• Analyzing samples from under fingernails → This is because an infected
person who scratched their anal area may have picked up some
pinworm eggs under the nails.
Dr. Calderon
LIFE CYCLE OF ENTEROBIUS VERMICULARIS
FIRSTLY, whipworm – just like Ascaris – must embryonate in the soil.

SECONDLY, note that there is NO LUNG MIGRATION. The implication
is this: there is no pulmonary presentation.
Dr. Calderon
SPECTRUM OF DISEASE: Trichuriasis
• Diarrhea
• Trichuris dysentery syndrome:
chronic dysentery and rectal
prolapse
• Rectal prolapse: from increased
peristalsis to expel the worms
• Appendicitis
The prolapsed, inflamed and edematous rectal tissue may even show visible
worms (Image source: Elsevier).
TREATMENT
• Mebendazole Gravid adult female Enterobius vermicularis deposit eggs on perianal
folds (1). Infection occurs via self-inoculation (transferring eggs to the mouth
The Unholy Trinity
with hands that have scratched the perianal area) or through exposure to
“Harold Brown, the late former parasitology professor at Columbia
eggs in the environment (e.g. contaminated surfaces, clothes, bed linens,
University College of Physicians and Surgeons, frequently referred to
etc.) (2). Following ingestion of infective eggs, the larvae hatch in the small
Ascaris, Trichuris, and hookworms as “the unholy trinity” to indicate
intestine (3) and the adults establish themselves in the colon, usually in the
that it was extremely common for a child to be infected with all three
cecum (4). The time interval from ingestion of infective eggs to oviposition by
parasites simultaneously.”
Hotez P. 2013. “The Unholy Trinity”: the Soil-Transmitted Helminth Infections Ascariasis, Trichuriasis, and the adult females is about one month. At full maturity adult females measure
Hookworm Infection, p 17-40. In Forgotten People Forgotten Diseases. ASM Press, Washington, DC. doi: 8 to 13 mm, and adult males 2 to 5 mm; the adult life span is about two
10.1128/9781555818753.ch2
So, which member of the unholy triad does NOT present with months. Gravid females migrate nocturnally outside the anus and oviposit
pulmonary symptoms? __________________ while crawling on the skin of the perianal area (5). The larvae contained
Dr. Calderon inside the eggs develop (the eggs become infective) in 4 to 6 hours under
optimal conditions (1). (Source: CDC)
PATHOGENESIS Autoinfection route: Rhabditiform larvae in the gut become infective
filariform larvae that can penetrate either the intestinal mucosa or the skin
• Female releases thousands of fertilized eggs on perianal skin
of the perianal area, resulting in autoinfection. Once the filariform larvae
o Eggs develop into larvae, causing perianal pruritus reinfect the host, they are carried to the lungs, pharynx and small intestine
• Autoinfection can occur as described above, or disseminate throughout the body. The significance of
autoinfection in Strongyloides is that untreated cases can result in
SPECTRUM OF DISEASE: Enterobiasis or oxyuriasis persistent infection, even after many decades of residence in a non-endemic
• Pruritus ani: most typical symptom, especially at night area, and may contribute to the development of hyperinfection syndrome
(Source: CDC).
• Eosinophilic enterocolitis
• Vulvovaginitis
DIAGNOSIS
• Salpingitis
• Harada-Mori culture
• Appendicitis
• Koga agar plate: most sensitive coprological method for larval
TREATMENT detection
• Baermann funnel gauze method, Beale’s string test, Enterotest
• Pyrantel pamoate
(string test)
MEMORY AID SOIL-TRANSMITTED HELMINTHS (STH)
“ATE”: Ascaris, Trichuris, Enterobius PATHOGENESIS
Soil-transmitted helminths have a common mode of • Larvae penetrate intestinal wall directly without leaving host
transmission: ingestion of embryonated eggs (which are and migrate to the lungs (autoinfection)
passed in feces and deposited in the soil). o Hyperinfection in immunocompromised patients
Take note that these are also the intestinal nematodes that can cause
appendicitis. SPECTRUM OF DISEASE: Strongyloidiasis
Note that Strongyloides can also be considered a soil-transmitted • Acute disease
helminth, according to the WHO.
o Ground itch at site of entry
o Mild watery diarrhea
V. STRONGYLOIDES STERCORALIS o Cochin China diarrhea: intermittent watery and bloody
PARASITE BIOLOGY diarrhea
• Threadworm o Eosinophilic pneumonia (Loeffler’s syndrome)
• Ovoviviparous (lay eggs which hatch before leaving host) • Chronic disease
• Soil-transmitted helminth (WHO) o Serpiginous track along buttocks, perineum and thighs (larva
• Facultative parasites currens)
o Duodenitis
INFECTIVE DIAGNOSTIC o Paradoxical asthma
TRANSMISSION o Hyperinfection syndrome
STAGE STAGE
Larval penetration Rhabditiform
Filariform larvae TREATMENT
of skin larvae
• Ivermectin
LIFE CYCLE OF STRONGYLOIDES STERCORALIS
VI. CAPILLARIA PHILIPPINENSIS
PARASITE BIOLOGY
• Only nematode whose life cycle involves a migratory bird
• Natural definitive hosts: Fish-eating birds
• Incidental definitive hosts: Humans
• Intermediate hosts: Freshwater or brackish water fish
TRANSMISSION
STAGE STAGE
Ingestion of Unembryonated
Infective larvae
undercooked fish egg
DIAGNOSIS
• Direct fecal smear
• Kato-katz technique
o Peanut-shaped eggs with striated shells and flattened
bipolar plugs
The Strongyloides stercoralis life cycle is complex, alternating between free-

living and parasitic cycles and involving autoinfection.
In the free-living cycle: Rhabditiform larvae are passed in the stool of an
infected definitive host (1), develop into either infective filariform larvae
(direct development) (6) or free-living adult males and females (2) that mate
and produce eggs (3), from which rhabditiform larvae hatch (4) and
eventually become infective filariform (L3) larvae (5). The filariform larvae
penetrate the human host skin to initiate the parasitic cycle (see below) (6). PATHOGENESIS
This second generation of filariform larvae cannot mature into free-living • Embryonated egg in the intestine releases larvae that reinvade
adults and must find a new host to continue the life cycle. the mucosa and causes autoinfection and hyperinfection
Parasitic cycle: Filariform larvae in contaminated soil penetrate human o Leads to ulcerative and compressive degeneration of
skin when skin contacts soil (6), and migrate to the small intestine (7). It has enterocytes, resulting in severe malabsorption
been thought that the L3 larvae migrate via the bloodstream and lymphatics
to the lungs, where they are eventually coughed up and swallowed. However,
L3 larvae appear capable of migrating to the intestine via alternate routes
(e.g. through abdominal viscera or connective tissue). In the small intestine,
the larvae molt twice and become adult female worms (8). The females live
embedded in the submucosa of the small intestine and produce eggs via
parthenogenesis (parasitic males do not exist) (9), which yield
rhabditiform larvae. The rhabditiform larvae can either be passed in the
stool (1) (see free-living cycle above), or can cause autoinfection (10).
LIFE CYCLE OF CAPILLARIA PHILIPPINENSIS Wuchereria Brugia
Characteristics
Appearance Smoothly curved Kinky

Terminal Nuclei Absent Present
Prevalence Widespread SEA only
Culex, Aedes,
Mosquito vectors Mansonia
Anopheles
Preference Scrotal lymphatics Limb lymphatics
Hydrocoele Elephantiasis
Clinical picture
Severity More severe Less severe
DIAGNOSIS
• Wet smear or thick blood smear
o Curved or kinky microfilariae
• Specimen collection best done at night between 8 PM and 4 AM
o Nocturnal periodicity
• DEC provocative test
o Allows blood smear collection in daytime
Typically, unembryonated, thick-shelled eggs are passed in the human • Knott’s concentration for low intensity infections
stool (1) and become embryonated in the external environment in 5-10 The standard method of diagnosing an active infection is to demonstrate
days (2); after ingestion by freshwater fish, larvae hatch, penetrate the microfilariae in a blood smear. These microfilariae circulate in the blood
intestine, and migrate to the tissues (3). Ingestion of raw or undercooked fish at night (nocturnal periodicity), hence, blood collection is ideally done at
results in infection of the human host (4). The adults of Capillaria this time to coincide with their appearance. A thick smear is then stained
philippinensis are very small and reside in the human small intestine, where with hematoxylin and eosin, or Giemsa. Concentration techniques can be
they burrow in the mucosa (5). In addition to the unembryonated, shelled used to increase sensitivity.
eggs which pass into the environment, the females can also produce eggs Alternatively, serologic methods can be useful. Patients with active
lacking shells (possessing only a vitelline membrane) (6), which become filarial infection typically have elevated serum levels of antifilarial IgG4.
embryonated within the female’s uterus or in the intestine. The released
Interestingly, because lymphedema may develop many years after the
larvae can re-invade the intestinal mucosa and cause internal
infection, laboratory tests are most likely to be negative in patients with
autoinfection (7). This process may lead to hyperinfection (a massive number
clinical lymphedema.
of adult worms). (Source: CDC) Dr. Calderon
SPECTRUM OF DISEASE: Capillariasis LIFE CYCLE OF WUCHERERIA AND BRUGIA

• Acute disease
o Borborygmus
o Intermittent diarrhea (8 to 10 stools/day)
o Fever, abdominal pain, eosinophilia
• Chronic disease
o Chronic watery diarrhea
o Edema, wasting
o Protein-losing enteropathy
o Hypogammaglobulinemia
TREATMENT
• Albendazole
• DOC: Mebendazole (Belizario 3rd ed)
MEMORY AID HABITAT OF INTESTINAL NEMATODES

Small intestine: CASH – Capillaria, Ascaris, Strongyloides, Hookworm
Large intestine: TE – Trichuris, Enterobius
During a blood meal, an infected mosquito (typically Mansonia spp.

VII. WUCHERERIA AND BRUGIA and Aedes spp.) introduces third-stage filarial larvae onto the skin of the
PARASITE BIOLOGY human host, where they penetrate into the bite wound (1). They develop into
adults that commonly reside in the lymphatics (2). Adults produce
• Blood and tissue nematode microfilariae, which are sheathed and have nocturnal periodicity. The
• Most debilitating nematode infection microfilariae migrate into lymph and enter the blood stream reaching the
• 2 important causative agents peripheral blood (3). A mosquito ingests the microfilariae during a blood
o Wuchereria bancrofti meal (4). After ingestion, the microfilariae lose their sheaths and work their
o Brugia malayi way through the wall of the proventriculus and cardiac portion of the midgut
• Usual scenario to reach the thoracic muscles (5). There the microfilariae develop into first-
stage larvae (6) and subsequently into third-stage larvae (7). The third-stage
o Farmer from abaca plantation
larvae migrate through the hemocoel to the mosquito’s proboscis (8) and can
infect another human when the mosquito takes a blood meal (1). (Source: CDC)
TRANSMISSION INFECTIVE STAGE DIAGNOSTIC STAGE
Mosquito bite 3rd stage larvae Microfilariae
PATHOGENESIS • Diagnostic stage: Microfilariae
• Larvae reach the lymphatic vessels and nodes where they (unsheathed)
develop into adult worms (usually localized in the lymph vessels • Clinical findings:
of lower extremities, inguinal lymph nodes, epididymis of males, o Dermal nodules
labia of females) o Hanging groin deformity
• Adult worms in the lymph nodes cause inflammation that o Lizard skin
obstructs lymphatic vessels, causing lymphedema o River blindness
• Microfilariae do not cause symptoms • Leading cause of preventable blindness in sub-Saharan Africa
• Diagnosis: Detection of microfilariae in skin snips or adults in
SPECTRUM OF DISEASE: Lymphatic filariasis biopsy specimens of skin nodules
• Acute disease • Treatment: Ivermectin
o Acute adenolymphangitis/ dermatolymphangioadenitis ORGAN MORPHOLOGY
o Filarial fever • Onchocercoma (subcutaneous nodule): fibrous
o Acute filarial lymphangitis (palpable cord) capsule surrounding adult worms, with
o Tropical pulmonary eosinophilia inflammatory infiltrates
§ Small epithelioid granulomas (Meyers-Kouwenaar bodies), Skin • Leopard, lizard or elephant skin: Epidermal
composed of aggregates of microfilariae surrounded by atrophy and elastic fiber breakdown, alternating
acidophilic hyaline material with hyperkeratosis; hyperpigmentation with
o Expatriate syndrome pigment incontinence, dermal atrophy and fibrosis
§ In individuals infected after migration to endemic regions
• Sclerosing keratitis (limbus)
§ Clinical and immunologic hyperresponsiveness to the
• Mazzotti reaction: Accentuation of keratitis with
mature or maturing worms
Eye antifilarial treatment
• Chronic disease
• Anterior chamber: Iridocyclitis and glaucoma
o Lymphedema (most common manifestation) which
progresses to elephantiasis • Choroid and retina: Atrophy and loss of vision
o Hydrocoele: common in Bancroftian filariasis
o Milky urine (chyluria) ✔GUIDE QUESTION
A 30-year-old Filipino male working in Sudan is being treated for
Onchocerca volvulus infection. He then develops fever, headache,
LOCAL EPIDEMIOLOGY dizziness, rashes, pruritus, pain in joints, muscles and lymph glands.
• Bancroftian Filariasis The physician suspects that he had a Mazzotti reaction, which is due to
o Sorsogon, Samar, Leyte, Palawan, Camarines, Albay, which of the following?
Mindoro, Marinduque, Romblon, all of Mindanao A. Increased GABA-mediated neurotransmission
• Malayan Filariasis B. Inflammatory reaction to lysis of the worms
C. Nicotinic stimulation at the myoneural junctions of nematodes
o Eastern Samar, Agusan del Sur, Palawan, Sulu
D. Stress-induced hemolysis
TREATMENT
• Diethylcarbamazine GUIDE QUESTION 9
RIVER BLINDNESS, https://qrs.ly/77ck6dt
ELEPHANTIASIS AND EYE WORM:
DEBILITATING WORM INFECTIONS
https://qrs.ly/h1bp479 X. TRICHINELLA SPIRALIS
PARASITE BIOLOGY
VIII. LOA LOA • Tissue nematode
• Hosts serve as both the final and intermediate hosts
• Intermediate host: pigs
TRANSMISSION
• African eye worm STAGE STAGE
• Transmitted by deer fly or mango fly (Chrysops) Ingestion of
Encysted larvae Encysted larvae
• Infective stage: L3 larvae undercooked meat
• Diagnostic stage: Microfilariae
DIAGNOSIS
• Definitive: Muscle biopsy
o Larvae within striated muscle
• Elevated CPKs
• Xenodiagnosis – involves
feeding suspected muscle to
• Loiasis is characterized by laboratory rats
o Subcutaneous edema (calabar swellings) • Bentonite flocculation test
o Worm crawling across the conjunctiva • ELISA: current recommendation
• DOC: diethylcarbamazine
PATHOGENESIS
IX. ONCHOCERCA VOLVULUS • Intestinal stage
o Liberated from pork by gastric juices
• Muscle stage
o Disseminate hematogenously to striated skeletal muscle
§ Encysted within a host-derived cell (nurse cell)
LIFE CYCLE OF TRICHINELLA SPIRALIS

• Transmitted by female blackfly (Simulium) See next image
• Infective stage: L3 larvae Trichinella is viviparous (it lays babies, not eggs). The females release
larvae that migrate to striated muscles where they encyst.
The sylvatic cycle (in wild animals) contributes to its distribution in
nature. Even if the infection is closely associated with eating pork, it may
also be acquired from eating other kinds of meat.
Dr. Calderon
SPECTRUM OF DISEASE: Trichinellosis
• Clinical conditions divided into 3 phases:
§ Enteric phase (incubation, intestinal invasion)
§ Invasion phase (larval migration, muscle invasion)
§ Convalescent phase (encystment and encapsulation)
• Cardinal signs and symptoms
§ Severe myalgia, periorbital edema, eosinophilia
• Self-limiting
• Mild disease
o Fever, muscle pain, periorbital edema, eosinophilia and
hemorrhagic phenomena (subconjunctival, splinter)
• Severe disease
o Myocarditis, encephalitis, pneumonia, respiratory myositis
TREATMENT
• Thiabendazole
XI. DRACUNCULUS MEDINENSIS

• Guinea fire worm
• Transmitted when copepods are
swallowed in water
• Pruritic painful papule
• Live worm in skin ulcer
Tx: Remove whole worm, wound care
XII. MISCELLANEOUS NEMATODES

Ancylostoma caninum, Angiostronglyus/
Toxocara canis Anisakis simplex
A. braziliense Parastronglyus cantonensis
T. canis from dogs A. caninum from dog intestine A. cantonensis from rat lung Anisakis from sushi
• Dog ascaris • Dog (caninum) and cat • Rat lungworm • Zoonotic roundworms
• Transmitted by ingestion of eggs (braziliense) hookworm • Natural DH: rat • Transmitted by ingestion of
• Humans are accidental hosts • Creeping eruptions • Accidental DH: humans undercooked fish
• Visceral larva migrans (cutaneous larva migrans) • IH: slugs and snails • Causes eosinophilic
• Ocular larva migrans • Transmitted by ingestion of gastroenteritis
• Uveitis raw mollusks or active • Mimics appendicitis
• Endophthalmitis penetration • “Tingling throat syndrome”
• Tx: Albendazole • Eosinophilic meningitis
• MCC of parasitic meningitis
CESTODES
OVERVIEW – CESTODES
CESTODE TRANSMISSION INTERMEDIATE HOST SITE AFFECTED TREATMENT
T. solium Eggs/larvae in undercooked pork Pigs Intestine Praziquantel
T. saginata Larvae in undercooked beef Cattle Intestine Praziquantel
D. latum Larvae in undercooked fish Fish Intestine Praziquantel
E. granulosus Eggs in food contaminated with dog feces Sheep Liver Albendazole
I. TAENIA SPP.
PARASITE BIOLOGY
• Intestinal cestodes
• T. solium: humans are both definitive and intermediate hosts
• T. saginata: humans are only definitive hosts
• Differentiated based on scolex and gravid proglottids (GP)
1° UB in
Cestode Suckers Rostellum
GP*
T. solium
4 Yes 5 – 10
(pork tapeworm)
T. saginata
4 No 15 - 25
(beef tapeworm)
*primary uterine branches in gravid proglottid
GENERALITIES
• Segmented, ribbon-like
• All are hermaphroditic.
• Structures:
§ Scolex: main organ of attachment to definitive host
§ Neck: region of growth
§ Segments or proglottids: becomes more mature distally, Taenia solium, gravid Taenia saginata, gravid
most distal are gravid segments proglottid with less branching proglottid with more
branching
MEMORY AID Taenia solium
The adult T. saginata is irritated by alcohol leading to passage of Taeniasis Cysticercosis
proglottids after a drinking bout. To remember, think T. saGINata. • Man is definitive • Man is an accidental intermediate
host host harboring the larval stage
INFECTIVE DIAGNOSTIC • IS: cysticercus (cysticerci) in the tissues
TRANSMISSION
STAGE STAGE cellulosae • IS: eggs
T. solium: • Mild non-specific • MoT: accidental ingestion of eggs via
Ingestion of cysticercus bovis, abdominal the fecal-oral route, e.g. autoinfection
undercooked eggs Gravid proglottids, complaints by a person who already has
“measly pork” T. saginata: eggs, scolex • Proglottids are not Taeniasis
/beef cysticercus as active → No • Most serious: neurocysticercosis
cellulosae obstruction of bile o Seizures, visual and motor deficits,
and pancreatic vomiting
DIAGNOSIS ducts and o Most serious: Racemous
• Stool examination, perianal swabs appendix (subarachnoid)
• To differentiate species: examination of gravid proglottids • Eyes: retinal or subretinal
flattened between two glass slides
o Injection of India ink through genital pore to count lateral TREATMENT
branches of uterus • Taeniasis: Praziquantel
• CT scan, MRI for neurocysticercosis • Neurocysticercosis: Praziquantel or albendazole +
• Ophthalmoscopy for ophthalmic cysticercosis corticosteroids
• Criteria for cure: (1) Recovery of scolex (2) Negative stool exam
PATHOGENESIS 3 months after treatment
• Minor intestinal damage from adult tapeworms
§ Irritation at the site of attachment MEMORY AID AUTOINFECTION
• Entangled proglottids may cause intestinal obstruction “Some Helminths Can Enter Colon Twice”
• Cysticerci can develop in striated muscle, brain, subcutaneous Strongyloides stercoralis
tissues, eye, heart, lung, peritoneum Hymenolepis nana
o Living cysticerci may cause inflammation Capillaria philippinensis
o Death of larva leads to inflammation that ends in calcification. Enterobius vermicularis
Cryptosporidium parvum
LIFE CYCLE OF TAENIA Taenia solium
Disclaimer: The “Helminths” is for mnemonic purposes only.
Note that Cryptosporidium is not a helminth.
II. DIPHYLLOBOTHRIUM LATUM

PARASITE BIOLOGY
• Longest medically important tapeworm
• Fish tapeworm/ broad tapeworm
• Has two elongated sucking grooves for attachment
• Have operculated eggs
All cestode eggs are non-operculated (no opening) EXCEPT for D latum
Dr. Rubio
• 1st intermediate host: copepods (Cyclops and Diaptomus)
• 2nd intermediate host: fish
• Infective stage to copepods: coracidium
• Infective stage to fish: procercoid larvae
TRANSMISSION
STAGE STAGE
Humans are the only definitive hosts for T. saginata and T. solium. Eggs or
gravid proglottids are passed with feces (1); the eggs can survive for days to Plerocercoid
Ingestion of Unembryonated
months in the environment. Cattle (T. saginata) and pigs (T. solium) become larvae or
undercooked fish egg
infected by ingesting vegetation contaminated with eggs or gravid sparganum
proglottids (2). In the animal’s intestine, the oncospheres hatch (3), invade
the intestinal wall, and migrate to the striated muscles, where they develop
into cysticerci. A cysticercus can survive for several years in the animal.
Humans become infected by ingesting raw or undercooked infected meat (4).
In the human intestine, the cysticercus develops over 2 months into an adult
tapeworm, which can survive for years. The adult tapeworms attach to the LIFE CYCLE OF D. LATUM
small intestine by their scolex (5) and reside in the small intestine (6).
(Source: CDC)
SPECTRUM OF DISEASE: Taeniasis, Cysticercosis

• Most common chief complaint: passage of proglottids or
segments in the stool
Taenia saginata
Taeniasis
• Intestinal infection (usually only one adult tapeworm)
• Epigastric pain, vague discomfort, hunger pangs, weight loss,
loss of appetite, pruritus ani
• Intestinal obstruction
• Proglottids are actively motile → can cause obstruction in the
bile and pancreatic ducts and appendix
SPECTRUM OF DISEASE: Diphyllobothriasis The adult Echinococcus granulosus (1) resides in the small intestine of the
definitive host (dog). Gravid proglottids release eggs (2) that are passed in
• Limited to one worm
the feces, and are immediately infectious. After ingestion by a suitable
• Abdominal pain and diarrhea intermediate host (sheep), eggs hatch in the small intestine and release six-
• Hyperchromic, megaloblastic anemia (due to vitamin B12 hooked oncospheres (3) that penetrate the intestinal wall and migrate
deficiency) with thrombocytopenia and leukopenia through the circulatory system into various organs, especially the liver and
lungs. In these organs, the oncosphere develops into a thick-walled hydatid
TREATMENT cyst (4) that enlarges gradually, producing protoscolices and daughter cysts
that fill the cyst interior. The definitive host becomes infected by ingesting the
• Praziquantel
cyst-containing organs of the infected intermediate host. After ingestion, the
• Criteria for cure: recovery of scolex protoscolices (5) evaginate, attach to the intestinal mucosa (6), and develop
into adult stages (1) in 32 to 80 days.
III. ECHINOCOCCUS GRANULOSUS Humans are aberrant or accidental intermediate hosts, and become infected
PARASITE BIOLOGY by ingesting eggs (2). Oncospheres are released in the intestine (3), and
hydatid cysts develop in a variety of organs (4). If cysts rupture, the liberated
• Composed of a scolex and only three proglottids protoscolices may create secondary cysts in other sites within the body
• One of the smallest tapeworms (secondary echinococcosis). (Source: CDC)
• Intermediate hosts: sheep/man In other words, the disease involves a dog-sheep cycle, but it becomes
• Definitive host: dog medically important in an accidental dog-human cycle
• Man is an accidental intermediate host. Dr. Calderon
PATHOGENESIS
• Cysts acts as space occupying lesions (SOLs)
INFECTIVE DIAGNOSTIC • if the cyst ruptures, life-threatening anaphylaxis can occur
TRANSMISSION
STAGE STAGE
Ingestion of eggs Embryonated egg Hydatid cysts SPECTRUM OF DISEASE: Human Cystic Echinococcosis
• Unilocular cysts
LIFE CYCLE OF E. GRANULOSUS • Hydatid cysts in liver (70%) – most
commonly in the inferior right lobe
• Pulmonary cysts (20 – 30%)
• Cerebral cysts (10%)
• Most common complication: intrabiliary rupture of the cyst
o Triad: intermittent jaundice, fever, eosinophilia
DIAGNOSIS
• Ultrasonography
• Gold standard serology: detection of IgG antibodies to hydatid
cyst fluid-derived native or recombinant antigen B subunit
(ELISA or immunoblot)
TREATMENT
• Surgical resection (>10 cm in diameter, secondary infection,
extrahepatic)
• Albendazole (< 7 cm, isolated, uncomplicated, negative
serology)
• PAIR procedure: Puncture, Aspiration, Injection, Respiration
CESTODES OF MINOR IMPORTANCE

Echinococcus multilocularis Hymenolepsis nana Hymenolepsis diminuta Dipylidium caninum
• Definitive hosts: Foxes • Dwarf tapeworm (smallest • Rat tapeworm • Dog tapeworm, double-pored
• Intermediate host: tapeworm) • Requires intermediate tapeworm
Rodents • Most frequently found tapeworm host • Most common tapeworm of dogs
• Transmission: accidental in developed countries • Transmission: ingestion and cats
ingestion of food • Common in orphanages, day care of infected rat flea with • Transmission: Ingestion of dog or
contaminated with fox centers, and mental institutions cysticercoid larvae cat fleas (Ctenocephalides canis/
feces • Only tapeworm which can • Eggs lack bipolar felis) with cysticercoid larvae
• Alveolar echinococcosis complete its entire life cycle in a filaments • Diagnosis: “barrel-shaped”
• Larvae form single host (does not require • Man is an accidental proglottids in stools
multiloculated cysts intermediate host) definitive host. • Treatment: Praziquantel
(honeycomb vesicles) • Ingestion of infected rice or flour • Treatment: Praziquantel
• Treatment: Albendazole; beetles with cysticercoid larvae
surgical cyst removal • Eggs are directly infectious for
humans
• Eggs either pass in the stool or can
reinfect the small intestine
(autoinfection)
• Eggs: 8-10 polar filaments and six-
hooked larva
• Treatment: Praziquantel
TREMATODES
OVERVIEW – TREMATODES
Trematode Transmission Sites Affected Intermediate Hosts Treatment
Schistosome S. japonicum Penetrate skin Liver Snail Praziquantel
Lung fluke P. westermani Ingested with raw crab Lung Snail and crab Praziquantel
Liver fluke C. sinensis Ingested with raw fish Liver Snail and fish Praziquantel
Flukes 1st Intermediate Host (Snail) 2nd Intermediate Host

Schistosoma japonicum Oncomelania hupensis quadrasi - -
Schistosoma
Schistosome Bulinus - -
haematobium
Schistosoma mansoni Biomphalaria - -
Paragonimus Antemelania asperata
Lung fluke Crabs Sundathelphusa philippina
westermani Antemelania dactylus
Trapa bicornis (water caltrop)
Eliocharis tuberosa (water
Intestinal
Fasciolopsis buski Segmentina, Hippeutis chestnut)
fluke
Aquatic Ipomea obscura (kang kong)
plants Nymphaea lotus (lotus)
Ipomea obscura
Lymnaea philippinensis
Liver fluke Fasciola spp. Nasturtium officinale
Lymnaea auricularia rubiginosa
(watercress)
Pila luzonica
Echinostoma ilocanum Gyraulus, Hippeutis Snails
Intestinal Vivipara angularis
fluke Freshwater, brackish water or marine Freshwater or brackish water
Heterophyid flukes
snails fish
Clonorchis sinensis Parafossarulus, Bulinus Fishes Cyprinidae (freshwater fish)
Liver fluke Opisthorchis viverrini
Bithynia Cyprinidae (freshwater fish)
Opisthorchis felineus
GENERALITIES LIFE CYCLE OF SCHISTOSOMA
• Unsegmented, leaf-like
• All are hermaphroditic except Schistosoma (dioecious).
• All require two intermediate hosts except Schistosoma
• The infective stage is metacercariae except for Schistosoma
(cercariae).
• The diagnostic stage is embryonated egg.
§ Except for Paragonimus, Fasciola, Fasciolopsis, and
Echinostoma (unembryonated egg)
• The first intermediate host is always a snail.

• The second intermediate host may be a fish, crustacean,
another snail, or fresh water plants.
• The drug of choice is praziquantel except for Fasciola which is
triclabendazole.
I. SCHISTOSOMA
(JAPONICUM, MANSONI, HAEMATOBIUM)
PARASITE BIOLOGY
• Oriental blood fluke
• Adult schistosomes exist as separate sexes (other trematodes Schistosoma eggs are eliminated with feces or urine, depending on
are hermaphrodites) species (1). Under appropriate conditions the eggs hatch and release
• Adults reside in the mesenteric/ portal or bladder veins miracidia (2), which swim and penetrate specific snail intermediate hosts (3).
The stages in the snail include two generations of sporocysts (4) and the
o Lay eggs that cause granulomas
production of cercariae, the infective stage to man (5). Upon release from the
snail, the infective cercariae swim, penetrate the skin of the human host (6),
INFECTIVE DIAGNOSTIC and shed their forked tails, becoming schistosomulae (7). The schistosomulae
TRANSMISSION
STAGE STAGE migrate via venous circulation to lungs, then to the heart, and then develop
Cercarial skin in the liver, exiting the liver via the portal vein system when mature, (8, 9).
Cercariae Eggs Male and female adult worms copulate and reside in the mesenteric venules,
penetration
the location of which varies by species (with some exceptions) (10).
For instance, S. japonicum is more frequently found in the superior
mesenteric veins draining the small intestine (A), and S. mansoni occurs SPECTRUM OF DISEASE: Schistosomiasis
more often in the inferior mesenteric veins draining the large intestine (B).
However, both species can occupy either location and are capable of moving
• Acute disease
between sites. S. intercalatum and S. guineensis also inhabit the inferior o Itching and dermatitis (swimmer’s itch) at site of cercarial
mesenteric plexus but lower in the bowel than S. mansoni. S. penetration
haematobium most often inhabits in the vesicular and pelvic venous o Katayama fever/ “snail fever”
plexus of the bladder (C), but it can also be found in the rectal venules. § Systemic hypersensitivity, resembling serum sickness
The females (size ranges from 7–28 mm, depending on species) deposit eggs • Chronic disease
in the small venules of the portal and perivesical systems. The eggs are moved o Intestinal Schistosomiasis – Schistosoma japonicum,
progressively toward the lumen of the intestine (S. mansoni, S. japonicum, S. Schistosoma mansoni
mekongi, S. intercalatum / guineensis) and of the bladder and ureters (S. § Chronic liver disease, portal hypertension → gastrointestinal
haematobium), and are eliminated with feces or urine, respectively (1). hemorrhage, massive splenomegaly
(Source: CDC)
o Urinary Schistosomiasis – Schistosoma haematobium
DIAGNOSIS § Painless hematuria, fibrosis of the bladder
• Kato-katz technique § Can cause squamous cell carcinoma of the bladder due to
• Rectal or liver biopsy chronic irritation by the S haematobium eggs
• Antibody detection o Colonic, pulmonary, cerebral schistosomiasis
• Circumoval precipitin test (ovoid egg with small hook) o Cor pulmonale
PATHOGENESIS
LOCAL EPIDEMIOLOGY
• Adult flukes living in the mesenteric or bladder veins
• Areas of Endemicity
• Evade host defenses by coating themselves with host antigens o Sorsogon, Samar, Leyte, Oriental Mindoro, Bohol, all of
• Egg deposition can occur in any organ but most commonly Mindanao EXCEPT Misamis Oriental
involves liver, intestines, and lungs.
• Main pathology: host granulomatous reaction to eggs TREATMENT
o Liver granulomas lead to presinusoidal obstruction,
• Praziquantel
hepatomegaly and portal hypertension
o Bladder granulomas lead to nodules, polypoid lesions, and
ulcerations in the lumens of the ureter and bladder, which in
turn causes urinary frequency, dysuria, and end stream
hematuria
S. japonicum S. mansoni S. haematobium
Egg
Oval. Small lateral spine is often Elongated with rounded anterior end
Elongated with prominent lateral
seen or may appear as a small and terminal spine at posterior end.
spine near posterior end. Anterior
hook or “knob” located in a Found in urine, occasionally in feces.
end tapered and slightly curved.
depression in the shell. Egg often covered with debris.
Oncomelania hupensis quadrasi Biomphalaria glabrata Bulinus truncates
Intermediate snail
host
Intestinal Schistosomiasis Urinary Schistosomiasis

• Liver granulomas lead to presinusoidal obstruction, hepatomegaly • Painless hematuria and fibrosis of
and portal hypertension the bladder
Spectrum of • GI hemorrhage, massive splenomegaly • Hydronephrosis
Disease: Chronic • Liver UTZ: clay pipe stem fibrosis with lacelike pattern • Associated with squamous cell
Schistosomiasis carcinoma of the bladder
✔GUIDE QUESTION II. PARAGONIMUS WESTERMANI

A 19/F from outside Metro Manila is referred to a tertiary medical
center for further evaluation of abdominal enlargement. She is from PARASITE BIOLOGY
Samar and has never traveled out of her island. Suspecting that she has • Lung fluke – adults reside in the lungs
an endemic fluke infection, the physician performs a rectal biopsy, • 1st intermediate host: Antemelania asperata (snail)
believing in its superiority over stool examination. Which of the • 2nd intermediate host: Sundathelphusa philippina (mountain
following findings confirms the diagnosis?
crab)
A. Eggs with vestigial spines on the lateral axes
Sundathelphusa philippina
B. Male and female flukes in copulation
(von Martens 1868)
C. Sausage-shaped eggs with bipolar plugs
Specialty dishes in which shellfish are
D. Both A and B are correct
consumed raw or prepared only in
vinegar, brine, or wine without cooking
GUIDE QUESTION 10 (e.g. burong talangka) play a key role in
the transmission of paragonimiasis.
https://qrs.ly/j4ck6k1
TRANSMISSION
STAGE STAGE
Ingestion of
Unembryonated
undercooked/ raw Metacercariae
egg
crab meat
Egg of Paragonimus, usually found in sputum, occasionally in
feces. Ovoidal or elongate with thick shell. Operculum is
slightly flattened and fits into shoulder area of shell. Posterior
end is thickened. Egg often asymmetrical with one side slightly
flattened.
LIFE CYCLE OF PARAGONIMUS WESTERMANI III. CLONORCHIS SINENSIS
PARASITE BIOLOGY
• Chinese liver fluke/ Oriental liver fluke

o Clonorchis sinensis
• 1st intermediate host: Parafossarulus, Bulinus (snail)
• 2nd intermediate host: Cyprinidae (fish)
• Adults reside in small and medium sized biliary ducts.
TRANSMISSION
STAGE STAGE
Ingestion of Embryonated
Metacercariae
undercooked/ raw fish egg
DIAGNOSIS
The eggs are excreted unembryonated in the sputum, or alternately they are • Direct fecal smear
swallowed and passed with stool (1). In the external environment, the eggs • Potassium permanganate stain
become embryonated (2) , and miracidia hatch and seek he first intermediate o Ovoid eggs with melon-like ridges and abopercular
host, a snail, and penetrate its soft tissues (3). Miracidia go through several
developmental stages inside the snail (4): sporocysts (4a), rediae (4b), with
protuberance
the latter giving rise to many cercariae (4c) which emerge from the snail. • Cholangiography (“arrowhead sign”)
The cercariae invade the second intermediate host, a crustacean such as a
crab or crayfish, where they encyst and become metacercariae. This is the PATHOGENESIS
infective stage for the mammalian host (5). Human infection with P. • The flukes move through the ampulla of Vater to the common
westermani occurs by eating inadequately cooked or pickled crab or crayfish
bile duct then to the distal biliary capillaries where maturation
that harbor metacercariae of the parasite (6). The metacercariae excyst in
the duodenum (7), penetrate through the intestinal wall into the peritoneal
into an adult worm occur.
cavity, then through the abdominal wall and diaphragm into the lungs, • Inflammatory response can cause desquamation of epithelial
where they become encapsulated and develop into adults (8). The worms can cells, adenomatous tissue formation, and hyperplasia and
also reach other organs and tissues, such as the brain and striated muscles, fibrosis of the biliary tract, predisposing to neoplastic
respectively. However, when this takes place completion of the life cycles is transformation.
not achieved, because the eggs laid cannot exit these sites. Time from
infection to oviposition is 65 to 90 days. Infections may persist for 20 years in LIFE CYCLE OF CLONORCHIS SINENSIS
humans. Animals such as pigs, dogs, and a variety of feline species can also
harbor P. westermani. (Source: CDC)
DIAGNOSIS
• Sputum concentration with 3% NaOH preparation
o Ovoid, thinner opercular end, thickened abopercular end
o Best sensitivity for microscopic diagnosis
• Enzyme immunoassay
• Complement fixation
PATHOGENESIS
• Granulomatous reaction that gives rise to a fibrotic cyst
containing blood-tinged purulent material, adult worms & eggs
• Secondary bacterial infection frequently occurs
SPECTRUM OF DISEASE: Paragonimiasis
• Chronic cough with bloody sputum
• Chest x-ray: ring-shadowed opacity
• Closely resembles tuberculosis – “In suspected cases of
tuberculosis, a history of crab-eating plus sputum examinations, SPECTRUM OF DISEASE: Clonorchiasis
image findings, and serodiagnosis are necessary to rule out
paragonimiasis.” (Nagakura et al 2002). • Acute disease
o Fever, eosinophilia, LAD and tender hepatomegaly
• Ectopic: cutaneous and cerebral paragonimiasis
• Chronic disease
TREATMENT o Hepatobiliary disease (calculi, acute suppurative cholangitis,
recurrent pyogenic cholangitis, cholecystitis, hepatitis)
• Praziquantel o Pancreatitis
o Cholangiocarcinoma
o Neurocirculatory dystonia
TREATMENT
• Praziquantel
TREMATODES OF MINOR IMPORTANCE
Fasciola hepatica,
Fasciolopsis buski Echinostoma ilocanum Heterophyes heterophyes
Fasciola gigantica
• Giant intestinal fluke • Mode of transmission: • Mode of transmission: • Temperate liver fluke and Tropical
• Largest intestinal fluke of humans Ingestion of infected Ingestion of infected fish liver fluke
and pigs snails • Adults reside in the small • Mode of transmission: Ingestion of
• Mode of transmission: Ingestion • Inflammation at site of intestine infected aquatic plants
of infected aquatic plants attachment • Mimics peptic ulcer • Acute or invasive phase: Triad of high
• Eggs indistinguishable from • Ulceration and disease fever, hepatomegaly, marked
Fasciola diarrhea (may be • Eggs are similar to eosinophilia
• Gland abscesses in the mucosa bloody) Opisthorchids • Chronic or latent phase: adults in bile
• Intoxication from absorption of • General intoxication ducts → obstruction
worm metabolites → generalized • Halzoun/ marrara: hemorrhagic
toxic and allergic symptoms nasopharyngitis and dysphagia due to
ingestion of raw Fasciola adult-
infected liver
• DOC: Triclabendazole
Notice the ‘pseudomembranes’ of the esophageal mucosa.

MEDICAL MYCOLOGY Also:
OVERVIEW OF FUNGI Pseudomembranous pharyngitis – Diphtheria
Pseudomembranous colitis – Clostridioides difficile
Dr. Calderon
FUNGAL STRUCTURE
• Has 2 basic forms:
FORM FEATURE
Yeast Unicellular, budding
Mold Multicellular, consists of hyphal elements
Mycelium – refers to the “intertwined mass of hyphae”
Dr. Rubio
DEFINITION OF TERMS
CONCEPT DEFINITION
• Refers to the filamentous cells of molds
Hyphae • Can be septate or aseptate hyphae
• Can be dematiaceous or hyaline
• Hyphal elements with septations
Septate
• Feature of MOST MEDICALLY
hyphae
IMPORTANT FUNGI
• Hyphal element WITHOUT SEPTATIONS
Aseptate →”multinucleated” or “coenocytic”
hyphae • Feature of ORDER MUCORALES (Mucor,
Rhizopus)
• Refers to “dark colored” hyphae
Dematiaceous • Due to the presence of melanin
✔GUIDE QUESTION hyphae • Mostly associated with soil exposure and
Which organism is associated with pseudomembranous esophagitis? subcutaneous mycoses
A. Mucor C. Aspergillus Hyaline
B. Candida D. Paracoccidioides • Refers to colorless hyphae
hyphae
The most prevalent cause of infectious esophagitis is esophageal
candidiasis. In the GIT, the esophagus is the second most CONCEPT DEFINITION
susceptible to candida infection, only after the oropharynx.
• Unicellular fungi, larger than bacteria,
Immunocompromised patients are most at risk, including patients
with HIV/AIDS, leukemia, diabetics, and those who are receiving
ovoid in shape
Yeast
corticosteroids, radiation, and chemotherapy. • Reproduced via budding (production of
blastoconidia)
• A unique feature of Candida albicans
Pseudohyphae
seen when it is grown at 20°C
• A unique feature of Candida albicans
Germ tube
seen when it is grown at 37°C
Esophageal candidiasis. Endoscopic finding: multiple whitish plaques
(black arrows) are seen and are usually taken for histology and
microscopic examination on brush.
Source: https://doi.org/10.1155/2019/3585136
CONCEPT DEFINITION OVERVIEW OF FUNGAL DISEASES
• Can be formed via asexual process A. FUNGAL ALLERGIES
(mitosis) or via sexual process • sick building syndrome
Fungal spores
(meiosis) • farmer’s lung
• An important feature for speciation • silo worker’s disease
• Ascospores – Phylum Ascomycota • allergic bronchopulmonary aspergillosis (Aspergillus
Sexual spores • Basidiospores – Phylum Basidiomycota fumigatus)
• Zygospores – Order Mucorales
Asexual spores – • Microconidia – small spores B. MYCOTOXICOSES
via size • Macroconidia – large or multicellular • may result from ingestion of fungal-contaminated foods
• Chlamydoconidia – from terminal or • e.g., St. Anthony’s fire from ergot-contaminated bread or
intercalary hyphae aflatoxin [a carcinogen] -contaminated peanuts
• Phialoconidia – from vase-shaped • ingestion of psychotropic (Psilocybe) or toxic (Amanita)
Asexual spores conidiogenous cell termed as “phialide” mushrooms.
via method of • Blastoconidia – from budding yeast
production • Arthroconidia – from fragmentation of C. FUNGAL INFECTIONS (MYCOSES)
hyphal cells • Mycoses range from superficial to overwhelming systemic
• Sporangiospores – characteristic infections that are rapidly fatal in the compromised host.
asexual spores of Order Mucorales • Mycoses are increasing in prevalence as a result of increased use
of antibiotics, corticosteroids, and cytotoxic drugs.
✔GUIDE QUESTION
Which is true about the growth of thermally dimorphic fungi? FUNGAL TOXINS AND ALLERGIES
A. Molds on artificial culture medium at room temperature, Amanita • liver necrosis due to amanitin and
yeasts in infected tissue mushrooms phylloidin
B. Yeasts on artificial culture medium at room temperature, molds
in infected tissue • ingestion of contaminated peanuts and grains
C. Molds and yeasts on artificial culture medium at room Aspergillus causes liver cancer due to aflatoxin
temperature flavus • aflatoxin B1 causes G:C → T:A mutation in
D. Molds and yeasts in infected tissue codon 249 of p53
Thermally dimorphic fungi, which switch to a yeast growth form • inhalation of the spores causes allergic
Aspergillus
during infection, grow in a mycelial (mold) form at room bronchopulmonary aspergillosis
fumigatus
temperature (25-30°C), and as a yeast at body temperature (IgE-mediated)
(37°C).
Such an ability to switch between a multicellular hyphal and LABORATORY DIAGNOSIS OF FUNGI
unicellular yeast growth form is a tightly regulated process
known as dimorphic switching. Dimorphic switching requires MEDICALLY IMPORTANT STAINING TECHNIQUES FOR FUNGI
the fungus to sense and respond to the host environment and is • KOH dissolves any tissue cells
10% KOH
essential for pathogenicity. • Makes the highly refractory fungal cells
examination
more visible
• Added to KOH to increase its sensitivity
Calcofluor
• Stains fungal cell wall and makes it
white
fluorescent
Gomori-
• Stains fungal cell wall black
methenamine
• Used to stain Pneumocystis carinii
silver (GMS)
Mucicarmine • Stains fungal capsule red
stain • Used to stain Cryptococcus neoformans
• Used “negative staining” to highlight the
India ink stain heavily thickened capsule of Cryptococcus
neoformans
MEDICALLY IMPORTANT CULTURE TECHNIQUES FOR FUNGI

Sabouraud’s • Standard culture for isolation of
dextrose agar (SDA) fungal agents
Inhibitory mold agar • Enhances the recovery of fungi
(IMA) from clinical specimens
OTHER DIAGNOSTIC TOOLS

• Helpful among immunocompetent
• Positive antibody test – may confirm the
Serology diagnosis
• Negative antibody test – may exclude the
diagnosis
• PCR
• MALDI-TOF-MS (matrix-assisted laser
Molecular
desorption ionization-time of flight mass
methods
Mold in the Cold, Yeast in the Heat! spectrometry)
• For rapid diagnosis of fungal organisms
FUNGAL PATHOGENESIS
• two types of host response: granulomatous or pyogenic
response
• some can be detected by using skin tests for delayed
hypersensitivity reaction
• reduced cell-mediated immunity predisposes to disseminated
disease
KEY FUNGAL STRUCTURES OBSERVED IN MICROSCOPIC
EXAMINATIONS OF CLINICAL SPECIMENS
PREDOMINANT
MYCOSES
MORPHOLOGY
Yeasts • Blastomycosis, Histoplasmosis,
(single or multiple Paracoccidioidomycosis,
buds) Penicilliosis, Sporotrichosis
Yeasts with capsules • Cryptococcosis
• Hyalohyphomycosis—species of
Hyphae
Aspergillus, Fusarium, Geotrichum,
(septate)
Trichosporon, et al.)
Hyphae
(septate in skin or • Dermatophytosis
nail specimens)
• Mucormycosis—species of
Hyphae
Rhizopus, Lichtheimia, DRUGS MECHANISM OF ACTION
(nonseptate)
Cunninghamella, etc. Polyenes • Binds to ergosterol in fungal cell
Hyphae • Phaeohyphomycosis—species of Amphotericin B membranes, forming leaky pores
(septate); Bipolaris, Cladosporium, Azoles
brownish cell walls Curvularia, Exserohilum, etc. • Inhibit fungal P450-dependent
Ketoconazole
Yeasts and enzymes (lanosterol
• Candidiasis—species of Candida Fluconazole
Pseudohyphae • 14-a-demethylase) blocking ergosterol
Itraconazole
Yeasts and Hyphae in synthesis; resistance can occur with
• Pityriasis versicolor Posaconazole
skin scrapings long-term use
Voriconazole
Spherules • Coccidiomycoses Terbinafine • Inhibits epoxidation of squalene
Sclerotic cell Echinocandins
• Chromoblastomycosis
(brownish cell walls) Caspofungin • Inhibit β-glucan synthase decreasing
Sulfur granules • Mycetoma Micafungin fungal cell wall synthesis
Anidulafungin
Arthroconidia in hair • Dermatophytosis • Blocks nucleic acid synthesis by
Flucytosine
Inhibiting DNA and RNA polymerases
Conidia in • Hyalohyphomycosis—species of
• interferes with microtubule function in
pulmonary cavity Aspergillus, Fusarium, etc.
dermatophytes and may also inhibit
Cysts (asci) in Griseofulvin
the synthesis and polymerization of
pulmonary • Pneumocystis jirovecii nucleic acids
specimens Which is the primary mechanism of resistance of C. albicans against
azole antifungals?
✔GUIDE QUESTION A. Mutations in the 14-alpha-sterol demethylase enzyme
Which stain binds to the complex carbohydrate cell wall of fungi and B. Mutations in microtubule-associated proteins
lights up a bright blue white color? C. Mutations in fungal squalene epoxidase
A. Periodic acid Schiff C. Calcofluor white D. Mutations in HMG-CoA reductase
B. Nigrosin D. Silver
Azole antifungals (e.g. fluconazole) target demethylase enzymes
Calcofluor white stain is a fluorescent stain that binds to involved in ergosterol synthesis. Mutations in these enzymes can
cellulose and chitin which is found in fungal cell walls. Fungal and consequently render the organism azole resistant.
parasitic organisms (specifically Pneumocystis jirovecii) will
appear fluorescent green or blue under UV light. This is the stain
used directly on clinical specimens. It is most sensitive for GUIDE QUESTION 12
visualizing few fungal elements.
https://qrs.ly/ajck6mz
The periodic acid–Schiff (PAS) method is useful for
demonstrating internal details. Staining produces ‘hot pink’ color.
Gomori’s methenamine silver (GMS) technique is considered
one of the better stains for fungi because it provides high contrast MAJOR CLASSIFICATIONS OF FUNGAL DISEASES (JAWETZ)
with minimal background staining. Consequently, it allows the
demonstration of sparsely present fungal elements in the sample. • All fungal disease or “mycoses” are NOT infective to other
organisms EXCEPT CUTANEOUS MYCOSES
The hematoxylin and eosin (H&E) stain is best used for studying
o Humans with mycoses are dead-end hosts.
the host reaction and for determining whether a fungus is hyaline
(colorless) or dematiaceous (naturally pigmented). REMEMBER:
Infective – refers to a communicable disease – “nakakahawa”
India ink or nigrosin staining is performed on CSF to diagnose
Infectious – the nature of the disease is microbial in origin
cryptococcal meningitis. The Cryptococcus yeast cell wall is
Example:
composed of a large polysaccharide capsule. India ink will stain
Pulmonary tuberculosis is INFECTIVE and INFECTIOUS
only the background (i.e. negative straining technique) and the
Aspergillosis is NOT INFECTIVE, yet INFECTIOUS
extracellular capsule will not stain and appears as a halo Dr. Rubio
surrounding the yeast.
The Gram stain is useful to demonstrate the presence of yeasts. • Involves the hair, and epidermis ONLY
The yeast organisms will stain dark blue/purple, and budding will
be easy to detect. Other fungal structures (e.g. hyphae) may stain
• Stratum corneum involvement
variably or even poorly. SUPERFICIAL • Pityriasis versicolor (tinea versicolor)
MYCOSES • Tinea nigra
• White piedra
GUIDE QUESTION 11 • Black piedra
https://qrs.ly/blck6lo • Involves the skin, hair and nails
• Only major classification of mycoses
CUTANEOUS
that is infective to other organisms
Which group of antifungal agents pertain to a novel, highly selective MYCOSES
class of semisynthetic polypeptides that inhibit important constituents
• Most prevalent mycosis in the world
of the fungal cell wall? • Dermatophytoses
A. Amphotericin C. Imidazole
B. Echinocandins D. Triazoles
C. Allylamines
• Agents usually reside in soil or on
vegetations
• Agents may enter the subcutaneous
tissue via traumatic inoculation
SUBCUTANEOUS • (+) granulomatous in nature
MYCOSES • (+) lymphatic spread
• Sporotrichosis
• Mycetoma
• Chromoblastomycosis Malassezia is present as a combination of both short pseudohyphae and
• Phaeohyphomycosis spores, the light microscopic appearance of which is referred to as
• Mode of transmission: inhalation of ‘spaghetti and meatballs’ or ‘bacon and eggs’ pattern.
infective stage of fungi
• Primary disease: pneumonia → may B. OTHER SUPERFICIAL MYCOSES
cause systemic manifestations
MYCOSIS AGENT FEATURE
• Endemic in certain geographic regions
Hortaea werneckii
• Usually asymptomatic among Tinea • Black discoloration of
ENDEMIC / (Exophiala
immunocompetent individuals nigra the palm
SYSTEMIC werneckii)
• Widespread systemic presentation in
MYCOSES Black • Hard black nodules on
the immunocompromised population Piedraia hortae
Piedra hair shaft
• Caused by dimorphic fungi
White • Soft white nodules on
• Coccidioidomycosis Trichosporon
Piedra hair shaft
• Histoplasmosis
• Blastomycosis
• Paracoccidioidomycosis
• Ubiquitous fungi to which healthy
people are exposed but usually resistant
• In general, CD4 counts of <200
cells/uL – increases susceptibility to Black piedra (left) and White piedra (right)
opportunistic fungi
OPPORTUNISTIC
MYCOSES
• Candidiasis II. CUTANEOUS MYCOSES
• Cryptococcosis DERMATOPHYTOSES (RING WORMS)
• Aspergillosis
• Secrete the enzyme keratinase, which digests keratin (infect
• Mucormycosis only superficial keratinized structure)
• Pneumocystis pneumonia • Unable to grow in 37oC or in the presence of serum, hence, no
• Penicilliosis deep infections
• 3 important dermatophyte genera and their sites of infection
I. SUPERFICIAL MYCOSES Organism Skin Hair Nails
A. MALASSEZIA FURFUR Trichophyton x x x
TINEA VERSICOLOR (AN-AN) Microsporum x x no infection
Epidermophyton x no infection x
• Superficial skin infection of cosmetic importance localized to the
stratum corneum • transmission: soil (geophilic), animals (zoophilic) e.g. dogs and
• Hypopigmented macules/patches in dark skin, cats, human (anthropophilic) e.g. sharing towels
hyperpigmented macules/patches in fair skin Infections due to zoophilic or geophilic dermatophytes may produce
• Degradation of lipids leads to production of acids, and eventual a more intense inflammatory response than those caused by
anthropophilic fungi, being least adapted to human hosts. But they
destruction of melanocytes – associated with seborrheic
RESOLVE MORE QUICKLY. (Jawetz)
dermatitis Dr. Calderon
• (+)spaghetti and meatballs appearance in 10% KOH Moreover, infections due to anthrophilic dermatophytes cause the
preparation greatest number of human infections. They are usually mild and chronic,
• Malassezia is extremely difficult to propagate in laboratory and may be DIFFICULT TO ERADICATE. (Jawetz)
Dr. Rubio
culture and is culturable only in media enriched with C12- to PATHOGENESIS
C14-sized fatty acids.
• chronic infections often located in the warm, humid areas of
body
✔GUIDE QUESTION
A 28/M consulted because of hypopigmented macules his chest, upper
• inflamed circular border containing papules and vesicles
back, shoulders and arms. Scrapings of the lesions were taken for surrounding a clear area of relatively normal skin
microscopic examination. Which of the following techniques may be • hypersensitivity causes dermatophytid reactions
employed to rapidly visualize the fungal elements on microscopy? o Dermatophytid is an inflammatory reaction to dermatophytosis
A. India ink preparation C. KOH preparation at a cutaneous site distant from the primary infection.
B. PAS staining D. Mucicarmine staining
Potassium hydroxide in a wet mount (KOH mount) of skin
scrapings breaks down the human cells, enhancing the visibility of
the unaffected fungus
Dr. Calderon
Microscopy of the scrapings revealed short, unbranched hyphae and
numerous spherical cells that resemble bacon and eggs. What is the DERMATOPHYTID ON THE FOREHEAD ASSOCIATED WITH
most likely causative agent? SCALP LESION OF TINEA CAPITIS.
A. Aspergillus fumigatus C. Malassezia furfur Source: American Academy of Pediatrics
B. Nocardia brasiliensis D. Fonsecaea pedrosoi

SPECTRUM OF DISEASE
• Tinea corporis (body): “ringworm”
• Tinea cruris (groin): “jock itch”
• Tinea pedis (feet): “athlete’s foot”
• Tinea capitis (scalp)
• Tinea unguium (nail): Onychomycosis
• Tinea manum
• Tinea barbae (facial hair)
DIAGNOSIS Which organism causes fungemia in premature infants on IV lipid
• 10% KOH: septate hyphae supplements?
A. Trichophyton sp. C. Blastomyces dermatitidis
• Sabouraud agar: hyphae and conidia B. Malassezia furfur D. Candida albicans
• yellow fluorescence on Wood’s lamp - certain species of
The lipophilic nature of Malassezia plays a role in the
Microsporum will fluoresce under ultraviolet light
pathogenesis of infection. Intravenous fat emulsions support the
• PCR growth of the fungus.
Dr. Calderon
TREATMENT
• Local antifungal creams (e.g. topical imidazole) III. SUBCUTANEOUS MYCOSES
• Oral Griseofulvin is used for tinea unguium and tinea capitis
• Oral terbinafine
• Keep skin dry
A. SPOROTHRIX SCHENCKII
SPOROTRICHOSIS
✔GUIDE QUESTION • dimorphic fungus that lives on vegetation
A 10/M with 2 weeks pruritic scalp, with patchy hair loss. PE: three • occurs most often in gardeners, especially those who prune
scaly and circular patches about 3 cm in diameter, as well as alopecia roses
and black dots in the areas of hair loss. He also has cervical • histopathology: (+) cigar shaped yeasts, asteroid bodies
lymphadenopathy. What is the most likely etiology?
• transmission: thorn prick
A. Cryptococcus neoformans C. Candida glabrata
B. Trichophyton tonsurans D. Coccidioides immitis • treatment: itraconazole, potassium iodide for cutaneous form;
amphotericin B for systemic disease
Tinea capitis (also known as "herpes tonsurans", "ringworm of
the hair", "ringworm of the scalp", "scalp ringworm", and "tinea
tonsurans") is a cutaneous fungal infection (dermatophytosis) of MEMORY AID SPOROTRICHOSIS
the scalp. It is caused by Trichophyton and Microsporum. Plant a rose in the POT.
Dr. Calderon
(Sporotrichosis may also be treated with POTassium iodide)
B. OTHER SUBCUTANEOUS MYCOSES

AGENT FEATURE
MYCOSIS
(NICE TO KNOW)
• Sclerotic cell walls
• Phialophora verrucosa • Cauliflower-like lesions
• Fonsecaea pedrosoi
Chromoblastomycosis (CMB) • Fonsecaea compacta
• Rhinocaldiella aquaspera
• Cladosporum carrionii
• Sulfur granules from

• Pseudallescheria boydii interconnecting draining
sinuses
• Madurella mycetomatis
Mycetoma • Madurella grisea
• Exophiala jeanselmei
• Acremonium falciforme
• Darkly pigmented septate hyphae in tissue

• Phialophora richardsiae
• Bipolaris spicifera
Phaeohyphomycosis • Wangiella dermatitidis
• Exserohilum rostratum
• Alternaria
• Curvularia
SOME CLINICAL FEATURES OF DERMATOPHYTE INFECTION

FUNGI MOST FREQUENTLY
SKIN DISEASE LOCATION OF LESIONS CLINICAL FEATURES
RESPONSIBLE
Tinea corporis Circular patches with advancing red, Trichophyton rubrum,
Non-hairy, smooth skin
(ringworm) vesiculated border, and central scaling. Pruritic Epidermophyton floccosum
Tinea pedis Interdigital spaces on feet of Acute: itching, red vesicular. Chronic: itching, T. rubrum, Trichophyton
(athlete’s foot) persons wearing shoes scaling, fissures mentagrophytes, E. floccosum
Tinea cruris Erythematous scaling lesion in intertriginous T. rubrum, T. mentagrophytes, E.
Groin
(jock itch) area. Pruritic floccosum
Scalp hair. Endothrix: fungus Circular bald patches with short hair stubs or
T. mentagrophytes, Microsporum
Tinea capitis inside hair haft. Ectothrix: broken hair within hair follicles. Kerion rare.
canis, Trichophyton tonsurans
fungus on surface of hair Microsporum-infected hairs fluoresce.
T. mentagrophytes, T. rubrum,
Tinea barbae Beard hair Edematous, erythematous lesion
trichophyton verrucosum
Nails thickened or crumbling distally, No fungi present in lesion. May
Tinea unguium Nail discolored; lusterless. Usually associated with become secondarily infected
tinea pedis with bacteria
IV. SYSTEMIC MYCOSES

OVERVIEW OF ENDEMIC MYCOSES
MYCOSIS ETIOLOGY ECOLOGY GEOGRAPHIC DISTRIBUTION TISSUE FORM
Global; endemic in Ohio,
Avian and bat Oval yeasts, 2 x 4 µm,
Histoplasma Missouri, and Mississippi River
Histoplasmosis habitats (guano); intracellular in
capsulatum valleys; central Africa (var.
alkaline soil macrophages
duboisii)
Semiarid regions of
Spherules, 10 – 80 µm,
Coccidioides posadasii southwestern United States,
Coccidioidomycosis Soil, rodents containing endospores, 2
or Coccidioides immitis Mexico, Central and South
– 4 µm
America
Mississippi, Ohio, and St. Thich-walled yeasts with
Blastomyces Unknown
Blastomycosis Lawrence River valleys, broad-based, usually
dermatitidis (riverbanks)
southeastern United States single, buds, 8 – 15 µm
Paracoccidioides Large, multiply budding
Paracoccidioidomycosis Unknown (soil) Central and South America
brasilensis yeasts, 15 – 30 µm
EPIDEMIOLOGY AND TRANSMISSION
• endemic in Ohio and Mississippi River valleys
• grows in soil contaminated with bird droppings (starlings) or
bat guano
• transmission by inhalation of airborne microconidia
PATHOGENESIS
• inhaled microconidia develop into budding yeast inside
macrophages
• spreads to liver and spleen
• dissemination in those who have defective CMI
MEMORY AID HISTOPLASMOSIS
A. COCCIDIOIDES IMMITIS HIstoplasma HIdes within macrophages.
CHARACTERISTICS
SPECTRUM OF DISEASE
• dimorphic fungus • Asymptomatic (in most persons)
o mold in soil
• Chronic Pneumonia: lesions calcify, which can be seen on chest
o spherule (not yeast) in tissue
X-ray (closely mimics PTB)
• endemic in arid regions of the southwestern United States and
• Disseminated: can occur in almost any organ, especially in lung,
Latin America
spleen, or liver
• white to tan cottony colonies
• Erythema nodosum
• Tongue ulcerations in AIDS patients
TRANSMISSION
• inhalation of arthrospores TREATMENT
DOC: Amphotericin B, Itraconazole
PATHOGENESIS If meningitis occurs: Fluconazole
• arthrospores form spherules
filled with endospores
• granulomata in bones and CNS
C. BLASTOMYCES DERMATITIDIS
• dissemination in those who CHARACTERISTICS
have defective CMI • dimorphic fungus
• round yeast with broad-based budding
CLINICAL FINDINGS • Endemic in eastern North America, (Ohio,
• Valley fever/San Joaquin valley fever/Desert rheumatism Mississippi)
o Self-limited influenza-like illness with fever, malaise, cough,
arthralgia, and headache TRANSMISSION
• Hilar adenopathy with pulmonary infiltrates, pneumonia, • inhalation of conidia
pleural effusions, or nodules
• Common opportunistic infection in AIDS patients from the SPECTRUM OF DISEASE
southwest United States • Chronic pneumonia
This condition is very common in Filipinos living in Latin America and • Ulcerated granulomas
Southwestern USA! • Verrucous skin lesions can simulate squamous cell carcinoma
Dr. Calderon
(SCC)
TREATMENT • Lytic bone lesions
• DOC: Amphotericin B, Itraconazole • Prostatitis
• If meningitis occurs: Fluconazole
MEMORY AID BLASTOMYCOSIS
Blasto Buds Broadly.
B. HISTOPLASMA CAPSULATUM
CHARACTERISTICS
• dimorphic fungus
• forms two types of asexual spores
o tuberculate macroconidia
§ typical thick walls and finger-like
projections
§ important in laboratory
identification
o microconidia
§ smaller, thin, smooth-walled spores
§ if inhaled, transmit the infection
B. CRYPTOCOCCUS NEOFORMANS
CHARACTERISTICS
• Oval yeast with narrow-
based bud surrounded by
a wide polysaccharide
capsule
• India ink preparation
• positive latex agglutina-
TREATMENT tion test (CALAS)
• DOC: Itraconazole
• Severe infection: Amphotericin B TRANSMISSION
• grows abundantly in soil containing bird (especially pigeon)
D. PARACOCCIDIOIDES BRASILIENSIS droppings
CHARACTERISTICS • transmission by inhalation of airborne yeast cells
• dimorphic fungus
SPECTRUM OF DISEASE
• thick yeast with multiple buds in wheel
configuration (mariner’s wheel) • asymptomatic lung infection
• restricted to Central and South America • meningitis
• encephalitis
TRANSMISSION • MCC of meningoencephalitis in HIV
• inhalation of conidia
A usual confusion among medical students is the clinical presentation of
Cryptosporidium vs Cryptococcus. Bothe organisms present with
SPECTRUM OF DISEASE distinguishable feature in the immunocompromised host:
• "Brazilian Blastomycosis” Cryptosporidium – diarrhea in the immunocompromised
• "South American Blastomycosis" Cryptococcus – meningitis in the immunocompromised
Dr. Rubio
• "Lutz-Splendore-de Almeida Disease" DIAGNOSIS
• "Paracoccidioidal Granuloma"
• India ink (clear halo) and
• chronic pneumonia
• Mucicarmine (red inner capsule)
• painful ulcers on mouth and nose
• Cryptococcal Antigen Latex Agglutination System (CALAS) of
• typical patient is male 30-50 years old → “man-hater fungus”
the CSF detects polysaccharide capsular antigen and is more
• rarely causes disease in fertile-age women, probably due to a
specific.
protective effect of estradiol
• Fungal culture
MEMORY AID PARACOCCIDIODOMYCOSIS
PARAcoccidio PARAsails with the captain’s wheel all the way TREATMENT
to Latin America. • drugs of choice
TREATMENT o amphotericin B and flucytosine
• chemoprophylaxis
• DOC: Itraconazole
o fluconazole
V. OPPORTUNISTIC MYCOSES C. ASPERGILLUS FUMIGATUS

A. CANDIDA ALBICANS CHARACTERISTICS
CHARACTERISTICS
• exist only as molds
• normal flora of URT, GIT, FGUT • septate hyphae that form V-shaped
• may appear as oval yeast with a single bud or as (dichotomous) branches
pseudohyphae (at 20C or room temperature)
• form germ tubes in serum and chlamydospores in culture (at TRANSMISSION
37C or body temperature) Fungal diseases: molds
• widely distributed in nature
• inhalation of airborne conidia
SPECTRUM OF DISEASE
Septate hyphae
• Immunocompetent with branching at
o oral thrush acute angles in
Aspergillosis
o vulvovaginitis → curd-like discharge
o intertrigo
o skin infections → satellite lesions
o onychomycosis
• Immunocompromised
o esophagitis
o subcutaneous nodules Coenocytic
o right-sided endocarditis (Aseptate) hypahe
with branching at
✔GUIDE QUESTION right angles in
Chronic mucocutaneous candidiasis is associated with a lack of which Mucormycosis
immune function?
A. Neutrophilic phagocytosis MEMORY AID ASPERGILLUS
B. T-cell function Think A!
C. B-cell function Acute Angles in Aspergillus.
D. Terminal complement
Chronic mucocutaneous candidiasis is a [primary (hereditary) PATHOGENESIS
immunodeficiency condition characterized by persistent or
• infections: wounds, burns, the cornea, external ear, sinuses
recurring infection with Candida. It is due to an inherent
malfunction of T-lymphocytes. • aspergilloma (fungus ball) in lung cavities
Dr. Calderon • allergic bronchopulmonary aspergillosis (ABPA)
o asthmatic symptoms with expectoration of brownish
bronchial plugs
GUIDE QUESTION 13
https://qrs.ly/gsck6n5
DIAGNOSIS E. PNEUMOCYSTIS JIROVECII
• Allergic bronchopulmonary aspergillosis: (FORMERLY CARINII)
o High level of IgE (IgE level > 1000 IU/dL) CHARACTERISTICS
o Sputum culture • indeterminate organism
o Wheezing patient and chest X-ray with fleeting infiltrates o The taxonomic classification of the Pneumocystis genus was
o Increased level of eosinophils debated for some time. It was initially mistaken for a
o Skin test: immediate hypersensitivity reaction trypanosome and then later for a protozoan. In the 1980s,
• Aspergilloma: chest X-ray or CT scan biochemical analysis of the nucleic acid composition of
• Invasive aspergillosis: sputum examination and culture Pneumocystis rRNA and mitochondrial DNA identified the
organism as a unicellular fungus rather than a protozoan.
TREATMENT Subsequent genomic sequence analysis of multiple genes
• drug of choice: amphotericin B including elongation factor 3, a component of fungi protein
• Allergic bronchopulmonary aspergillosis: corticosteroids synthesis not found in protozoa, further supported this notion.
• Aspergilloma: removal via thoracic surgery • major surface glycoprotein undergoes programmed
• Invasive aspergillosis: voriconazole, possibly Caspofungin (very rearrangements
high mortality) • diagnosis by staining BAL washings
o toluidine blue
o methenamine silver stain
ASPERGILLUS
• quantitative PCR for may be useful in distinguishing between
VS MUCORMYCOSIS colonization and active infection
https://qrs.ly/ztck6nh
PATHOGENESIS
• transmission occurs by inhalation of cysts
D. RHIZOPUS ORYZAE AND MUCOR SPP. • cysts in alveoli induce an inflammatory response consisting
MUCORMYCOSIS plasma cells
• saprophytic molds with nonseptate hyphae withOUT walls o frothy exudate that blocks oxygen exchange
and branches at RIGHT ANGLES (90 degrees)
SPECTRUM OF DISEASE
• rhino-orbital-cerebral infection with eschar formation
• patients with diabetic ketoacidosis, burns, or leukemia • PCP occurs when CD4<200
o most common AIDS-defining illness
✔GUIDE QUESTION • GOLD STANDARD IMAGING – CT SCAN: diffuse interstitial
The following medically important fungal genera have propensity to pneumonia with ground glass infiltrates bilaterally in
invade through blood vessel walls leading to local tissue infarction and • 100% mortality if untreated
necrosis, EXCEPT which one?
A. Epidermophyton C. Mucor TREATMENT AND PREVENTION
B. Aspergillus D. Rhizopus
• drug of choice: trimethoprim-sulfamethoxazole
Some fungi can lead to acute, rapidly evolving, often fatal • For sulfa allergy
infections due to vasculotropic invasive mycoses. These o atovaquone
angioinvasive (i.e. vessel-invading) fungal infections cause
o pentamidine
significant morbidity and mortality because of their propensity to
invade blood vessel walls, resulting in catastrophic tissue o dapsone (prophylaxis only)
ischemia, infarct, and necrosis. Mucor, Aspergillus, Rhizopus are Start prophylaxis when CD4+ count drops to < 200 cells/mm3 in HIV.
angioinvasive. Dr. Calderon
Epidermophyton, a dermatophyte, is unlikely to be angioinvasive

because of its biological limitations.
SYMPTOMS AND CONDITIONS ASSOCIATED WITH OPPORTUNISTIC MYCOSES

SYMPTOMS COMMON UNDERLYING CONDITION FUNGAL DISEASE
Vaginitis (erythema and pain) Antibiotic use, pregnancy, diabetes, AIDS Candida vaginitis
Facial swelling; lethargy; red exudate from
Ketoacidotic diabetes, leukemia Rhinocerebral mucormycosis
eyes and nares; necrotic tissue
Neonates with IV lipid supplements Fungemia: Malassezia
Fever without pulmonary symptoms
Indwelling IV catheters Fungemia: Candida
Fever; pain on urination Urinary catheter Urinary candidiasis
Difficulty in swallowing AIDS Esophageal candidiasis
Cryptococcal meningitis, Histoplasma or
AIDS coccidioidal meningitis, Candida
cerebritis
Meningeal symptoms
Severe neutropenia Aspergillus central nervous system
Hodgkin’s lymphoma; diabetes infection
Cryptococcal meningitis (chronic)
Immunocompromised patient, particularly Invasive Aspergillosis
if neutropenic
Pulmonary symptoms AIDS Pneumocystis pneumonia
Histoplasmosis, coccidioidomycosis
Urban homeless alcoholics Sporotrichosis (pulmonary)
Cough without upper respiratory
Previous lung damage, especially cavities Aspergilloma (fungus balls)
symptoms, hemoptysis
Endocarditis Intravenous drug abuse Candida or Aspergillus endocarditis
Enteritis (often with anal pruritus) Antibiotic use Candida enteritis
Whitish covering in mouth Premature infants, children on antibiotics Candida thrush
Corners of mouth sore Elderly suffering from malnourishment Perlèche
Sore gums Dentures Denture stomatitis
Skin lesions; endophthalmitis Indwelling catheter Candidemia
BRS Microbiology and Immunology (Board Review Series)
Basing on morphological and biochemical characterization of the
BACTERIOLOGY organism, the infection is most likely due to Staphylococcus
✔GUIDE QUESTION aureus. Methicillin-resistant S aureus (MRSA), which can be
A 28/M with a history of chronic alcoholism presents with fever and hospital or community acquired, is an increasingly common cause
productive cough. He was apparently well until 3 days prior to consult of impetigo; this pathogen is observed more often with the non-
when he developed cough, shaking chills, and headache. His cough has bullous form of impetigo than the bullous form.
been associated with the production of yellowish-green sputum, which Methicillin resistance in S aureus is mediated by the mecA gene,
occasionally was blood-tinged with brownish streaks. which encodes for a novel penicillin-binding protein (PBP), PBP-
Blood culture grew Gram-positive cocci in pairs and short chains. 2a, with reduced binding affinity for antibiotic. In MRSA, exposure
Which laboratory test will facilitate identification of the genus? to methicillin inactivates the 4 high-binding-affinity PBPs
A. Coagulase test C. Novobiocin sensitivity test normally present. PBP-2a, which displays a low affinity for
B. Catalase test D. Bacitracin sensitivity test methicillin, takes over the functions of these PBPs, permitting the
cell to grow.
In this case, the patient most likely has pneumonia, of which the Dr. Calderon
most common cause is Streptococcus pneumoniae. The growth of
Gram-positive cocci in pairs and short chain suggests the
organism is probably either Staphylococcus or Streptococcus. The
item asks for the test that will suggest the genus. catalase test
differentiate staphylococci (catalase-positive) from streptococci
(catalase-negative).
Dr. Calderon
A 5/M with perioral blistered lesions with honey-colored crusts.
Culture: (+) Gram-positive cocci, beta-hemolytic on blood agar plate,
catalase-positive, coagulase-positive. Sensitivity: resistant to
methicillin. What is the most likely organism?
A. Staphylococcus aureus C. Streptococcus agalactiae
B. Streptococcus pyogenes. D. Staphylococcus saprophyticus
GRAM-POSITIVE BACTERIA
The image on the left shows examples of the different types of hemolysis. Plates were inoculated in
cursive writing. Note that the growth on these plates does not show up well because transmitted
light was used to show the hemolysis. (Top) Alpha-hemolysis is partial hemolysis of the red blood
cells with a change in the color of hemoglobin resulting in a translucent area with a greenish
coloration. (middle) Gamma-hemolysis is not hemolysis. (Bottom) Beta-hemolysis is complete
lysis of the red blood cells, which result in a trans parent area around the colony.
From Engleberg NC, et al. Schaechter’s Mechanism of Microbial Disease. 5th ed. Baltimore, MD: Wolters Kluwerr Health; 2013.)
Here’s a video on hemolysis:
HEMOLYSIS
https://qrs.ly/pybp9v1
HEMOLYSIS
From Engleberg NC, et al. Schaechter’s Mechanism of Microbial Disease. 5th ed. Baltimore,
MD: Wolters Kluwerr Health; 2013.)
Dr. Calderon
STAPHYLOCOCCI - OVERVIEW SPECTRUM OF DISEASE: PYOGENIC

GRAM STAIN OTHER FEATURES ORGANISM • Skin & Soft Tissue Infections
catalase positive, Staphylococcus o bullous impetigo, folliculitis, furuncles, carbuncles, cellulitis,
coagulase positive aureus hidradenitis suppurativa, mastitis, surgical site infections
catalase positive, • Acute Endocarditis
gram positive Staphylococcus o most common cause of acute endocarditis
coagulase negative,
cocci in epidermidis o native valve (tricuspid valve) in IV drug abusers (IVDA)
novobiocin sensitive
clusters • Pneumonia
catalase positive,
Staphylococcus o nosocomial pneumonia, VAP, necrotizing pneumonia,
coagulase negative,
saprophyticus complicated by empyema, abscess or pneumatocele
novobiocin resistant
o post-viral pneumonia
• Osteomyelitis & Septic Arthritis
A. STAPHYLOCOCCUS AUREUS o from hematogenous spread or local introduction at wound site
CHARACTERISTICS o Brodie abscess
• gram-positive cocci in grape-like clusters § sequestered focus of osteomyelitis arising in the
• b-hemolytic yellow or golden colonies on blood agar metaphyseal area of a long bone
• catalase-positive
• coagulase-positive SPECTRUM OF DISEASE: TOXIGENIC
• salt-tolerant on mannitol salt agar (halotolerant) • Gastroenteritis
• “Gold” color is due the pigment staphyloxanthin o acute onset (4 hrs) of vomiting and diarrhea due to ingestion
of preformed heat-stable enterotoxin
o source: salad made with mayonnaise (potato or tuna salad)
• Scalded Skin Syndrome (Ritter disease)
o exfoliatin cleaves desmoglein in desmosomes
§ separation of epidermis at stratum granulosum
§ distinguish from TEN (Lyell disease) where separation
occurs at dermo-epidermal junction
• Toxic Shock Syndrome
HABITAT o due to TSST-1
• human nose (anterior nares) and skin o fever, hypotension, sloughing of the filiform papillae →
TRANSMISSION strawberry tongue, desquamating rash and multi-organ
involvement (>3)
• direct contact (hands)
o usually no site of pyogenic inflammation; blood CS negative
• fomites
o usual scenario: tampon-using menstruating women or in
• contaminated food patients with nasal packing for epistaxis
VIRULENCE FACTORS: TREATMENT
IMMUNOMODULATORS
• penicillinase-resistant
Protein A • prevents complement activation methicillin-sensitive SA penicillins
Coagulase • builds an insoluble fibrin capsule (MSSA) • (nafcillin, oxacillin, &
Hemolysins dicloxacillin)
• toxic to hematopoietic cells
(cytotoxins) methicillin-resistant SA • contain altered PBP
PV Leukocidin • specific for white blood cells (MRSA) • DOC is vancomycin
Catalase • detoxifies hydrogen peroxide vancomycin-resistant SA
• DOC is linezolid
Penicillinase • inactivates penicillin derivatives (VRSA)
✔GUIDE QUESTION
TISSUE PENETRANCE A 14-year-old Caucasian male presents with painful erythematous and
Hyaluronidase • hydrolyzes hyaluronic acid honey-colored crusted lesions around his mouth. Culture of the lesions
Fibrinolysin reveals gram-positive cocci in clusters. Further analysis reveals
• dissolves fibrin clots bacteria that are beta-hemolytic, coagulase positive, and appear golden
(staphylokinase)
• spread in fat-containing areas of on the blood agar plate. Which of the following helps the bacterium in
Lipase this infection bind to immunoglobulin and prevent phagocytosis when
the body
invading its host?
TOXINS A. Protein A C. Exfoliatin A
• superantigen causing epidermal B. Staphylokinase D. Protein M
Exfoliatin A and B
separation Protein A prevents phagocytosis by binding to the Fc region of IgG.
Enterotoxins • superantigens causing food Protein M is a cell-wall component that prevents phagocytosis in
(heat-stable) poisoning group A streptococci (Streptococcus pyogenes). Though M protein
helps the bacterium avoid phagocytosis initially, when the
Toxic shock syndrome • superantigen leading to toxic adaptive immune system is activated, antibodies against the M
toxin (TSST-1) shock syndrome protein antigen are created. These antibodies bind to the surface
• causes marked necrosis of the of the bacterium and promote phagocytosis through
Alpha toxin
skin and hemolysis opsonization. Antibodies against M protein may also cross-react
with antigens of the heart via molecular mimicry - this may result
in myocarditis.
Methicillin resistance in Staphylococcus aureus is carried in which
gene?
A. blaZ C. dfrB
B. mecA D. gyrA
Methicillin resistance in S aureus is mediated by the mecA gene,
which encodes for a novel penicillin-binding protein (PBP), PBP-
2a, with reduced binding affinity for antibiotic. In MRSA, exposure
to methicillin inactivates the 4 high-binding-affinity PBPs
normally present. PBP-2a, which displays a low affinity for
methicillin, takes over the functions of these PBPs, permitting the
cell to grow.
Lippincott Illustrated Reviews: Microbiology (Lippincott Illustrated Reviews Series)
B. STAPHYLOCOCCUS EPIDERMIDIS SPECTRUM OF DISEASE

CHARACTERISTICS • most common cause of
• gram-positive cocci in clusters o prosthetic valve endocarditis
o septic arthritis in prosthetic joints
o ventriculoperitoneal shunt infections
• coagulase-negative
TREATMENT
• novobiocin-sensitive
• whitish, non-hemolytic colonies on blood agar • removal of prosthetic device
• over 50% are methicillin-resistant and thus require vancomycin
C. STAPHYLOCOCCUS SAPROPHYTICUS
CHARACTERISTICS
• gram-positive cocci in clusters
• coagulase-negative
MEMORY AID NOVOBIOCIN SENSITIVITY • novobiocin-resistant
• whitish, non-hemolytic colonies on blood agar
NO StRES
• Nitrite negative (unlike E. coli)
NOvobiocin
Saprophyticus Resistant
EPIDEMIOLOGY
Epidermidis Sensitive
• 2nd most common cause of UTIs in sexually active women
HABITAT TRANSMISSION
• normal skin flora • autoinfection CLINICAL FINDINGS
• direct contact (hands) • dysuria, pyuria, and bacteriuria
PATHOGENESIS
• low-virulence organism TREATMENT
• glycocalyx adheres well to foreign bodies and form biofilms • TMP-SMX, quinolones
o prosthetic heart valves
o prosthetic joints
o ventriculoperitoneal shunts
o indwelling catheters
STREPTOCOCCI – OVERVIEW
GRAM STAIN OTHER FEATURES ORGANISM A. STREPTOCOCCUS PYOGENES

Catalase negative, alpha CHARACTERISTICS
Streptococcus
hemolytic, bile soluble, • gram-positive cocci in chains
pneumoniae
optochin-sensitive • catalase-negative
Catalase negative, alpha viridans • beta-hemolytic
hemolytic, bile insoluble, streptococcal
• bacitracin-sensitive
optochin-resistant sp.
Gram-positive • Lancefield group A
Catalase negative, beta
cocci in Streptococcus • positive PYR test
hemolytic, bacitracin-
chains pyogenes o The PYR test measures hydrolysis of l-pyrrolidonyl-β-
sensitive
naphthylamide and release of β-naphthylamine, which in the
Catalase negative, beta
Streptococcus presence of p-dimethylaminocinnamaldehyde forms a red
hemolytic, bacitracin-
agalactiae compound.
resistant
o Advantage: takes less than 1 minute to determine whether the
Catalase negative, Group D reaction is positive (S. pyogenes or group D streptococci) or
gamma hemolytic streptococci negative (all other streptococci).
MEMORY AID BACITRACIN SENSITIVITY
B – BRAS
Bacitracin
group B strep Resistant
group A strep Sensitive
HABITAT TRANSMISSION SPECTRUM OF DISEASE: IMMUNOLOGIC

• human throat (oropharynx) • respiratory droplets • Acute Rheumatic Fever
• skin o Post-pharyngitic
PATHOGENESIS: o cross-reacting antibodies to M proteins and antigens of joint,
heart, and brain tissue
VIRULENCE ENZYMES
o Jones Criteria:
• degrades hyaluronic acid
Hyaluronidase § migratory polyarthritis
(spreading factor)
§ pancarditis
Streptokinase § erythema marginatum
• activates plasminogen
(fibrinolysin) § Sydenham chorea
DNase • degrades DNA in exudates or § subcutaneous nodules
(streptodornase) necrotic tissue
C5A peptidase • inactivates complement C5A MEMORY AID JONES CRITERIA
TOXINS P–E–C–C–S
Erythrogenic toxin • produce scarlet fever Polyarthritis
Streptolysin O • highly antigenic Erythema marginatum
(oxygen-labile) • causes AB formation Chorea (Sydenham)
Streptolysin S (oxygen-stable) Carditis (Pancarditis)
Subcutaneous nodules
Pyrogenic exotoxin A • superantigen similar to TSST
• protease that rapidly destroys • Glomerulonephritis
Exotoxin B o post-impetigo (commonly the M12 type) OR post-pharyngitic
tissue
o M protein incites immune complex deposition on the
M protein is a major virulence factor for the group A streptococcus. It glomerular basement membrane
inhibits the activation of complement and protects the organism from o ssx: hypertension, periorbital edema, hematuria
phagocytosis. It is also the weakest point in the organism's defense.
Among the so many virulence factors linked to GABHS, remember M TREATMENT
first.
Dr. Calderon • DOC is Penicillin G
PATHOGENESIS: EVIDENCES OF INFECTION • patients with a history of rheumatic fever require long-term
• anti-streptolysin O (ASO) titers to document antecedent antibiotic prophylaxis to prevent recurrence of the disease
pharyngitis ✔GUIDE QUESTION
• anti-DNAse B titers to document antecedent skin infection An 8/M presents with fever, migrating joint pains in the knees and
o Streptolysin O is irreversibly inhibited by cholesterol in skin elbows, and has raised erythematous serpentine-like lesions on his
lipids back. The patients clinical presentation is most likely due to which
pathophysiologic mechanism?
• anti-streptokinase antibodies decrease efficacy of
A. IgG antibodies complexes with self or foreign antigens resulting
streptokinase in managing MI in complement activation
B. Pre-sensitized CD4+ helper T-cell releases cytokines when re-
SPECTRUM OF DISEASE: PYOGENIC exposed to the offending material
• Skin & Soft Tissue Infections C. Antigens cross-link IgE antibodies triggering vasoactive amine
o Impetigo contagiosa: release
§ perioral blistered lesions with honey-colored crust D. Cross-reaction of antibodies to bacterial antigens with self-
antigens leading to cytotoxicity
§ accumulation of neutrophils beneath stratum corneum
§ complication: poststrep GN J♡NES criteria for rheumatic fever:
o Erysipelas • Joints – polyarthritis
§ superficial infection extending into dermal lymphatics • ♡ - Carditis
o Cellulitis • Nodules (subcutaneous)
§ deeper infection involving subcutaneous/dermal tissues • Erythema marginatum
§ facilitated by hyaluronidase (spreading factor) • Sydenham chorea
o Necrotizing fasciitis
The item describes a case of rheumatic fever (RF), a type II
§ rapidly progressive infection of deep subcutaneous tissues hypersensitivity reaction. In this reaction, IgM and IgG bind to
§ facilitated by exotoxin B antigen to activate complement, and can either be cytotoxic or
§ Fournier's gangrene: form of necrotizing fasciitis involving non-cytotoxic depending on the target of the antibodies.
the male genital area and perineum; often caused by mixed Below review the features of the other hypersensitivity reactions
organisms but can be caused by GABHS (see also Pathology):
• Pharyngitis Type I hypersensitivity is caused by antigen cross-linking of IgE
o most common bacterial cause of sore throat on sensitized mast cells. This causes the release of vasoactive
o inflammation, exudate, fever, leukocytosis, and tender CLAD mediators (e.g., histamine, leukotrienes, and prostaglandin D2)
o pyogenic complications: peritonsillar and retropharyngeal and inflammatory mediators (e.g., TNF-alpha and leukotriene
(Quincy) abscess, otitis, sinusitis, meningitis B4). This mechanism is responsible for asthma, allergic rhinitis
(hay fever), anaphylaxis, angioedema, urticaria, and allergies to
SPECTRUM OF DISEASE: TOXIGENIC medications and food. Asthma, in particular, is characterized by
cough and shortness of breath that is worse at night and
• Scarlet Fever associated with end-expiratory wheezing.
o Post-pharyngitic
Type III hypersensitivity reactions are immune complex-
o due to erythrogenic toxin, seen in lysogenized strains
mediated. In these reactions, antigen-antibody complexes deposit
o fever, strawberry tongue, centrifugal rash (sandpaper-like), in healthy tissues, initiating localized inflammatory responses in
Pastia lines, desquamation these tissues. Examples of conditions caused by type III
o Dick test for susceptibility – method of determining hypersensitivity reactions are systemic lupus erythematosus,
susceptibility to scarlet fever by injection into the skin of 0.1 serum sickness, and post-streptococcal glomerulonephritis.
cubic centimeter of scarlet fever toxin (do not confuse this with Type IV hypersensitivity reactions are cell-mediated. In these
the Schick test for diphtheria susceptibility) reactions, T-cells are sensitized to an antigen. On subsequent
• Streptococcal Toxic Shock Syndrome exposure to that antigen, effector T-cells and macrophages will
o clinically similar but milder than S. aureus TSS be activated. Examples of type IV hypersensitivity reactions
o due to pyrogenic exotoxin A include type I diabetes mellitus, multiple sclerosis, and
Hashimoto’s thyroiditis.
o recognizable site of pyogenic inflammation
o blood cultures are often positive
B. STREPTOCOCCUS AGALACTIAE Cefalexin, a first-generation cephalosporin, is active against non-

(GROUP B STREPTOCOCCI) resistant strains of Staphylococcus aureus (e.g. hidradenitis,
carbuncle, folliculitis) – but not the organisms mentioned in A, B,
CHARACTERISTICS HABITAT and C.
• gram-positive cocci in • vagina Dr. Calderon
chains
• Catalase-negative TRANSMISSION D. STREPTOCOCCUS PNEUMONIAE
• Beta-hemolytic • transvaginal CHARACTERISTICS
• Bacitracin-resistant • transplacental • Gram-positive "lancet-shaped" cocci in pairs or chains
• Lancefield group B • Catalase-negative
• hydrolyze hippurate • Alpha-hemolytic
• CAMP test–positive • Bile soluble and optochin-sensitive
• grow using Lim broth • positive Quellung reaction
SPECTRUM OF DISEASE
• urinary tract infection in pregnant women
• neonatal pneumonia, sepsis and meningitis
o most common cause
o predisposing factors
§ intrapartum fever (T>38)
§ PROM (>18h)
§ vaginal colonization
§ complement deficiency Positive Quellung reaction: (+) capsular swelling when mixed with a small
• endometritis amount of antiserum (serum with antibodies to the capsular antigens) and
methylene blue
TREATMENT
• DOC is penicillin G MEMORY AID JONES CRITERIA
• penicillin G + aminoglycoside for serious infections Optochin Sensitivity Quellung Reaction
• all pregnant women should be screened for GBS colonization OVERPASS QUELLUNG reaction =
at 35-37 weeks AOG Optochin capsular
o chemoprophylaxis with IV Penicillin or Ampicillin 4 hours Viridans Resistant SWELLUNG (swelling)
Pneumoniae Sensitive
prior to delivery
Encapsulated Bacteria
Some Killers Have Pretty Nice and Shiny Bodies.
C. GROUP D STREPTOCOCCI Streptococcus pneumoniae
CHARACTERISTICS Klebsiella pneumoniae
• gram-positive cocci in chains Haemophilus influenzae
Pseudomonas aeruginosa
• catalase-negative
Neisseria meningitidis
• gamma hemolytic colonies
Salmonella typhi
• Lancefield group D B group streptococci
• bile insoluble and optochin-resistant
• hydrolyzes esculin in bile-esculin agar (BEA) HABITAT AND TRANSMISSION
• positive PYR test • habitat is upper respiratory tract
• E. faecalis can grow in 6.5% NaCl while S. bovis cannot • transmission via respiratory droplets
HABITAT PATHOGENESIS
• human colon • capsule retards phagocytosis
• urethra and female genital tract can be colonized • IgA protease for colonization
• c-substance reacts with CRP
TRANSMISSION
• may enter bloodstream during gastrointestinal (GI) or SPECTRUM OF DISEASES: PYOGENIC
genitourinary tract procedures • Pneumonia
o most common cause of CAP
SPECTRUM OF DISEASES o Blood-tinged, pink, or rusty sputum
• UTIs due to indwelling urinary catheters and urinary tract o Blood cultures often positive
instrumentation • Otitis media, sinusitis, meningitis
• biliary tract infections • Septic shock
• endocarditis in patients who underwent GIT surgery due to E. o splenectomy predisposes to sepsis
faecalis
• Marantic endocarditis in patients with abdominal malignancy TREATMENT
due to S. bovis • Penicillin G
• Levofloxacin or Vancomycin combined with Ceftriaxone for
TREATMENT penicillin resistance
• Penicillin plus gentamicin
• Vancomycin for penicillin-resistance PREVENTION
• Linezolid for vancomycin-resistant strains • polyvalent (23-type) polysaccharide vaccine
• conjugated vaccine: pneumococcal polysaccharide coupled
✔GUIDE QUESTION with carrier protein (diphtheria toxoid)
Cefalexin may be useful to treat which infection?
A. Enterococcal endocarditis ✔GUIDE QUESTION
B. Listerial meningitis
While testing various strains of Streptococcus pneumoniae, a researcher
C. MRSA pneumonia
discovers that a certain strain of this bacteria is unable to cause disease
D. Hidradenitis suppurativa
in mice when deposited in their lungs. What physiological test would
E. All of the above
most likely deviate from normal in this strain of bacteria as opposed to
NONE of the cephalosporins are active against the following: a typical strain?
• Enterococci A. Bile solubility C. Quellung reaction
• Listeria monocytogenes B. Optochin sensitivity D. Hemolysis on BAP
• MRSA
The item describes that a non-virulent strain of pneumococci was PATHOGENESIS: VIRULENCE FACTORS
given to the animals, which did not cause disease. This is perhaps • antiphagocytic capsule (poly-D-glutamate)
because the bacteria did not possess a capsule (remember
Griffith’s experiment?). So, the question here is asking for a test for • calmodulin-dependent adenylate
virulence. If virulence is mainly conferred by the capsule (e.g. as
Edema factor (EF)
cyclase
antiphagocytic factor), then the Quellung reaction can help can
• inhibits a signal transduction in cell
differentiate the virulent (encapsulated) from the non-virulent Lethal factor (LF)
(naked) strain.
division
Dr. Calderon Protective • mediates the entry of the other two
antigen (PA) components into cell
E. VIRIDANS STREPTOCOCCI
(S. MUTANS, S. SANGUIS)
CHARACTERISTICS
• gram-positive cocci in chains
• Catalase-negative
• Alpha-hemolytic
• Bile insoluble and optochin-resistant
HABITAT AND TRANSMISSION

• habitat is oropharynx
• enters bloodstream during dental procedures
MEMORY AID OPTOCHIN RESISTANCE

Viridans streptococci live in the mouth because they are not
afraid of-the-chin (op-to-chin resistant) https://whyfiles.org/shorties/089anthrax_receptor/index.html
SPECTRUM OF DISEASE
PATHOGENESIS
• Cutaneous Anthrax
• glycocalyx enhances adhesion to damaged heart valves o direct epidermal contact with spores causes formation of a
• protected from host defenses within vegetations malignant pustule with subsequent eschar and central
necrosis
SPECTRUM OF DISEASE o 20% mortality rate
• S. mutans, for dental caries • Inhalational Anthrax
• S. sanguis, for subacute bacterial endocarditis (SBE) o inhaled spores from animals (woolsorter’s disease) or from
o most common cause of subacute and native valve weaponized preparations (bioterrorism)
endocarditis o prolonged latent period (2 mos) before rapid deterioration
• S. intermedius, for brain abscesses o massively enlarged mediastinal lymph nodes, pulmonary
hemorrhage, meningeal symptoms
TREATMENT o 100% mortality rate without immediate treatment
• Penicillin G with or without an aminoglycoside (Gentamicin) • Gastrointestinal Anthrax
• Vancomycin for penicillin-resistance o ingestion of live spores leads to UGI ulceration, edema and
• Linezolid for vancomycin-resistant strains sepsis (rapidly-progressive course)
o mortality rate approaches 100%
GRAM-POSITIVE RODS TREATMENT
GRAM • cutaneous anthrax
OTHER FEATURES ORGANISM
STAIN o DOC is ciprofloxacin
aerobic, nonmotile, • inhalational/gastrointestinal anthrax
Bacillus anthracis
box-car-shaped o DOC is ciprofloxacin or doxycycline with one or two
aerobic, motile, additional antibiotics (rifampin, vancomycin, penicillin,
Bacillus cereus
reheated fried rice imipenem, clindamycin, clarithromycin)
spore-
anaerobic,
forming Clostridium tetani
tennis-racket-like ✔GUIDE QUESTION
gram
anaerobic, Clostridium In 2001, a series of letters containing spores of Bacillus anthracis were
positive
bulging cans botulinum mailed to members of the media and to the United States Senate offices.
rods
anaerobic, lecithinase Clostridium The result was 22 cases of anthrax with five deaths. The heat resistance
gas-forming perfringens of bacterial spores, such as those of B. anthracis, is due in part to their
anaerobic, Clostridioides dehydrated state and in part to the presence of large amounts of which
of the following?
pseudomembranes difficile
A. Peptidoglycan C, Chitin
non-spore- aerobic, nonmotile, B. Teichoic acids D. Calcium dipicolinate
Corynebacterium
forming curved, Chinese
diphtheriae Spores of Bacillus species are dormant and extremely resistant to
gram characters
many environmental stresses including, heat, desiccation,
positive aerobic, curved, Listeria radiation, and a variety of toxic chemicals. As a consequence,
rods tumbling motility monocytogenes spores can survive for extremely long periods, certainly hundreds
of years and perhaps much longer. Spore resistance is due to a
I. BACILLUS ANTHRACIS variety of factors, including the outer spore coats and the relative
impermeability of the spore's inner membrane.
CHARACTERISTICS
Dipicolinic acid forms a complex with calcium ions within the
• aerobic, gram-positive box-car like rods endospore core. This complex binds free water molecules, causing
• nonmotile dehydration of the spore. Two genera of bacterial pathogens are
• spore-forming known to produce endospores: the aerobic Bacillus and anaerobic
• Medusa head morphology Clostridium.
o dry "ground glass" surface and irregular edges with
projections along lines of inoculation SUPPLEMENT
MCC of death is pulmonary hemorrhage in the ff:
HABITAT AND TRANSMISSION • Anthrax (pulmonary) aka wool sorter’s disease
• habitat is soil • Leptospirosis, severe (Weil’s syndrome)
• transmission by contact with infected animals or inhalation of • Congenital syphilis
spores from animal hair and wool (woolsorter’s disease)
II. BACILLUS CEREUS HABITAT AND TRANSMISSION

CHARACTERISTICS • habitat is soil
• entry through traumatic implantation into tissues with low
• aerobic, gram-positive spore-forming rod
oxygenation leads to spore termination, growth, & toxin
• motile
production
PATHOGENESIS
• spores on grains such as rice survive steaming and rapid frying
• spores germinate under anaerobic conditions in the wound
• spores germinate when rice is kept warm for many hours (e.g.,
• tetanus toxin (tetanospasmin)
reheated fried rice)
o protease that cleaves proteins involved in the release of
glycine from Renshaw cells in spinal cord
MEMORY AID BACILLUS CEREUS
o Prevents release of GABA by cleaving of synaptobrevin 2
Food poisoning from reheated fried rice? EMETIC
Be serious! Bacillus cereus Tetanospasmin
SITE OF MECHANISM OF
PATHOGENESIS RESULT
ACTION ACTION
• Heat-Labile Enterotoxin Inhibits release of
o cholera-like enterotoxin causes ADP-ribosylation, increasing GABA by cleavage Rigidity: trismus,
cAMP of proteins risus sardonicus,
• Heat-Stable Enterotoxin Presynaptic
critical for proper opisthotonos,
o staphylococcal-like enterotoxin functions as superantigen terminals
function of apnea/laryngospasm,
synaptic vesicle dysphagia, ↑DTRs
BACILLUS CEREUS FOOD-ASSOCIATED INFECTION release
Blocks
Neuromuscular Weakness or
neurotransmitter
junction paralysis
release
Loss of inhibition may also affect preganglionic sympathetic neurons in
the lateral gray matter of the spinal cord and produce sympathetic
hyperactivity and high circulating catecholamines. Autonomic
dysfunction may occur: hypertension, tachycardia, dysrhythmia,
hyperpyrexia, profuse sweating, peripheral vasoconstriction
Dr. Calderon
TREATMENT
• debridement of primary wound
• Metronidazole or penicillin - Metronidazole (400mg rectally or
500 mg IV every 6 h for 7 days) is the preferred antibiotic. An
alternative is penicillin (100,000–200,000 IU/kg per day),
although this drug theoretically may exacerbate spasms
(Harrisons)
• TIG (at the wound site)
• Vaccination with tetanus toxoid
o given in childhood and every 10 years thereafter
ALGORITHM FOR CLINICAL AND

PATHOLOGIC PROGRESSION OF TETANUS
Harrison’s Principles of Internal Medicine
SPECTRUM OF DISEASE: FOOD POISONING

EMETIC FORM DIARRHEAL FORM
Implicated food Rice Meat, vegetables
Incubation
< 6 (mean, 2) > 6 (mean, 9)
period (hours)
Vomiting, nausea, Diarrhea, nausea,
Symptoms
abdominal cramps abdominal cramps
Duration
8 – 10 (mean, 9) 20 – 36 (mean, 24)
(hours)
Enterotoxin Heat-stable Heat-labile
SPECTRUM OF DISEASE
• Ophthalmitis
o occur after traumatic penetrating eye injuries of the eye with a
soil-contaminated object
o complete loss of light perception within 48 hours of injury
TREATMENT
• food poisoning (emetic/diarrheal)
o symptomatic treatment only
• ophthalmitis
o vancomycin, clindamycin, ciprofloxacin or gentamicin
III. CLOSTRIDIUM TETANI

CHARACTERISTICS
• anaerobic, gram-positive, spore-forming rods
• spore is at one end (terminal spore) so organism looks like a
tennis racket
TETANUS PROPHYLAXIS HABITAT AND TRANSMISSION
VACCINATION HISTORY • habitat is soil and human colon
Uncertain • myonecrosis results from contamination of wound with soil or
>3 doses
WOUND or <3 doses feces
Toxoid TIG Toxoid TIG • food poisoning is transmitted by ingestion of contaminated food
(TeANA) (ATS) (TeANA) (ATS)
PATHOGENESIS
NO
YES only if • Gas Gangrene
Clean, minor YES NO NO o alpha toxin, a lecithinase that cleaves cell membranes
last dose
>10 years o Gas produced by anaerobic metabolism
NO • Food Poisoning
YES only if o production of enterotoxin which acts as superantigen
Contaminated YES YES NO
last dose SPECTRUM OF DISEASE: TOXIGENIC
>5 years • Gas Gangrene
o pain, edema and cellulitis with crepitation
IV. CLOSTRIDIUM BOTULINUM o hemolysis and jaundice are common
CHARACTERISTICS • Food Poisoning
o 8- to 16-hour incubation period
• anaerobic, gram-positive, spore-forming rods
o characterized by watery diarrhea with cramps & little
HABITAT AND TRANSMISSION vomiting
• habitat is soil o resolves in 24 hours
• organism and botulinum toxin transmitted in improperly TREATMENT
preserved food • wound debridement and penicillin for gas gangrene
o alkaline vegetables such as green beans, peppers, and
• supportive management for food poisoning
mushrooms
o smoked fish PREVENTION
o canned goods (bulging) • proper wound care
o honey • adequate cooking
PATHOGENESIS
• botulinum toxin (heat-labile neurotoxin) blocks acetylcholine VI. CLOSTRIDIUM DIFFICILE (Old Name)
release causing flaccid paralysis (descending pattern) CLOSTRIDIOIDES DIFFICILE (New Name)
• eight immunologic types of toxin CHARACTERISTICS
o types A, B, and E are most common in humans • anaerobic, gram-positive, spore-forming rods
• Botox is a commercial preparation of exotoxin A • exotoxin in stool detected by cytopathic effect (final phase by
o uses: wrinkle removal, torticollis which viral cells infect cells) on cultured cells or ELISA
SPECTRUM OF DISEASE: TOXIGENIC HABITAT AND TRANSMISSION
• Food-Borne Botulism • carried in the colon
o eye symptoms o 3% of the general population
§ BOV, diplopia, ptosis, mydriasis o up to 30% of hospitalized patients
o bulbar signs (4 Ds): diplopia, dysphonia, dysarthria, dysphagia • transmitted by the fecal-oral route
o anticholinergic effects
• hands of hospital personnel are important intermediaries
§ dry mouth, constipation, abdominal pain
o bilateral descending flaccid paralysis
PATHOGENESIS
o respiratory paralysis
• antibiotics suppress normal flora, allowing C. difficile to
QUICK HITS! TRIAD OF BOTULISM overgrow
1. Symmetric descending flaccid paralysis (with prominent o clindamycin, 2nd & 3rd gen cephalosporins, ampicillin
bulbar involvement) • exotoxins A (enterotoxin) and B (cytotoxin) inhibit GTPases,
2. Absence of fever leading to apoptosis and death of enterocytes
3. Intact sensorium o pseudomembranes are the visual result
• Infant Botulism (Floppy Baby Syndrome) • infection can precipitate flare-ups of ulcerative colitis
o when babies ingest spores found in household dust or honey
o due to absence of competitive bowel microbes SPECTRUM OF DISEASE: TOXIGENIC
• Wound Botulism • Pseudomembranous Colitis
o traumatic implantation and germination of spores at the o Non-bloody diarrhea associated with pseudomembranes
wound site (yellow-white plaques) on the colonic mucosa
o toxic megacolon can occur
TREATMENT TREATMENT
• adequate ventilatory support • causative antibiotic should be withdrawn
• elimination of the organism from GIT • oral metronidazole or vancomycin should be given and fluids
o judicious use of gastric lavage and metronidazole or penicillin replaced - oral vancomycin because it has poor intestinal
• trivalent botulinum antitoxin (types A, B, E) absorption, hence, it ‘coats’ the lesions with antibiotic
• surgery if toxic megacolon develops
PREVENTION
MEMORY AID CLOSTRIDIUM
• proper sterilization of all canned and vacuum-packed foods
Clostridium TETani = TETanic paralysis
• adequate cooking
Clostridium BOTulinum = BOTulism from bad BOTtles of food
• discard bulging/swollen cans Clostridium PERFringens = PERForates a gangrenous leg
(gas gangrene)
V. CLOSTRIDIUM PERFRINGENS Clostridioides DIfficile = DIarrhea
CHARACTERISTICS OTHER CLOSTRIDIA
• anaerobic, gram-positive, spore-forming rods • C. septicum: Nontraumatic myonecrosis in
• double hemolysis on blood agar immunocompromised patients
• growth on egg-yolk agar • C. sordellii: Toxic shock syndrome associated with septic
o nonmotile but with rapidly spreading growth on culture abortion
media • C. tertium: Traumatic wound infections
MOST COMMON SPECIES OF CLOSTRIDIUM (SPORE FORMER) IN CLINICAL SAMPLES
SPECIES COLONY GRAM STAIN CHARACTERISTICS
“Box-car” (short and fat) shaped rods;
C. Large, white, with double-zone Lipase negative; lecithinase positive;
short chains may be seen; rare spores
perfringens hemolysis indole negative; reverse CAMP positive
seen
Often stain Gram-negative or variable;
C. ramosum Large, spready white colony cells are more slender and longer than C. Commonly isolated from clinical samples
perfringens; spores not commonly seen
Large, Gram-positive rods with
subterminal spores seen; lecithinase Less frequently isolated than C.
C. sordelii White
positive; lipase negative; indole and perfringens, C. ramosum, and C. septicum
urease positive
Thin bacilli with terminal spores: “snow-
shoe” or “tennis racket” appearance; May be part of gastrointestinal flora;
C. tetani
lecithinase negative; lipase weak positive; cause of tetanus
indole variable and urease negative
Long, filamentous bacilli with rare When isolated from blood cultures,
C. septicum White, swarming colonies subterminal spores seen; lecithinase , indicates a possible gastrointestinal
lipase, and urease negative malignancy
White colonies with distinctive
Cause of pseudomembranous colitis and
“horse-barn” odor; selective
C. difficile Thin, long bacilli with spores seen antibiotic-associated diarrhea; rarely
CCFA media: yellow, ground-
found outside of the gastrointestinal tract
glass-appearing colonies
VII. CORYNEBACTERIUM DIPHTHERIAE MEMORY AID

CHARACTERISTICS DIPHTHERIA BETA-PROPHAGE
• aerobic, non-spore-forming, non-motile gram-positive rods ABCDEFG of Diphtheria ABCDE of beta-prophage-
• club or comma-shaped rods arranged in V or L shape ADP-ribosylation encoded toxins
• looks like Chinese characters Beta-prophage ShigA-like toxin (EHEC)
• metachromatic granules Corynebacterium Botulinum toxin
• Culture: Potassium tellurite: dark black colonies Diphtheriae Cholera toxin
• Loeffler’s medium: after 12 hours of growth, stain with Elongation Factor-2 Diphtheria toxin
methylene blue. Granules (metachromatic) Erythrogenic toxin
• Reddish metachromatic (Babes-Ernst / Volutin) granules (S. pyogenes)
can be seen
SPECTRUM OF DISEASE
• modified Elek test: for detection of toxigenicity
• prominent thick, gray, pseudomembranes over tonsils and
throat
• habitat is human throat
• complications
• transmission via respiratory droplets o airway obstruction
o Myocarditis - A-V conduction block, dysrhythmia
PATHOGENESIS o Neural involvement: peripheral nerve palsies, GBS, palatal
• exotoxin inhibits protein synthesis by adding ADP-ribose to paralysis, neuropathies, cranial nerve and/or muscle paralysis
elongation factor-2 (EF-2)
o subunit A, has ADP-ribosylating activity TREATMENT
o subunit B, binds the toxin to cell surface • antitoxin and penicillin G
o exotoxin encoded by b-prophage
• pseudomembranes result from death of mucosal epithelial cells PREVENTION
• toxoid vaccine, usually in combination with tetanus toxoid and
pertussis vaccine (DTaP)
• Schick test: injection of diphtheria exotoxin into the skin, to
determine whether a person is susceptible to infection by
diphtheriae (not to be confused with Dick test in scarlet fever)
VII. LISTERIA MONOCYTOGENES

CHARACTERISTICS
• aerobic, non-spore-forming, gram-positive rods
• arranged in V- or L-shape
• tumbling motility
• narrow zone of beta-hemolysis
• cold enhancement: paradoxical growth in cold temperature
HABITAT
• colonizes GI and female GUT
• widespread in animals, plants, and soil
TRANSMISSION
• across placenta or by contact during delivery
• ingestion of unpasteurized milk products, e.g., cheese
PATHOGENESIS
• internalin: interacts with E-cadherin on the surface of cells
• listeriolysin: escape from phagosomes
• actin rockets (actin polymers): propels the bacteria through
the membrane of one human cell and into another
Microbiology: An Evolving Science (Fourth Edition)
SPECTRUM OF DISEASE • Adult Listeriosis
• Early-Onset Neonatal Listeriosis o bacteremia, sepsis, or meningitis in pregnant, elderly, or
(granulomatosis infantiseptica) immunocompromised individuals
o transplacental transmission TREATMENT
o characterized by late miscarriage or birth complicated by • ampicillin with or without gentamicin
sepsis, multiorgan abscesses, and disseminated granulomas
• Late-Onset Neonatal Listeriosis PREVENTION
o transmitted during childbirth and manifests as meningitis or • pregnant women and immunocompromised patients should not
meningoencephalitis ingest unpasteurized milk products or raw vegetable
GRAM NEGATIVE BACTERIA
actually Mueller-Hinton agar with 5% chocolate sheep blood plus

GRAM-NEGATIVE COCCI the following antibiotics (VPN):
GRAM STAIN OTHER FEATURES ORGANISM • Vancomycin (inhibits gram-positive organisms)
encapsulated, ferments Neisseria • Polymyxin* (inhibits gram-negative organisms excluding
gram negative maltose and glucose meningitidis Neisseria species)
diplococci insignificant capsule, Neisseria • Nystatin (inhibits fungi)
ferments glucose only gonorrhoeae *Alternatively, polymyxin can sometimes be replaced with colistin
(hence, VCN) or trimethoprim.
MEMORY AID NEISSERIA Dr. Calderon
Neisseria MeninGitidis
ferments Maltose and Glucose I. NEISSERIA MENINGITIDIS
Neisseria GOnorrhoeae
ferments Glucose Only CHARACTERISTICS
• gram-negative "kidney-bean" diplococci
✔GUIDE QUESTION • large polysaccharide capsule
Gram stain of synovial fluid from the knee of a 20/F with suspected
• oxidase-positive colonies on chocolate agar
bacterial arthritis reveals Gram-negative diplococci. To isolate the
Neisseria gonorrhoeae, the specimen should be plated on which of the • ferments maltose and glucose
following?
A. Chocolate agar HABITAT AND TRANSMISSION
B. Thayer-Martin medium • habitat is the URT
C. Chocolate agar enriched with factors X and V
• transmission via respiratory droplets
D. In an armadillo
• humans are the only natural hosts
The presence of bacteria in the synovial fluid suggests an • high carriage rate in close quarters
infection. Synovial fluid analysis is also useful to help distinguish
o military recruits, dormitories, camps, travel (e.g. epidemic
crystal arthropathy from infectious arthritis, although the two
occasionally coexist. related to traveling to Saudi Arabia for the Hajj pilgrimage)
Cultures of likely sites of Neisseria gonorrhoeae infection are the Neonates are very susceptible from 6 to 24 months, when protective anti-
most important tests to perform for the diagnosis of disseminated meningococcal lgG is low.
Dr. Calderon
gonococcal infection (DGI) and consequent gonococcal arthritis.
Synovial fluid cultures are positive for N gonorrhoeae in no more PATHOGENESIS
than 50% of cases and alone are insufficient to establish the • antiphagocytic polysaccharide capsule
diagnosis. • endotoxin (LPS)
Neisseria gonorrhoeae is a fastidious organism. It is typically • IgA protease
cultured using an agar medium such as chocolate agar plate. • complement deficiencies in the late-acting complement
Normally, sterile clinical specimens (e.g. blood, synovial fluid, components (C6–C9) predispose to illness
CSF) should be inoculated onto enriched chocolate agar or o cannot form membrane-attack complexes
another nonselective medium.
Thayer-Martin agar, an antibiotic-containing selective medium,
is used for unsterile specimens (e.g. urethral, endocervical). It is
SPECTRUM OF DISEASE The polysaccharide capsule of Neisseria meningitides serogroup B is
• Meningitis poorly immunogenic even with protein conjugation. The
polysaccharide of serogroup B meningococcus is similar to certain
o most common cause among aged 2-18 yrs
human glycoproteins, such as intracellular adhesion molecules. This
o fever, headache, stiff neck, and an increased level of PMNs in similarity to human molecules likely explains the poor
spinal fluid immunogenicity. An alternate approach to vaccine development
required using meningococcal B proteins as the antigens.
II. NEISSERIA GONORRHOEAE

CHARACTERISTICS
• gram-negative "kidney-bean" diplococci
• insignificant capsule
• oxidase-positive colonies on Thayer-Martin medium
• ferment glucose only
✔GUIDE QUESTION
SIGNS OF MENINGEAL IRRITATION
The modified Thayer-Martin medium contains which antibiotics?
A. Voriconazole, cefuroxime, netilmicin
B. Vancomycin, colistin, nystatin
WHY IS MENINGITIS
C. Vancomycin, ciprofloxacin, neosporin
SO DANGEROUS? D. Voriconazole, cotrimoxazole, nystatin
https://qrs.ly/zpbp491
• Vancomycin – inhibits gram-positive organisms
• Polymyxin* - inhibits gram-negative organisms excluding
• Meningococcemia Neisseria species
o dissemination of meningococci into the bloodstream • Nystatin - inhibits fungi
o multiorgan disease, consumptive coagulopathy, petechial or *Sometimes replaced with colistin (hence, VCN) or trimethoprim.
Dr. Calderon
purpuric rash (purpura fulminans)
• Waterhouse-Friderichsen Syndrome
o most severe form of meningococcemia
o high fever, shock, widespread purpura, disseminated • habitat is the human genital tract
intravascular coagulation, thrombocytopenia, and adrenal • transmission by sexual contact or during passage through birth
insufficiency canal
§ bilateral hemorrhagic destruction of the adrenal glands
PATHOGENESIS
TREATMENT • pili - promote adherence to epithelial cells, antigenic variation,
• penicillin G (no significant resistance) anti-phagocytosis (binds bacteria tightly to host cell protecting
it from phagocytosis)
PREVENTION • lipo-oligosaccharide (LOS)
• vaccine contains capsular polysaccharide of strains A, C, Y, and • IgA protease
W-135 (memorize these four letters: ACYW) • Outer membrane protein porins: promote invasion into
o coupled to a carrier protein (e.g. diphtheria toxoid) epithelial cells
• rifampin chemoprophylaxis to close contacts o Opa proteins - promote adherence and invasion into
epithelial cells; expression results in opaque colonies
Conjugation of the polysaccharide from the capsule with a protein carrier
• complement deficiencies in the late-acting complement
enhances immunogenicity. I will explain this concept further later when
we touch base with Haemophilus influenzae. components (C6–C9) predispose to illness
Dr. Calderon o cannot form membrane-attack complexes
✔GUIDE QUESTION • usual co-infection with Chlamydia trachomatis
Which of the following virulence factors allows adherence of bacteria to
the mucous membranes of the respiratory, genitourinary and SPECTRUM OF DISEASE: LOCALIZED
gastrointestinal tracts? • Ophthalmia Neonatorum
A. Panton-Valentine Leukocidin o purulent conjunctivitis in newborns
B. Hyaluronidase • Gonococcal Urethritis
C. Coagulase
D. IgA protease
o urethritis and epididymitis in men
o most common cause of urethritis
IgA proteases cleave immunoglobulin A molecules at certain proline • Pelvic Inflammatory Disease
bonds in the hinge region. In this way, the enzyme allows the certain
bacteria to adhere to mucous membranes (which are lined with IgA).
o most common cause of PID
o complications:
Gram-negative:
§ sterility
• Neisseria gonorrhoeae (GU)
§ ectopic pregnancy
• Neisseria meningitides (respiratory)
• Haemophilus influenzae (respiratory)
§ chronic pelvic pain
Gram-positive: § dyspareunia
• Streptococcus pneumoniae (respiratory) § Fitz-Hugh-Curtis syndrome (perihepatitis): violin-string
Remember: Mucous membranes of the respiratory, genitourinary adhesions
and gastrointestinal tracts are lined with IgA (Remember: IgA
proteases are useful for bacterial pathogenesis). SPECTRUM OF DISEASE: DISSEMINATED
Dr. Calderon
Which capsular type of Neisseria meningitidis lacks immunogenicity even • Septic Arthritis
with protein conjugation, hence, not included in the vaccine? o most common cause in sexually active adults
A. A D. Y o arthritis, tenosynovitis, or pustules in the skin
B. B E. W-135
C. C DIAGNOSIS
N. meningitidis is classified into at least 13 serogroups based on • Nucleic acid amplification test (NAAT) – gold standard for the
characteristics of the polysaccharide capsule. Most invasive disease diagnosis of gonorrheal infections
(e.g. CNS, sepsis) is caused by serogroups A, B, C, W, and Y. The
relative importance of serogroups depends on geographic location TREATMENT
and other factors such as age. Serogroups B, C, and Y are the most
frequent causes of disease in the U.S., each accounting for about one • Ceftriaxone + Doxycycline due to frequent co-infection with
third of reported cases. Serogroup A is common in Sub-Saharan Chlamydia trachomatis
Africa but is rare in the U.S.
PREVENTION
• barrier contraception (condoms)
• treat sexual partner
• erythromycin ointment or silver nitrate to prevent conjunctivitis
✔GUIDE QUESTION
A 26-year-old male presents to his primary care physician with
complaints of burning with urination, penile discharge, and
intermittent fevers. A urethral smear shows gram negative diplococci
within white blood cells. The organism grows well when cultured on
Thayer-Martin agar. The patient is prescribed a course of ceftriaxone
and the infection resolves without further complication. One year later,
the patient returns with the same infection. Which of the following best
explains this lack of lasting immunity?
A. Antigenic variation
B. Polysaccharide capsule
C. Bruton's agammaglobulinemia There is also a positive Quellung test because of its capsule, similar to
D. Lack of necessary vaccination Streptococcus pneumoniae. Remember: Quellung = capsular swelling!
E. HIV infection HABITAT AND TRANSMISSION
Neisseria gonorrhoeae varies the composition of at least three • habitat is upper respiratory tract
major components of its outer membrane: • transmission via respiratory droplets
• pili, which mediate initial attachment to host cells (most
commonly) PATHOGENESIS
• membrane protein P.II, responsible for closer attachment • type b (Polyribitol phosphate) = 95% of invasive disease
resulting in phagocytosis
• lipo-oligosaccharide (LOS)
• IgA protease
Antigenic variation not only enables the pathogen to avoid the • affects children from 6 months to 1 year
immune response in its current host, but also allows re-infection o decline in maternal IgG and immature immune system
of previously infected hosts. If the pathogen's dominant antigen
can be altered (e.g. pilin antigenic variation), the pathogen can SPECTRUM OF DISEASE
then evade the host's acquired immune system.
• sinusitis, otitis media, pneumonia
• meningitis
III. OTHER NEISSERIACEAE • epiglottitis
• Eikenella corrodens and Kingella kingae cause culture- o most common cause
negative subacute bacterial endocarditis in patients with pre- o cherry red epiglottis
existing heart disease o thumb sign
• COPD exacerbations
Thumb sign (arrow)
MEMORY AID HACEK ORGANISMS
The thumb sign in epiglottitis is a manifestation of an edematous and
nagha-HACEK ng lagim sa mga may sakit sa puso enlarged epiglottis. Here it is seen on lateral soft-tissue radiograph of the
Haemophilus aphrophilus neck, suggestive of acute infectious epiglottitis.
Actinobacillus actinomycetemcomitans Dr. Calderon
Cardiobacterium hominis MEMORY AID HAEMOPHILUS INFLUENZAE

Eikenella corrodens
HaEMOPhilus influenzae causes
Kingella kingae
Epiglottitis
Meningitis
GRAM-NEGATIVE RODS: RESPIRATORY TRACT Otitis media
OVERVIEW – GRAM-NEGATIVE RODS – RESPIRATORY Pneumonia
GRAM TREATMENT
OTHER FEATURES ORGANISM
STAIN • ceftriaxone
enriched chocolate agar,
Haemophilus
Polyribitol phosphate PREVENTION
influenzae type b
capsule • HiB vaccine containing the type b capsular polysaccharide
gram
Bordet-Gengou agar, Bordetella conjugated to diphtheria toxoid
negative
whooping cough pertussis o given between 2 and 18 months of age
rods
poorly gram staining, silver
Legionella ✔GUIDE QUESTION
stain, charcoal yeast agar,
pneumophila A 4/M patient is scheduled to receive the Hib conjugate vaccine. The
air-conditioning
parents are given detailed information about the vaccine, but the
mother asks, "Why is 'tetanus toxoid conjugate' listed on the package
I. HAEMOPHILUS INFLUENZAE insert?" She adds that her son already received the DTaP vaccine. The
parents request an explanation for the reason the Hib vaccine contains
CHARACTERISTICS
both the capsular polysaccharide of Hib as well as the conjugated
• small gram-negative (coccobacillary) rods tetanus toxoid. Which of the following best describes the purpose of
• requires factor X (hemin) and V (NAD) for growth (chocolate Hib vaccine conjugation?
agar) A. Booster dose against tetanus
• Culture specimen on blood agar that has been heated to 80oC for B. Eliminates the need for booster doses
15 minutes (now called chocolate agar). This high temperature C. Induces immunity against non-typeable H. influenzae
D. Elicits T cell-dependent immune response
lyses the red blood cells releasing both hematin (called X factor)
and NAD+ (called V factor). Like Neisseria, H. influenzae grows A conjugate vaccine is a type of vaccine which combines a weak
best when the chocolate agar is placed in a high CO2 environment antigen (e.g. capsular component) with a strong antigen (e.g.
toxoid) as a carrier so that the immune system has a stronger
at 37oC.
response to the weak antigen (e.g. eliciting a T-cell response).
• satellite phenomenon around S. aureus colonies - hemolysis by
S. aureus liberates factor V needed by H. influenzae (see photo The immune system reacts to vaccines which evoke an immune
response by production of antibodies (aka B-cell or humoral
below)
immunity) and T cells (aka cell-mediated immunity). The T cells
‘remember’ the antigen (keyword: memory) so that if the body
encounters it later, antibodies can be produced by B cells to break
down the antigen. For bacteria with a polysaccharide coating (e.g.
Hib, pneumococcus, meningococcus), the immune response
generates B cells independent of T cell stimulation.
By conjugating the polysaccharide (capsule) to a protein carrier NATURAL HISTORY
(toxoid), a T cell response can be induced. Normally,
polysaccharides by themselves cannot be loaded onto the major
histocompatibility complex (MHC) of antigen presenting cells
(APC) because MHC can only bind peptides. In the case of a
conjugate vaccine, the carrier peptide linked to the
polysaccharide target antigen is able to be presented on the MHC
molecule and the T cell can be activated.
As a result, the vaccine is ‘improved’ as T cells stimulate a more
vigorous immune response and also promote a more rapid and
long-lasting immunologic memory. The conjugation of
polysaccharide target antigen to the carrier protein also
increases efficiency of the vaccine as a non-conjugated
vaccine against the polysaccharide antigen is not effective in
young children. The immune systems of young children are not
able to recognize the antigen as the polysaccharide covering
disguises the antigen. By combining the bacterial polysaccharide
with another antigen, the immune system is able to respond.
To accurately determine the cause of repeated bouts of otitis media that
have begun to affect a toddler’s hearing, inner ear fluid is obtained by • Incubation Period
careful puncture of her tympanic membrane with a sterile needle. o 7-10 days
Gram stain of the aspirate reveals short Gram-negative rods and • Catarrhal phase
polymorphonuclear leukocytes. No organisms are isolated on blood o 1-2 weeks
agar but colonies are observed on chocolate agar. What is the most
o rhinorrhea, malaise, fever, sneezing, anorexia
likely cause of this infection?
A. Haemophilus influenzae non-typeable o Antibiotics most effective
B. Haemophilus influenzae type b • Paroxysmal phase
C. Klebsiella pneumoniae o 2-4 weeks
D. Streptococcus pneumoniae o ‘Whoop’ → burst of non-productive coughs
o Increased number of lymphocytes in blood smear
o Antibiotics ineffective during this stage
GUIDE QUESTION 14
• Convalescent stage
https://qrs.ly/8ock6ni o 3-4 weeks (or longer)
o Diminished paroxysmal cough
o Development of secondary complications (pneumonia,
seizure, encephalopathy)
II. BORDETELLA PERTUSSIS
CHARACTERISTICS TREATMENT
• small gram-negative rods • Erythromycin
• culture on Bordet-Gengou agar or Regan-Lowe charcoal
medium PREVENTION
• acellular vaccine in combination with diphtheria and tetanus
HABITAT AND TRANSMISSION toxoids (DTaP)
• habitat is upper respiratory tract
• transmission via respiratory droplets
III. LEGIONELLA PNEUMOPHILA
PATHOGENESIS CHARACTERISTICS
• filamentous hemagglutinin • poorly gram-negative rods
o pili rod that extends from the surface of B. pertussis, enabling o visualize with silver stain
the bacteria to bind to ciliated epithelial cells of the bronchi • facultative intracellular bacteria
o mediates attachment • culture on charcoal yeast extract agar
• pertussis toxin o increased amounts of iron and cysteine
o causes ADP-ribosylation o optimal between 28 and 40°C; organisms are dormant below
o activates G proteins that increases cAMP resulting in: 20°C and are killed at temperatures above 60°C
§ increased sensitivity to histamine • rapid urinary antigen test - Urinary antigen can be detected by
§ increased insulin release radioimmunoassay with high sensitivity and specify and will
§ peripheral lymphocytosis remain positive for months after infection. Urine antigen test
• extracytoplasmic (false) adenylate cyclase only detects L. pneumophilia serogroup 1, but this accounts for
o ‘weakens’ neutrophils lymphocytes and monocytes 90% of cases.
o inhibits phagocytosis • Legionnaires disease (LD) was recognized in 1976 after an
• tracheal cytotoxin outbreak of pneumonia at an American Legion convention in
o damages ciliated cells Philadelphia
o causes whooping
MEMORY AID FACULTATIVE INTRACELLULAR BACTERIA
SPECTRUM OF DISEASE Some Bugs May Live FacultativeLY.
• Pertussis or Tuspirina Salmonella
o paroxysmal pattern of hacking coughs, accompanied by Brucella
production of copious amounts of mucus, that end with an Mycobacterium
inspiratory "whoop" (watch the video, particularly at 0:29) Listeria
Francisella
Legionella
Yersinia
WHOOPING COUGH
- MAYO CLINIC HABITAT AND TRANSMISSION
https://qrs.ly/2ubp4az
• Ubiquitous in man and natural water environments
• Freshwater amoebae appear to be the natural reservoir for the
organisms.
• transmission via aerosol (e.g. AC, cooling towers)
• person-to-person transmission does not occur
PATHOGENESIS MEMORY AID LACTOSE FERMENTERS
• endotoxin LaCtose is KEE. Grow in MacConKEE agar.
• Cu-Zn superoxide dismutase and catalase-peroxidase - protect Citrobacter
bacteria from macrophage superoxide and hydroperoxide Klebsiella
oxidative burst Escherichia coli
• Pili and flagella - promote attachment and invasion Enterobacter
• Secretion of protein toxins, e.g. RNAase, phospholipase A and
phospholipase C HABITAT AND TRANSMISSION
• organism replicates intracellularly • habitat is human colon
o cell-mediated immunity is important • colonizes the vagina and urethra
o inhibits phagolysosome fusion • transmission
• predisposing factors o ascending infection in UTI
o old age, smoking, high alcohol intake, immunosuppression o during birth in neonatal meningitis
o fecal–oral route in diarrhea
SPECTRUM OF DISEASE
• ATYPICAL PNEUMONIA PATHOGENESIS
o pneumonia accompanied by confusion, non-bloody diarrhea, • pili or fimbriae – attachment, colonization factor, associated
hyponatremia, proteinuria and hematuria with UTI (cystitis, pyelonephritis)
• PONTIAC FEVER • flagellum (H)
o mild, flulike illness • capsule (K) – associated with pneumonia and neonatal
meningitis (K1)
TREATMENT • endotoxin (O)
• azithromycin or erythromycin • enterotoxins
o ST and LT cause watery diarrhea, increase cAMP (similar to
PREVENTION cholera toxin)
• reducing cigarette and alcohol consumption o verotoxin (Shiga-like toxin) causes bloody diarrhea (HUS),
• eliminating aerosols from water sources inhibits protein synthesis by inactivating the 60S subunit of
• high temperatures and hyperchlorination in hospital water eukaryotic cells (E. coli O157:H7, STEC, EHEC)
supply
MEMORY AID ENTEROBACTERIACEAE
GRAM NEGATIVE RODS - GIT AND GUT Think MESSY SPECK! Enterobacteria drink
Morganella Serratia COFFEe!
OVERVIEW – GRAM-NEGATIVE RODS – GIT AND GUT
Escherichia Proteus Capsular antigen (K)
GRAM STAIN OTHER FEATURES ORGANISM
Shigella Enterobacter O antigen
Lactose fermenter, Salmonella Citrobacter Flagellar antigen (H)
Escherichia coli
green sheen Yersinia Klebsiella Ferments glucose
Lactose fermenter, Klebsiella Enterobacteriaceae
urease positive, ESBL pneumoniae
Comma-shaped,
Gram-negative motile, oxidase Vibrio cholerae
rods positive
Comma-shaped,
Campylobacter
microaerophilic,
jejuni
Skirrow’s agar
Comma-shaped, Helicobacter
urease positive pylori
motile, oxidase
negative, H2S Salmonella spp.
producer
non-motile, oxidase
non-lactose- negative, H2S non Shigella spp.
fermenting, producer
gram negative swarming, oxidase
Proteus
rods negative, H2S
mirabilis
producer, urease
oxidase positive, H2S
Pseudomonas
non producer,
aeruginosa
obligate aerobe
I. ESCHERICHIA COLI Lippincott Illustrated Reviews: Microbiology (Lippincott Illustrated Reviews Series)
CHARACTERISTICS SPECTRUM OF DISEASE
• facultative gram-negative rods
• Urinary Tract Infection
• lactose-fermenting colonies on EMB or
o most common cause of community-acquired UTI
MacConkey agar
• Neonatal Meningitis
• green sheen on EMB agar; metallic sheen
o 2nd most common cause
• typing by O and H antigens
Green metallic sheen on EMB

MEMORY AID NEONATAL MENINGITIS
B–E–L
B group streptococci (S. agalactiae)
Escherichia coli
Listeria monocytogenes
• Intestinal Infections II. SALMONELLA SPP.
STRAIN ABBREVIATION SYNDROME CHARACTERISTICS
Enterotoxigenic
ETEC Watery diarrhea • facultative gram-negative rods
E. coli
• non-lactose-fermenting
Watery diarrhea of long
Enteropathogenic duration, mostly in • produces H2S
EPEC • Widal test detects antibodies in patient's serum
E. coli infants, often in
developing countries • cultured in XLD medium
Bloody diarrhea;
Enterohemorrhagic hemorrhagic colitis and HABITAT
EHEC • human colon only (S. typhi)
E. coli hemolytic uremic
syndrome (HUS) • enteric tract of humans and animals, e.g., chickens and domestic
Enteroinvasive livestock (S. enteritidis)
EIEC Bloody diarrhea
E. coli
Persistent watery diarrhea TRANSMISSION
Enteroaggregative
EAEC in children and patients • fecal–oral route
E. coli
infected with HIV
T – travel
P – pediatric, poverty, Philippines
H – hemorrhagic diarrhea + HUS
I – invasive, so hemorrhagic diarrhea but without HUS
A - AIDS
Dr. Calderon
TREATMENT
• ampicillin or sulfonamides for UTI
• 3° cephalosporins for meningitis and sepsis
• rehydration is effective in traveler's diarrhea
PREVENTION The cycling of Salmonella through animals and humans
• limiting urinary catheterization The human-to-human transmission and cycle is indicative of Salmonella
• switching IV lines promptly typhi.
• drinking boiled water Dr. Calderon
PATHOGENESIS
✔GUIDE QUESTION
A 27-year-old male suddenly develops severe abdominal cramping and • Enterocolitis (S. enteritidis/ S. typhimurium)
bloody diarrhea. The patient reports consuming rare hamburger four o invasion of the epithelial and subepithelial tissue of the small
days prior to the onset of the symptoms. Which of the following best and large intestines
describes the toxin-mediated mechanism of this disease process? o infectious dose is high
A. Depolymerization of actin filaments in gastrointestinal mucosal § gastrectomy or use of antacids lowers the infectious dose
cells, leading to mucosal cell death significantly
B. Increased intracellular cAMP in gastrointestinal mucosal cells,
• Typhoid Fever (S. typhi)
resulting in decreased absorption and increased secretion in the
digestive tract o due to Vi (virulence) capsular antigen
C. Inhibition of elongation factor-2 (EF-2), resulting in decreased o organisms enter, multiply in Peyer patches, and then spread
protein synthesis in gastrointestinal mucosal cells to reticulo-endothelial system
D. Inhibition of the 60S ribosomal subunit, resulting in o predilection for invasion of the gallbladder, which can result
decreased protein synthesis in gastrointestinal mucosal cells in establishment of the chronic carrier state
The presentation of bloody diarrhea following ingestion of • Septicemia (S. choleraesuis)
undercooked beef (e.g. rare hamburger) suggests exposure to o bacteremia results in the seeding of many organs, with
enterohemorrhagic E. coli (aka E. coli O157:H7). The organism is osteomyelitis, pneumonia, and meningitis as the most
most commonly transmitted to human hosts through the
common sequelae
consumption of undercooked meat as well as raw, leafy vegetables.
o commonly in patients with sickle cell anemia or cancer
The Shiga-like toxin (just like the real Shiga toxin produced by
Shigella) inhibits 60S ribosomal subunits, resulting in decreased
SPECTRUM OF DISEASE
protein synthesis in gastrointestinal mucosal cells. The toxin also
enhances cytokine release to cause the clinical manifestations of • Enterocolitis
hemolytic-uremic syndrome, which include thrombocytopenia, o incubation period of 12–48 hours
microangiopathic hemolytic anemia, and acute kidney injury. o nausea and vomiting and then progresses to abdominal pain
Microthrombi form on damaged endothelium within the glomeruli, and nonbloody diarrhea
leading to mechanical hemolysis, platelet consumption, and • Typhoid Fever
decreased renal blood flow.
o incubation period 5 to 21 days
Here’s a detailed Pathology video that explicitly accounts the
pathogenesis of E. coli O157:H7. By explicit I meant there are very CULTURE
WEEK PRESENTATION
technical (molecular) terms here, but do not worry about SOURCE
memorizing them. I just want you to see the big picture, particularly Stepwise fever, anorexia, malaise,
Blood, bone
the pathogenesis of HUS. Let this part complement your study of 1 relative bradycardia and
pathology and IM. marrow
bacteremia
Abdominal pain, bloating, Urine, rose
E. COLI 0157:H7 2 constipation, rose spots, spots, bone
PATHOGENESIS hepatosplenomegaly, jaundice marrow
& COMPLICATIONS Stool, bone
https://qrs.ly/hbbpbw1 3 Bleeding, ileitis, pneumonia
marrow
4 Recovery or death Bone marrow
Let’s recall important exotoxin mechanisms detailed in this item:
• Exotoxin A and B of Clostridioides difficile – cause Bile, stool,
Post Chronic carrier state
depolymerization of actin filaments in gastrointestinal mucosal bone marrow
cells, leading to mucosal cell death (i.e. pseudomembranes) • Septicemia
• Cholera toxin - increases intracellular cAMP in gastrointestinal o fever but little or no enterocolitis and then proceed to focal
mucosal cells, resulting in decreased absorption and increased symptoms associated with the affected organ
secretion in the digestive tract o frequently bone, lung, or meninges
Exotoxin A of Pseudomonas aeruginosa – inhibits elongation
factor-2 (EF-2), resulting in decreased protein synthesis in
gastrointestinal mucosal cells
Dr. Calderon
TREATMENT TREATMENT
• Ceftriaxone • fluid and electrolyte replacement
• Philippines: amoxicillin, chloramphenicol, co-trimoxazole • in severe cases, ciprofloxacin
PREVENTION PREVENTION
• public health measures, e.g., sewage disposal, chlorination, hand • public health measures, e.g., sewage disposal, chlorination,
washing, food safety hand washing, food safety
• vaccines for S. typhi
IV. VIBRIO SPP.
✔GUIDE QUESTION
CHARACTERISTICS
An 8-year-old African male with sickle cell anemia develops
osteomyelitis. Which is the most likely etiology? • comma-shaped gram-negative rods
A. Streptococcus C. Pseudomonas • motile
B. Salmonella D. Candida • oxidase-positive
Overall, the most common cause of osteomyelitis in an otherwise • cultured on thiosulfate citrate bile salts sucrose (TCBS) agar
healthy patient is Staphylococcus aureus. • shooting star motility
Dr. Calderon
HABITAT
OSTEOMYELITIS IN SPECIFIC CONDITIONS • human colon only (V. cholerae)
CONDITION MOST LIKELY CAUSE • saltwater (V. parahaemolyticus and V. vulnificus)
Burns • Pseudomonas aeruginosa
TRANSMISSION
• Staphylococcus aureus
IV drug abusers • fecal–oral route (V. cholerae)
• Pseudomonas aeruginosa
• contaminated raw seafood (V. parahaemolyticus)
Sickle cell anemia • Salmonella choleraesuis
• trauma to skin, especially in shellfish handlers, or by ingestion of
raw shellfish (V. vulnificus)
III. SHIGELLA SPP.
CHARACTERISTICS
• non-lactose-fermenting, gram-negative rods
• produce no gas from the fermentation of glucose
• do not produce H2S
• nonmotile
• have O antigens
• cultured in XLD medium
HABITAT TRANSMISSION
• human colon only • fecal–oral route PATHOGENESIS
• enterotoxin (choleragen) acts by ADP ribosylation
MEMORY AID SHIGELLA TRANSMISSION • mucinase enhances attachment to the intestinal mucosa
4 Fs: Food, Fingers, Feces, Flies • high infectious dose
• pandemics caused by Vibrio cholerae O1 biotype El Tor
PATHOGENESIS (cholera El Tor)
• Shigella invade the distal ileum and colon
o Invades submucosa of intestinal tract (distal ileum and colon),
but not the lamina propria → local inflammation with
ulceration → bleeding
o Shigella has a low infective dose (200 bacilli) → so, it is highly
infectious, as compared to Salmonella which has an infective
dose between 105 and 108 (100 K to 100 million bacterial
cells), hence, less infectious.
o Invasion of M cells is key to pathogenicity.
• Important species and strains:
o Shigella sonnei – Duval’s bacillus
§ most common cause of bacillary dysentery
o Shigella dysenteriae type 1 – Shiga bacillus
§ most severe form of bacillary dysentery
§ most common cause of epidemic dysentery
• some produce an enterotoxin (Shiga toxin)
Cholera toxin (a.k.a. choleragen, sometimes abbreviated as CTX, Ctx or
CT) is a protein complex responsible for the massive, watery diarrhea (e.g.
EPONYMS (Nice to know) rice water stools) characteristic of cholera infection.
Shigella dysenteriae
Group Shiga bacillus See the figure above: Here CT acts by causing constitutive activation of
Shigella dysenteriae type I adenylate cyclase, leading to elevated cAMP in intestinal epithelial cells.
A Schmitz bacillus
Shigella dysenteriae type 2 cAMP activates protein kinase A, which causes the opening of ion
Flexner bacillus; channels in the membrane, leading to chloride and bicarbonate secretion
Group
Shigella flexneri Hiss & Russell by intestinal crypt cells and disruption in absorption by villus cells.
B
bacillus WHOOPS! On the other hand, the pertussis toxin of Bordetella pertussis
Group Newcastle (whooping cough) acts in a similar manner with the exception that it
Shigella boydii
C Manchester bacillus ADP-ribosylates the Gi subunit, rendering it unable to inhibit cAMP
Group production (inhibition of the inhibitory, hence, excitatory net effect.)
Shigella sonnei Duval bacillus
D So, to summarize, the mechanisms are opposite but yield the same net
effects:
SPECTRUM OF DISEASE • Choleragen – ADP-ribosylation leads to stimulated Gs protein →
increased cAMP
• Bacillary Dysentery
• Pertussis – ADP-ribosylation of Gi protein → inhibits Gi (inhibits
o incubation period: 1–4 days inhibitory) → increased cAMP
o fever and abdominal cramps, followed by diarrhea, initially Dr. Calderon
watery then bloody
o diarrhea frequently resolves in 2 or 3 days
SPECTRUM OF DISEASE TREATMENT
• Cholera • symptomatic treatment only
o watery diarrhea in large volumes (rice-water stools) • erythromycin for severe disease
o patients with severe hypovolemia may have sunken eyes, dry
mouth, cold clammy skin, decreased skin turgor, or wrinkled PREVENTION
hands and feet, aka ‘washerwoman's hands’ • public health measures
o complications
§ cardiac and renal failure
§ non-gap acidosis
VI. HELICOBACTER PYLORI
§ hypokalemia CHARACTERISTICS
• Gastroenteritis • curved gram-negative rods
o generally self-limited with an explosive onset of watery • urease-positive
diarrhea and nausea, vomiting, abdominal cramps, headache, • microaerophilic
and low-grade fever MEMORY AID UREASE-POSITIVE BACTERIA
• Wound Infections
Particular Kinds Have Urease.
o associated with exposure to contaminated water
Proteus mirabilis
Klebsiella pneumoniae
TREATMENT
Helicobacter pylori
• Cholera Ureaplasma urealyticum
o fluid and electrolyte replacement
o tetracycline or azithromycin shortens duration HABITAT AND TRANSMISSION
• V. parahaemolyticus, V. vulnificus Infection • habitat is the human stomach
o minocycline plus fluoroquinolone or cefotaxime • transmission is by ingestion
PREVENTION
• public health measures PATHOGENESIS
o only improvements in sanitation can lead to effective control • damages goblet cells of the gastric mucosa
of the disease • production of large amounts of ammonia from urea by the
• short-term immunity using cholera vaccine organism's urease
o may cause herd immunity o ammonia also neutralizes stomach acid, allowing the organism
to survive
V. CAMPYLOBACTER JEJUNI • detected using the following tests:
o EGD with biopsy showing H. pylori
CHARACTERISTICS
o urease breath test
• comma-shaped gram-negative rods o H. pylori stool antigen
• microaerophilic
• positive oxidase and catalase tests SPECTRUM OF DISEASE
• grows well at 42°C on Skirrow agar • Peptic Ulcer Disease
• most common cause of bacterial gastroenteritis o recurrent pain in the
upper abdomen,
HABITAT AND TRANSMISSION frequently
• habitat is human and animal feces (cattle, chickens, and dogs) accompanied by
• transmission is by the fecal–oral route bleeding into the
gastrointestinal tract
PATHOGENESIS • Disease Associations
o gastric carcinoma
o MALT lymphomas
ANTI-H. PYLORI ANTIBIOTICS

• Amoxicillin
• Clarithromycin
• Metronidazole
• Tetracycline
VII. KLEBSIELLA PNEUMONIAE

CHARACTERISTICS
• facultative gram-negative rods with large polysaccharide
SPECTRUM OF DISEASE capsule
• watery, foul-smelling diarrhea followed by bloody stools • extended spectrum beta-lactamase (ESBL) activity in drug-
accompanied by fever and severe abdominal pain resistant strains
• may mimic ulcerative colitis • urease-positive
• disease associations
o Guillain-Barré syndrome HABITAT TRANSMISSION
§ antigenic cross-reactivity between oligosaccharides in • upper respiratory and • aspiration or inhalation
bacterial capsule and glycosphingolipids on surface of neural GIT • ascending spread of fecal flora
tissues
§ Campylobacter infection is the most commonly identified SPECTRUM OF DISEASE
cause of GBS • Pneumonia
o reactive arthritis (Reiter syndrome) o thick, bloody sputum ("currant-jelly" sputum)
o usually nosocomial
MEMORY AID REITER SYNDROME o most common cause in alcoholics
Triad of urethritis, uveitis, and arthritis • Urinary Tract Infections
CAN’T PEE
CAN’T SEE TREATMENT
CAN’T CLIMB A TREE • culture-guided treatment (cephalosporins alone or with
aminoglycosides)
VIII. PROTEUS MIRABILIS • Gastrointestinal Infections

o typhlitis (necrotizing enterocolitis)
CHARACTERISTICS
o Shanghai fever (mild form of typhoid)
• facultative gram-negative rods o peritonitis in patients undergoing peritoneal dialysis
• non-lactose-fermenting • Urinary Tract Infections
• urease-positive o 3rd most common cause of nosocomial UTIs
• swarming motility • Sepsis
PATHOGENESIS o ecthyma gangrenosum
• urease hydrolyzes the urea in urine to form ammonia § hemorrhagic lesions
o raises pH producing alkaline urine o febrile neutropenia
o encourages the formation of struvite stones, composed of § leukemia or lymphoma post chemo- or radiation therapy
magnesium-ammonium-phosphate § severe burns
SPECTRUM OF DISEASE TREATMENT

• Complicated Urinary Tract Infection • combination of active antibiotics required because of
o UTI associated with nephrolithiasis resistance to multiple antibiotics
o staghorn calculi form on renal calyces o antipseudomonal penicillins (ticarcillin, piperacillin)
TREATMENT o penicillin plus beta-lactamase inhibitor (ticarcillin-
• TMP-SMX or ampicillin clavulanate, piperacillin-tazobactam)
o third generation cephalosporins (ceftazidime)
• surgery for large stones
o fourth generation cephalosporins (cefepime)
o monobactam (aztreonam)
IX. PSEUDOMONAS AERUGINOSA o carbapenems (imipenem, meropenem)
CHARACTERISTICS o fluoroquinolones (ciprofloxacin)
• gram-negative rods • examples of suitable combinations
• obligate aerobe o CEFTAZIDIME + AMIKACIN
• non-lactose-fermenting o PIPERACILLIN + AMIKACIN
• oxidase-positive o AZLOCILLIN + CIPROFLOXACIN
• pyocyanin (blue-green pigment) • rifampicin is added for refractory cases
• sweet grape-like odor
• grown on Cetrimide agar PREVENTION
• disinfection of water-related equipment
MEMORY AID PSEUDOMONAS
• hand washing
Pseudomonas AERuginosa is an obligate AERobe • prompt removal of catheters
• environmental water sources, e.g., in hospital respirators and SUPPLEMENT NICE TO KNOW GRAM NEGATIVE AEROBES
humidifiers The organisms I am listing below fall under the category of
• inhabits the skin, upper respiratory tract, and colon of about emerging nosocomial infections. They share some characteristics
10% of people of Pseudomonas (I usually call them the ‘cousins’ of
Pseudomonas):
• transmission via water aerosols, aspiration, and fecal • Gram-negative aerobe
contamination • Nosocomial
PATHOGENESIS • Multi-drug resistant → The idea is this: the treatment is similar
to that of Pseudomonas but, of course, only when proven by
• endotoxin C&S in the lab. So, think: pip-taz, meropenem, aztreonam,
• exotoxin A aminoglycosides, quinolones, etc.
o tissue necrosis and inactivates EF-2 Dr. Calderon
o type III secretion system facilitates exotoxin transfer NICE TO KNOW GRAM-NEGATIVE AEROBES
• elastase and proteases • Acinetobacter baumannii
• pyocyanin damages the cilia and mucosal cells • Flavobacterium meningosepticum (Elizabethkingia
• verdoglobin from hemoglobin breakdown → any of several meningosepticum)
green compounds derived from hemoglobin or related compounds • Achromobacter xylosoxidans
by cleavage of the porphyrin ring
SPECTRUM OF DISEASE X. ACINETOBACTER BAUMANNII
• Skin and Soft Tissue Infections • Pleomorphic aerobic gram-negative bacillus commonly
o burn wound infections isolated from the hospital environment and hospitalized
o hot tub folliculitis → typically self-limiting patients
§ spa pools, whirlpools, or inadequately chlorinated • Water organism, preferentially colonizes aquatic
swimming pools and hot tubs (Remember: Pseudomonas environments.
loves ‘wet’ environments) • In a hospital setting, Acinetobacter commonly colonizes
o skin graft-loss due to infection irrigating solutions and intravenous solutions
o green nail syndrome • Low virulence, but capable of causing infection
• Bone and Cartilage Infections o Respiratory secretions and urine, represent colonization
o puncture wound osteomyelitis rather than infection
o pubic osteomyelitis in IV drug abusers • Occur usually in organ systems that have a high fluid content
• Ear Infections • Nosocomial meningitis may occur in colonized neurosurgical
o otitis externa patients with external ventricular drainage tubes
o malignant otitis externa in diabetics • Multi-resistant aerobic gram-negative bacillus sensitive to
o chronic suppurative otitis media relatively few antibiotics
• Pneumonia • Multidrug-resistant Acinetobacter is not a new or emerging
o ventilator-acquired pneumonia phenomenon, but A baumannii has always been an organism
o high-risk CAP inherently resistant to multiple antibiotics
§ immunocompromised
§ broad spectrum antibiotics
§ steroid therapy
§ structural lung lesions
- bronchiectasis
- cystic fibrosis
XI. FLAVOBACTERIUM MENINGOSEPTICUM B. FRANCISELLA TULARENSIS

• formerly Chryseobacterium meningosepticum now called TULAREMIA
Elizabethkingia meningosepticum • small gram-negative rods
• Nonfermenting, nonmotile, oxidase-positive Gram-negative • reservoir: rabbits, deer, and rodents
aerobic bacillus • transmission: ticks (e.g., Dermacentor), aerosols, contact, and
• Ubiquitous in the environment, found in freshwater, ingestion
saltwater, and soil • treatment: streptomycin or gentamicin
• Recently termed Elizabethkingia meningosepticum (or
meningoseptica) C. YERSINIA PESTIS
• A ubiquitous Gram-negative bacillus BUBONIC, PNEUMONIC and SEPTICEMIC PLAGUE
• Historically associated with neonatal meningitis and • most virulent bacteria
infections in immunocompromised patients • small gram-negative rods with bipolar (safety pin) staining
o Neonatal infections often occur as outbreaks with • reservoir: wild rodents
environmental contamination being the source • transmission: flea (Xenopsylla cheopis) bite, inhalation
• Infections are not common but are clinically important • PE: buboes, cutaneous hemorrhage
because the organism is naturally resistant to multiple • treatment: streptomycin and tetracycline
antibiotics • No vaccine available
XII. ACHROMOBACTER XYLOSOXIDANS Forms of plague
A.K.A ALCALIGENES XYLOSOXIDANS • Bubonic → sudden onset of fever, headache, chills, and
• Causes opportunistic infections in compromised patients weakness and one or more swollen, tender and painful lymph
o Cancer patients nodes (buboes); usually results from an infected flea bite
• Catalase- and oxidase-positive, motile, gram-negative rod • Septicemic → fever, chills, extreme weakness, abdominal pain,
that oxidizes xylose and glucose shock, and possibly bleeding into the skin and other organs.
Skin and other tissues may turn black and die, especially on
• Exists in a water environment and may be confused with
fingers, toes, and the nose. Septicemic plague can occur as the
Pseudomonas species.
first symptoms of plague, or may develop from untreated
• Unlike Pseudomonas, Achromobacter has peritrichous
bubonic plague. This form results from bites of infected fleas
flagella
or from handling an infected animal.
• Emerging, unusual Gram-negative infection in CF
• Pneumonic → fever, headache, weakness, and a rapidly
developing pneumonia with shortness of breath, chest pain,
XIII. BACTEROIDES FRAGILIS cough, and sometimes bloody or watery mucous; may develop
CHARACTERISTICS from inhaling infectious droplets or from untreated bubonic
• anaerobic, gram-negative rods or septicemic plague that spreads to the lungs. This is the
• predominant anaerobe of human colon most serious form of plague.
• spreads to blood or peritoneum during bowel trauma, People most commonly acquire plague when they are bitten by a flea that
perforation or surgery is infected with the plague bacteria. People can also become infected from
direct contact with infected tissues or fluids while handling an animal that
is sick with or that has died from plague. Finally, people can become
PATHOGENESIS
infected from inhaling respiratory droplets after close contact with cats
• infections commonly due to combinations of bacteria in and humans with pneumonic plague.
synergistic pathogenicity Again, remember that the VECTOR is the FLEA. This is crucial (and
• LPS with low endotoxic activity historically important, at least to me) because the boards once asked the
• capsule (antiphagocytic and anticomplement) vector of plague. Many students answered RAT – because they referred to
• foul-smelling discharge → because of short-chain fatty-acid what the mnemonic says (YEYE the RAT as RESERVOIR), that’s ONE BIG
products of fermentation POINT missed. So, be extra careful when comprehending questions, OK?
Here’s a morsel of the history of medicine: Let me show you a recent
visual that explains the magnitude of the effect of the plague, and why it
SPECTRUM OF DISEASE earned the title “most virulent disease” ever!
• abdominal abscess
• peritonitis VISUALIZING THE
HISTORY OF PANDEMICS
TREATMENT https://qrs.ly/1tbpc7s
• metronidazole, clindamycin or cefoxitin
• surgical drainage of abscess Dr. Calderon
OTHER BACTERIA D. PASTEURELLA MULTOCIDA

In this section, I provide you a quick overview of the ‘rest’ of the bacteria. BITES and OSTEOMYELITIS
But, of course, as a Filipino, you should be extra familiar with TB. • short, encapsulated gram-negative rod that exhibits bipolar
Dr. Calderon
staining (‘closed safety pin appearance’, see figure below)
• buttery colonies with musty
I. ZOONOSES odor due to indole production
MEMORY AID ZOONOSES • reservoir: cats and dogs
Bugs From Your Pets. • transmission: animal bites
Brucella abortus • treatment: penicillin G
Francisella tularensis
Yersinia pestis
Pasteurella multocida
A. BRUCELLA ABORTUS
BRUCELLOSIS (UNDULATING FEVER)
• small gram-negative rods without a capsule Pasteurella multocida, in closed safety pin (“perdible!”) appearance
• transmission: contaminated dairy or direct contact
• treatment: doxycycline plus rifampin MEMORY AID ZOONOSES
Bruce the COW
MEMORY AID BRUCELLOSIS Francis the RABBIT
Unpasteurized dairy products give you Undulating fever. Yeye the RAT (reservoir! Vector is the flea, OK?)
Papa the CAT
II. MYCOBACTERIA PATHOGENESIS: TYPES OF LESIONS

• Exudative Lesions
o pus from acute inflammatory response
• Granulomatous Lesions
o central area of Langhans giant cells surrounded by a zone of
epithelioid cells
o tubercle is a granuloma surrounded by fibrous tissue that has
undergone central caseation
MEASURES OF EXPOSURE
• Purified Protein Derivate Skin Test
o positive test ("seroconversion") indicates:
§ current infection/active disease
§ past exposure but not necessarily active disease
§ BCG vaccination
o negative test indicates:
§ no infection
A. MYCOBACTERIUM TUBERCULOSIS § anergy → immunocompromised, malnutrition, steroids, and
sarcoidosis
CHARACTERISTICS
o type IV hypersensitivity mediated
• aerobic, acid-fast rods
o Ziehl-Neelsen (or Kinyoun)
DRUGS USED IN TB TREATMENT
• high lipid content
MECHANISM OF MECHANISMS OF
o mycolic acids and wax D Drug
ACTION RESISTANCE
• produces catalase and niacin
• Inhibit DNA- • Mutations in DNA-
• slow-growing on Löwenstein-Jensen medium Rifampicin
dependent RNA dependent RNA
• luciferase assay for drug resistance (RIF)
polymerase polymerase
• Mutations of
catalase-
• habitat is human lungs Isoniazid • Inhibit mycolic peroxidase reduce
• transmission is via respiratory droplets produced by coughing (INH) acid synthesis intracellular
transformation to
PATHOGENESIS: VIRULENCE FACTORS active form
• immune system itself causes damage Pyrazinamide • Interferes with
o TB contains no endotoxins or exotoxins -
(PZA) NAD
• exported repetitive protein (sulfatides) • Inhibit arabinosyl
o prevents phagosome-lysosomal fusion transferase which
• cord factor - most important virulence factor Ethambutol
blocks -
o inhibits WBC migration (EMB)
arabinogalactan
o causes characteristic serpentine growth pattern synthesis
o induces TNF-α release • Interferes with the • Mutations of genes
• tuberculin surface protein Streptomycin 30s subunit of encoding the 30s
o triggers cell-mediated immunity → caseation and granulomas ribosomes subunit
o triggers delayed hypersensitivity reaction
o a surface protein
TUBERCULOSIS: PATHOGENESIS
Robbins and Cotran Pathologic Basis of Disease, 9th ed. 2015
THIS IS VERY IMPORTANT! Likelihood of

As a type IV hypersensitivity, TB will require CD4 (TH1) cells. An intact transmitting Low High
cell mediated immunity is necessary to mount a granulomatous reaction. leprosy
Patients with immunodeficiency might manifest a lack of granuloma Cell-mediated
formation, hence, disseminated TB (e.g. HIV, senescence, genetic T-cell response to M. Present Reduced or absent
defects). Consider that a granuloma is a sign of intact immunity. Now, the leprae
figure: In figure A, the first exposure of the alveolar macrophages to TB
Lepromin skin
will alert them to phagocytose it – simply because it is a foreign body. Positive Negative
Remember that this first exposure to the TB bacillus could be TB in the test
form of a live BCG vaccine or the actual infection itself (whichever comes • Skin or nerve biopsy will reveal acid-fast bacilli (lepromatous) or
first!). After which, the alveolar macrophage has to wrestle with the TB, granulomas (tuberculoid)
but sometimes the TB ‘prevails’ by remaining alive within macrophages, • Lepromin skin test - Although not useful for diagnosis, it allows
owing to its antiphagocytic mechanisms (e.g. sulfatides that prevent positioning of patients on the immunologic spectrum
phagosome-lysosome fusion). Then, the surviving intracellular TB will be Dr. Calderon
‘seeded’ to multiple sites as the alveolar macrophage migrates to the
lymph nodes. Why would it go to the lymph node? Well, to ‘tell’ the MEMORY AID LEPROSY
immune system it found an invader! This partly explains why BCG has
to be ‘alive’ (although attenuated) because it is the interaction of the
LEpromatous leprosy is LEthal.
macrophage with the ‘living’ cell that stimulates the succeeding
reactions. Now that the macrophage is ‘carrying’ the antigens of TB, it SPECTRUM OF DISEASE
will later ‘present’ it to the immune system (i.e. antigen presentation to • Leprosy / Hansen Disease
the lymphoid cells). In other words, the macrophage is going to alert the
o most common cause of crippling of the hand
immune system by ‘presenting’ the antigen to the lymphoid cells. Here you
should appreciate how the alveolar macrophage acts as an antigen-
o Damage in the following nerves is associated with
presenting cell (APC), a.k.a. whistleblower or sumbungero. Now, figure B: characteristic impairments in leprosy:
You appreciate this chain of events: the alveolar macrophage acts as an § Ulnar and median: clawed hand
APC and produces IL-12. In turn, IL-12 stimulates TH1 differentiation. TH1 § Posterior tibial: plantar insensitivity and clawed toes
produces IFN-γ to activate the rest of the macrophages to become § Common peroneal: foot drop
bactericidal and to form granulomas and caseation necrosis. In other § Radial cutaneous, facial, and greater auricular nerves (may
words, the goal of antigen presentation by one macrophage is to alert the also be involved)
other macrophages. Now, be very conscious of the cytokines involved
• Erythema Nodosum Leprosum
because sometimes these are asked in the boards. Finally, it is important
that you correlate this concept to pathology – and IM and Pedia – so I o Seen in lepromatous form
refer you to your discussion there, or to this quick video recap: o Tender red nodules or humps on both shins
o Signals acute flare-ups of disease
o Treated with Thalidomide → category X drug; associated with
Tuberculosis
phocomelia if given during pregnancy
| Clinical Presentation
https://qrs.ly/8pbp588 TREATMENT AND PREVENTION
• tuberculoid leprosy
Dr. Calderon
o dapsone and rifampin
✔GUIDE QUESTION • lepromatous leprosy
Among the events that lead to mounting an immune response o dapsone, rifampin, and clofazimine
to TB, which one precedes the others? • erythema nodosum leprosum
A. Activation of macrophages by T-cells o thalidomide
B. Bacterium-mediated inhibition of phagosome-
lysosome fusion III. ACTINOMYCETES
C. Formation of epithelioid cells
D. Th1 cell activation A. ACTINOMYCES ISRAELII
ACTINOMYCOSIS
• anaerobe (normal oral flora)
GUIDE QUESTION 15
• setting: local trauma (broken jaw or dental extraction)
https://qrs.ly/zvck6og • PE: hard, nontender swelling with sinus tracts draining sulfur
granules
• treatment: penicillin G + drainage
ATYPICAL MYCOBACTERIUM B. NOCARDIA ASTEROIDES
B. MYCOBACTERIUM AVIUM-INTRACELLULARE NOCARDIOSIS
COMPLEX (MAI, MAC) • aerobic, filamentous gram-positive rods with aerial hyphae
• cause pulmonary disease in immunocompromised hosts (AIDS • weakly acid-fast (Fite-Faraco)
patients with CD4 <50) • transmission: inhalation of particles from soil
• manifests as mycetomas and lung and brain abscesses (orange
C. MYCOBACTERIUM LEPRAE colonies)
CHARACTERISTICS • treatment: TMP-SMX + drainage
• aerobic, acid-fast rods
• can’t be cultured in vitro: mouse footpad or in the armadillo MEMORY AID ANTIBIOTICS FOR ACTINOMYCETES
S–N–A–P
HABITAT AND TRANSMISSION Sulfa for Nocardia; for Actinomyces, use Penicillin.
• reservoir: humans and armadillos
• transmission: prolonged exposure to nasal secretions of patients IV. MYCOPLASMA PNEUMONIAE
with the lepromatous form CHARACTERISTICS
• smallest free-living organisms
PATHOGENESIS • not seen on Gram-stain
TUBERCULOID LEPROMATOUS o no cell wall
FEATURE
LEPROSY LEPROSY o only bacteria with sterol in cell membrane
Number of lesions One or few Many lesions • cultured in Eaton’s agent → requires cholesterol and nucleic
Tissue acids; penicillin is added to inhibit growth of contaminating
Little Marked
destruction bacteria; dome-shaped colonies with “fried egg” appearance or
Number of acid- “mulberry” appearance (in the case of Mycoplasma pneumoniae)
Few Many
fast bacilli
HABITAT AND TRANSMISSION • Secondary Syphilis
• habitat is human respiratory tract o condyloma lata, maculopapular rash, fever headache, malaise,
• transmission is via respiratory droplets anorexia, lymphadenopathy
o occurs after 1 to 3 months
PATHOGENESIS • Tertiary Syphilis
• toll-like receptor 2 protein (P1 adhesin) o many years after inoculation
o attachment, inhibition of ciliary motion and necrosis o clinical spectrum
• hydrogen peroxide § granulomas (gummas)
o contributes to the damage to the respiratory tract cells § neurosyphilis
• autoantibodies against red cells (cold agglutinins) and brain, - tabes dorsalis
lung, and liver cells - Argyll-Robertson pupil / Prostitute’s pupil
- dementia paralytica
SPECTRUM OF DISEASE § cardiovascular (aortitis)
- obliterative invasion of small blood vessels and vasa
• most common type of atypical pneumonia (walking
vasorum, causing endarteritis
pneumonia)
• Congenital Syphilis
• clinical findings not compatible with chest x-ray
o snuffles / saddle nose
• extra-pulmonary manifestations:
o mulberry molars
o hemolysis, Stevens-Johnson syndrome, Raynaud, Guillain-
o Hutchinson triad: Hutchinson teeth, deafness, keratitis
Barre syndrome
o saber shins
o rhagades (angle of mouth)
TREATMENT
o Higoumenakis sign (clavicle) → unilateral enlargement of the
• DOC: erythromycin or azithromycin sternoclavicular portion of the clavicle, leads to detachment
• penicillins and cephalosporins are inactive because the o Clutton’s joints (synovitis)
organism has no cell wall o pulmonary hemorrhage
V. SPIROCHETES SEROLOGIC TESTS FOR SYPHILIS

A. TREPONEMA PALLIDUM • Nontreponemal - screening tests, easy to perform, low cost
CHARACTERISTICS o Venereal Disease Research Laboratory (VDRL) - require
microscopic examination to detect flocculation
• coiled spirochete o Rapid plasma reagin (RPR)
• not seen on Gram-stain because too thin o Antigen: cardiolipin, cholesterol, and purified lecithin
• cannot be cultured in vitro o Others: Unheated serum reagin (USR) and toluidine red
o lacks Krebs cycle enzymes unheated serum test (TRUST)
• microaerophilic • Treponemal antibody tests— for confirmation
o measure antibodies against T pallidum antigens
HABITAT AND TRANSMISSION § T pallidum enzyme immunoassay (TPEIA)
• habitat is the human genital tract § The antigens in non-treponemal tests contain specific
• transmission is by sexual contact and from mother to fetus amounts of cardiolipin, cholesterol, and purified lecithin in
across the placenta quantities sufficient to yield a standardized amount of
reactivity.
SPECTRUM OF DISEASE § Historically, the cardiolipin was extracted from beef heart or
• Syphilis liver with added lecithin and cholesterol to enhance reaction
o Four stages with syphilitic “reagin” antibodies. Reagin is a mixture of IgM
o Congenital form and IgG antibodies reactive with the cardiolipin–
• Characteristic plasma cell-predominant inflammatory infiltrate cholesterol–lecithin complex.
MEMORY AID
False Positive VDRL FTA-ABS
Results Find The Antibody –
V–D–R–L ABSolutely
Viruses (EBV, Hepatitis) 1. most specific
Drugs (marijuana) 2. earliest positive
Rheumatic fever, RA 3. remains positive longest
Lupus, Leprosy
TREATMENT
• benzathine penicillin G
• Jarisch-Herxheimer reaction
o influenza-like symptoms few hours after receiving penicillin,
due to lysis of treponemes
PREVENTION
• use of condoms, antibiotics after exposure, serologic follow-up
B. BORRELIA BURGDORFERI
CHARACTERISTICS
• weakly staining, gram-negative spirochetes
• largest medically-important bacteria
• stain well with aniline dyes (Giemsa or Wright stain)
• cultured on BSK medium
Lifted from Robbins and Cotran Pathologic Basis of Disease, 9th ed. 2015
• Primary Syphilis HABITAT AND TRANSMISSION
o within hours, enters lymphatics and multiplies • Animal Reservoirs
o local, nontender ulcer (chancre) usually forms in 2–10 weeks o white-footed mouse
o Highly infectious, heals spontaneously in 3-6 weeks o white-tailed deer
§ differentiate from painful CHANCROID due to H. ducreyi • Transmission
o bite from deer ticks (Ixodes scapularis, Ixodes pacificus)
SPECTRUM OF DISEASE: LYME DISEASE SPECTRUM OF DISEASE
• Stage 1: erythema chronicum migrans • Incubation Period
• Stage 2: myocarditis (AV block), meningitis, Bell palsy o ranges from 2 to 20 days
• Stage 3: autoimmune migratory polyarthritis (onion skin • Acute Leptospiremic Phase
lesions), acrodermatitis chronica atrophicans o fever, chills, intense headache
MEMORY AID LYME DISEASE o calf tenderness
§ due to rapid multiplication of leptospires in muscles with
BAKE a Key LYME pie
high oxygen tension
Bell Palsy
o conjunctival suffusion
Arthritis
§ due to damaged and leaky conjunctival vessels
Kardiac block
§ painful and itchy but with minimal tearing
Erythema chronicum migrans
• Immune Leptospiruric Phase
TREATMENT o aseptic meningitis
• early localized or disseminated Lyme disease § CSF pleocytosis with or without meningeal symptoms
o doxycycline (DOC), amoxicillin, cefuroxime § coincides with appearance of antibody titers
• late manifestations o pulmonary involvement
o intravenous penicillin or ceftriaxone § snow-flake lesions in CXR
o hepatic necrosis
PREVENTION o glomerulonephritis
• using insecticides § due to immune-complex deposition
• applying insect repellents to clothing • Weil Syndrome
• wearing protective clothing that reduces exposure of skin to o most severe form of leptospirosis
insects o triad: jaundice, bleeding, uremia
o orange cast skin (severe jaundice)
C. LEPTOSPIRA INTERROGANS o most common cause of death is respiratory failure due to
CHARACTERISTICS massive pulmonary hemorrhage
• thin, coiled spirochetes
TREATMENT
• hook at one or both pointed ends (Shepherd’s crook)
• obligate aerobe • mild leptospirosis
• grown on Ellinghausen-McCullough-Johnson-Harris (EMJH) o doxycycline, ampicillin or amoxicillin
medium or Fletcher medium • severe leptospirosis
o penicillin G, ampicillin, ceftriaxone or cefotaxime
HABITAT AND TRANSMISSION • Jarisch-Herxheimer reaction may develop within hours after
starting therapy
• habitat: wild and domestic animals
• transmission via animal urine
PREVENTION
o dog, livestock, and rat urine
o usual setting wading in floodwaters • doxycycline chemoprophylaxis
• vaccination of domestic livestock and pets
PATHOGENESIS • rat control
• leptospires penetrate intact mucous membranes or skin
through small cuts or abrasions VI. CHLAMYDIA SPP.
• multiply rapidly and damage endothelium of small blood A. CHLAMYDIA TRACHOMATIS
vessels
CHARACTERISTICS
• organisms found in blood and CSF early in the disease and in
urine during the later stages • obligate intracellular bacteria
• immune complex-mediated meningitis and glomerulonephritis • energy parasites that use host ATP
• cell wall lacks muramic acid
DETECTION • grown in cycloheximide culture
• cytoplasmic inclusions in Giemsa
• darkfield microscopy is insensitive
• cultures on EMJH/Fletcher medium only become positive after MEMORY AID OBLIGATE INTRACELLULAR BACTERIA
2 weeks of incubation Stay inside cells when it is Really Cold
• gold standard is leptospire microscopic agglutination test (lepto Rickettsia
MAT) Chlamydia
FORMS
• Elementary Body
o inactive, extracellular
o enters cells by endocytosis
• Reticulate Body
o metabolically active, intracellular
o seen microscopically
MEMORY AID FORMS OF CHLAMYDIA HABITAT AND TRANSMISSION

Elementary body = Enfectious, Enters cell via Endocytosis • habitat
Reticulate body = Replicates in cell by fission o human genital tract
o eyes
• transmission ✔GUIDE QUESTION
o sexual contact Which of the following refers to an obsolete skin test for venereal
§ most common STD overall lymphogranuloma that uses antigens prepared from chlamydia grown
o transvaginal in the yolk sac of a chick embryo?
A. Frei test
o hand-to-eye contact
B. Elek test
PATHOGENESIS C. Quellung test
• balance that is often reached between host and parasite, D. Bile-optochin test
resulting in prolonged persistence of infection This test was developed in the 1920’s to identify lympho-
• infection persists in the presence of high antibody titers granuloma venereum. Antigen is prepared from sterile pus
aspirated from previously unruptured abscesses. It then produces
SPECTRUM OF DISEASE a reaction in patients with lymphogranuloma venereum when
• Trachoma injected intradermally. This test is no longer used today, but might
o C. trachomatis types A-C be important for historical reasons.
o chronic keratoconjunctivitis progressing to scarring and Let’s recap the other tests:
blindness Elek test – Corynebacterium diphtheriae
o Halberstädter-Prowazek inclusions - Round to oval Quellung test – capsular swelling
cytoplasmic inclusion bodies near the nuclei of conjunctival Bile-optochin test – streptococci
Dr. Calderon
epithelial cells in trachoma.
MEMORY AID TRACHOMA = TYPES A, B, C B. CHLAMYDIA PNEUMONIAE
ABC: Africa • ATYPICAL PNEUMONIA
Blindness o similar to Mycoplasma pneumoniae
Chronic infection o associated with atherosclerosis
• Genital Tract Infections § Sero-epidemiological evidence of higher titers of anti-C.
o C. trachomatis types D–K pneumoniae antibodies in CV patients vs control
o most common cause of STDs § Detection of the organism within atherosclerotic lesions, but
§ NGU in males; PID in females not in adjacent normal tissue by immunohistochemistry,
§ usual coinfection with gonorrhea PCR and EM and by culture
o birth complications: § C. pneumoniae can either initiate lesion development or
§ neonatal conjunctivitis cause exacerbation of lesions in rabbit and mouse animal
§ neonatal pneumonia models respectively.
o associated with Reiter syndrome o Diagnosis: microimmunofluourescence (MIF) serologic
• Neonatal Pneumonia test – most sensitive method for diagnosis of C pneumonia
o C. trachomatis types D–K infection
o late-onset (2-4 weeks)
o striking tachypnea, characteristic paroxysmal cough (staccato C. CHLAMYDIA PSITTACI
cough), absence of fever, and eosinophilia • PSITTACOSIS
• Lymphogranuloma Venereum o bird exposure (bird fancier’s disease)
o C. trachomatis types L1–L3 § parrots, parakeets, macaws, cockatiels
o papule or vesicular which ulcerates and leads to suppurative o sudden onset pneumonia with malaise, fever, anorexia, sore
inguinal lymphadenitis (buboes) throat, photophobia, and severe headache
o positive Frei test
§ intradermal injection of antigen TREATMENT
DIAGNOSIS (CHLAMYDIA TRACHOMATIS) • STD – azithromycin
• Nucleic acid amplification test (NAAT) – gold standard for the • conjunctivitis – erythromycin
diagnosis of genital tract infections • LGV – doxycycline
• Immunofluorescence – gold standard for the diagnosis of • psittacosis – azithromycin
trachoma
• IgM antibody titer of 1:32 or more – diagnostic for neonatal
pneumonia
VII. RICKETTSIAE
• classical detection using Weil-Felix reaction → cross-reaction with antigens of OX strains of Proteus vulgaris
• drug of choice for all rickettsial infections is doxycycline
DISEASE CAUSE VECTOR INCUBATION ONSET RASH ESCHAR MORTALITY
Rocky Mountain Rickettsia Macular with
Tick 7 Abrupt No 10-25%
spotted fever rickettsia centripetal spread
Rickettsia Macular with
Epidemic typhus Body louse 8 Abrupt No 20%
prowazekii centrifugal spread
Endemic typhus Rickettsia typhi Rat flea 7-14 Gradual Maculopapular No Low
Orientia Mites Maculopapular with
Scrub typhus 10-12 Abrupt No 1-15%
tsutsugamushi (chiggers) centrifugal spread
Mites Generalized
Rickettsial pox Rickettsia akari 9-14 Abrupt Yes Low
(chiggers) papulovesicular
Q fever Coxiella burnetti None 4-90 Chronic None No 65%
Ehrlichia Maculopapular or
Ehrlichiosis Ticks 7-21 Abrupt No 2-3%
chaffeensis petechial
✔GUIDE QUESTION
MISCELLANEOUS BACTERIA Bacillary angiomatosis presents with cutaneous nodules very similar in
A. BARTONELLA HENSELAE appearance to those found in which disease?
CAT SCRATCH DISEASE A. Burkitt lymphoma
• gram-negative rod B. Nasopharyngeal carcinoma
C. Kaposi sarcoma
• normal oral flora of cats
D. Cholangiocarcinoma
• cat-scratch fever in immunocompetent individuals
• bacillary angiomatosis in immunocompromised
• transmission: cat bite or scratch
It is especially difficult to differentiate clinically between bacillary COVID-19 (CORONAVIRUS DISEASE 19)
angiomatosis and Kaposi's sarcoma (KS). Both may present with
AUGUST UPDATE
moist, erosive cutaneous vascular lesions in immunocompromised
patients. A tissue biopsy is required for diagnosis. Failure to – CAUSES, SYMPTOMS, DIAGNOSIS,
distinguish KS from bacillary angiomatosis is problematic TREATMENT, PATHOLOGY
because, unlike KS, bacillary angiomatosis responds dramatically https://qrs.ly/7qbp59p
to antibiotic therapy. Furthermore, bacillary angiomatosis may
be life threatening if untreated.
OVERVIEW OF VIRUSES
• Viruses are acellular infectious agents
B. GARDNERELLA VAGINALIS • Obligate intracellular parasites
BACTERIAL VAGINOSIS • Consist of DNA or RNA genome, but not both, surrounded by a
• facultative gram-variable rod protein coat
• clue cells present • May also be enveloped or naked
• positive whiff test (fishy • Contain the genes necessary for directing their own replication
odor) • Require host structures and enzymes to complete replication
• malodorous vaginal discharge • The fate of the host cell following infection ranges from lysis and
release progeny virions to gradual, prolonged release of viral
particles
✔GUIDE QUESTION
Which organism predominates the vaginal ecosystem in otherwise
healthy adults? I. VIRAL STRUCTURE
A. Lactobacillus acidophilus • range in size from 20-300 nm
B. Escherichia coli • all viruses have a protein coat (capsid)
C. Gardnerella vaginalis o composed of repeating capsomers
D. Chlamydia trachomatis o in some viruses, covered with lipoprotein envelope
• nucleic acid genome + capsid = nucleocapsid
GUIDE QUESTION 16
VIRAL SYMMETRY
https://qrs.ly/8wck6os
• Symmetry: spherical (icosahedral) or helical
• All helical viruses are enveloped
• Icosahedral viruses can be enveloped or naked
• All DNA viruses are icosahedral except Poxvirus
C. HAEMOPHILUS DUCREYI
• Only RNA viruses have helical symmetry
CHANCROID o Most assume a spherical shape except rhabdoviruses, which
• small gram-negative rod have a bullet-shaped capsid.
• culture on chocolate agar with heme (factor X) o Most RNA viruses have helical symmetry except:
• PE: painful genital ulcer § Flaviviruses
§ Caliciviruses
D. YERSINIA ENTEROCOLITICA § Reoviruses RNA viruses with
MESENTERIC ADENITIS (pseudoappendicitis) § Picornavirus icosahedral symmetry
• gram-negative rods § Togaviruses
• reservoir: domestic animals § Hepevirus
• transmission: oro-fecal route
E. KLEBSIELLA GRANULOMATIS
GRANULOMA INGUINALE (DONOVANOSIS)
• encapsulated, pleomorphic gram-negative bacillus
• bipolar densities (Donovan bodies) look like closed safety pins
• small painless papule ulcerates to form beefy red ulcer with VIRAL PROTEINS
velvety surface • surface proteins
• pseudobuboe formation → lump in the groin similar in o attachment to host cell receptors
appearance to bubo (remember bubonic plague?); it is actually a • DNA or RNA polymerases
granuloma and not an inflamed lymph node, hence, it is a ‘false’ • matrix protein
bubo o interaction between nucleocapsid and envelope
• treatment: azithromycin • antigenic (serotypic) variants
o evasion of host defenses
VIROLOGY VIRAL ENVELOPE
This section on the fundamentals of virology is something that you • lipid membrane derived from the host cell
probably know already (as discussed in the generalities section), but o acquired as the virus exits from the cell in a process called
allow me to lead you to some online resources where you can review these budding
items. You might think that these ‘peculiar’ details are unimportant, but o all enveloped viruses acquire their envelope from plasma
sometimes the boards can give you a clinical scenario (e.g. a textbook case membrane EXCEPT herpes virus (from nuclear membrane)
of measles), then ask ‘peculiar’ questions (e.g. shape of the virus, whether
its DNA or RNA is single- or double stranded). Nevertheless, I lead you to
• enveloped viruses are less stable and more easily inactivated
easy-to-understand resources here. When we reach phase 1, we will MEMORY AID NAKED VIRUSES
discuss you some questions on how these concepts are tested. NAKED CPR and PAPP smear
Should I know the coronavirus by heart? Calici Parvo
Dear, it is still being studied. Note, however, that medically speaking, (as Picorna Adeno
represented in the older literature), coronaviruses are really of less Reo Papilloma
clinical importance (except SARS and COVID-19, of course!). Generally, as
far as the boards are concerned, coronaviruses are the 2nd most common
Polyoma
cause of the common colds (the first being rhinoviruses). Nevertheless, we NAKED VIRUSES: Viruses that do not have membranes
are unsure whether and to what extent you will be tested about COVID- Give PAPP smears and CPR to a naked hippie (herpesvirus)
19. It is better to be prepared anyway, and at least you should know the Naked DNA Virus Naked RNA Virus
general characteristics of coronaviruses. Papillomavirus Calicivirus
Dr. Calderon
Adenovirus Picornavirus
Parvovirus Reovirus
Polyomavirus Hepevirus
✔GUIDE QUESTION
The interstitial space between the nucleocapsid and the envelope is
called the _____.
A. Tegument
B. Penton
C. Hemagglutinin
D. Procapsid
The matrix is also known as the tegument..
Dr. Calderon
II. VIRAL GENETICS VIRAL LIFE CYCLE AND PHARMACOTHERAPY

VIRAL GENOME
• all viruses are haploid except retroviruses
• contain either DNA or RNA, but not both
• genomes can be either single-stranded or double-stranded
• genomes of RNA viruses can be either positive-polarity or
negative-polarity
• some RNA viruses have a segmented genome
MEMORY AID SEGMENTED GENOME

B–O–A–R
Bunyaviruses
Orthomyxoviruses (influenza)
Arenaviruses
Reoviruses
NEGATIVE-STRAND RNA VIRUSES

• must transcribe negative strand to positive
• virion brings its own RNA-dependent polymerase REPLICATION STAGE DRUGS AVAILABLE
1 Adsorption Fusion inhibitors, e.g. T-20
RNA VIRUSES 2 Penetration, uncoating Amantadine
• Two types of RNA viruses: positive-stranded or negative- Acyclovir
stranded Zidovudine
• Positive-Stranded RNA Viruses 3 Viral nucleic acid synthesis Lamivudine
o RNA is just like a messenger RNA (mRNA) Nevirapine
o When a positive-stranded RNA virus enters a host cell, its RNA Ribavirin
can immediately translated by the host’s ribosomes into 4 Viral protein synthesis Interferons
protein 5 Assembly Protease inhibitors
6 Release –
UNCOATING OF AN ENVELOPED VIRUS

• Negative-stranded RNA viruses
o When negative-stranded RNA viruses enter the cell, they are
not able to begin translation immediately
o Must transcribe negative strand to positive (–) → (+)
o Virion brings its own RNA-dependent polymerase, which
will carry out the transcription of the negative-strand into
positive.
Receptors used by viruses

VIRUS RECEPTORS
MEMORY AID NEGATIVE-STRAND RNA VIRUSES CMV • Integrins (heparan sulfate)
Always Bring Polymerase Or Fail Replication. EBV • CD21
Arenaviruses HIV • CD4, CXCR4, CCR5
Bunyaviruses Parvovirus B19 • P antigen on RBCs
Paramyxoviruses Rabies • Nicotinic AChR
Orthomyxoviruses Rhinovirus • ICAM-1
Filoviruses
Rhabdoviruses VIRAL GENETICS
DNA VIRUSES • mutations can produce antigenic, drug-resistant or
• Unlike RNA, DNA cannot be translated directly into proteins. attenuated variants
• It must be transcribed into mRNA with subsequent translation • genomic reassortment causes epidemics
of mRNA into structural proteins and enzymes o example: influenza viruses
• complementation: one virus produces a protein that can be
used by another virus
o example: hepatitis D and hepatitis B
• phenotypic mixing: two different viruses infect the same cell
• Most DNA viruses have BOTH a negative strand and a positive
strand except PARVOVIRUSES, which have single-stranded DNA OUTCOMES OF VIRAL INFECTION
genome Cytopathic • visual or functional change in infected
• All double-stranded DNA have icosahedral symmetry except effect cells
POXVIRUS in which DNA has complex structural proteins Malignant • oncogenic viruses induce transformation
looking much like a box. transformation and unrestrained growth
• Negative strand refers to the DNA strand that is read; used as a • infected cells appear normal, but are
Commensal
template for transcription into mRNA, producing large numbers of progeny
Symbiosis
• Positive strand is ignored. viruses
VIRULENCE FACTORS VIRAL VACCINES
• cytokine decoys • Live-Attenuated Vaccines
o bind cytokines and block their ability to interact with their o Induce humoral and cell-mediated immunity but may
intended targets revert to virulence on rare occasions
• virokines o Dangerous to give to immunocompromised patients or their
o reduce the expression of antigen presenting cells and close contacts
inactivate complement o Examples: (MISS CRY)
• antigenic variants of surface proteins § MMR (the only live-attenuated vaccine that can be given to
HIV-positive patients who do not show signs of immuno-
PERSISTENT VIRAL INFECTIONS deficiency)
Carrier • produce virus for long periods of time § Influenza (intranasal)
state • can serve as a source of infection for others § Smallpox
§ Sabin’s polio vaccine
Latent • not producing virus at the present but can be
§ Chicken pox
Infections reactivated at a subsequent time
§ Rotavirus
Slow Virus • long incubation period, often measured in § Yellow fever
Infections years • Killed Vaccines
o Induce only humoral immunity but are stable
III. LABORATORY DIAGNOSIS o Examples: (RIP Always; SalK=Killed)
PRESUMPTIVE IDENTIFICATION § Rabies
§ Influenza (injected)
• Cytopathic effect
§ Salk’s polio vaccine
• Hemadsorption: attachment of RBCs to surface of infected cells
§ Hepatitis A
• Interference: interference with CPE by another virus
• Recombinant Vaccines
• Decrease in acid production by infected, dying cells (using
o Examples:
phenol red)
§ Hepatitis B (recombinant HBsAg)
§ HPV (Types 6, 11, 16, 18)
DEFINITIVE DIAGNOSIS
✔GUIDE QUESTION
• Complement fixation
Which is the first vaccine known to prevent a human cancer?
• Hemagglutination inhibition A. HIV C. HPV
• Neutralization B. HBV D. HCV
• Fluorescent antibody assay
OK, your intuition might tell you it should be HPV, but the first
• Radioimmunoassay evidence of cancer prevention by vaccination in humans was
• Enzyme-linked immunosorbent assay (ELISA) provided by HBV vaccination in infants. Chronic HBV is related to
approximately 60%-90% of hepatocellular carcinomas (HCC) in
SEROLOGIC TESTS adults and nearly 100% of childhood HCC in areas endemic for
HBV infection. The first universal HBV vaccination program was
• Seroconversion: finding antibody in one who previously had
launched in Taiwan and has continued for more than 20 years.
none
• Presence of IgM: can be used to diagnose current infection Remember, HBV vaccine is not really intended directly against the
cancer. The concept being tested here is that lowering the risk of
• Presence of IgG: cannot be used to diagnose current infection; HBV can subsequently lower the risk of the related cancer.
antibody may be due to an infection in the past Dr. Calderon
The most common sites of viral infection and disease is the _____.
DETECTION OF VIRAL ANTIGENS A. Skin
• Presence of viral proteins, commonly used in diagnosis B. Oropharynx and respiratory tract
C. Gastrointestinal tract
• Example: p24 of HIV and HbSAg D. CNS
• Presence of viral DNA or RNA of the gold standard in viral
Remember: AERO-DIGESTIVE tract!
diagnosis Dr. Calderon
IV. DNA VIRUSES
MEMORY AID DNA VIRUSES

DNA Viruses are HHAPPPPy viruses.
Hepadna
Herpes
Adeno
Pox
Parvo
Polyoma
Papilloma
All DNA viruses have double- All DNA viruses are icosahedral
Parvovirus Poxvirus
stranded DNA EXCEPT EXCEPT
All DNA viruses have linear DNA Papilloma, Polyoma, All DNA viruses replicate in the
Poxvirus
EXCEPT and Hepadna nucleus EXCEPT
NAKED DNA VIRUSES TRANSMISSION

MODE OF
• direct contact or sexually
VIRUS ONCOGENIC VACCINE
TRANSMISSION
Respiratory, PATHOGENESIS
Adenovirus No Yes • infect squamous cells and induce formation of cytoplasmic
fecal-oral
Human Sexual, skin vacuole (koilocytes)
Yes Yes • genes E6 and E7 – THIS IS VERY IMPORTANT!
papillomavirus contact
Parvovirus Respiratory, o inactivation of tumor suppressor genes
No No o E6 inhibits p53
B19 transplacental
o E7 inhibits Rb
1. PARVOVIRIDAE
SPECTRUM OF DISEASE
PARVOVIRUS B19 (FIFTH DISEASE)
• HPV-1 to 4
CHARACTERISTICS o skin and plantar warts
• naked virus with icosahedral symmetry • HPV-6 and 11
• single-stranded DNA genome o genital warts (condyloma acuminata)
• one serotype o respiratory tract papilloma
o most common viral STD
TRANSMISSION • HPV-16, 18, 31, 33
• respiratory droplets and transplacental o carcinoma of cervix, penis, and anus
SPECTRUM OF DISEASE
• Erythema Infectiosum (Fifth Disease)
o bright red cheek rash (slapped cheeks) with fever, coryza, and
sore throat
• Aplastic crisis
o interferes with erythroid progenitor cells TREATMENT
o transient but severe aplastic anemia in children sickle cell • genital warts: podophyllin
anemia, thalassemia or spherocytosis • skin warts: liquid nitrogen
• Fetal Infections • plantar warts: salicylic acid
o 1st trimester: fetal death
o 2nd trimester: hydrops fetalis PREVENTION
• Arthritis • vaccine for HPV-6, 11, 16 and 18
o immune-complex arthritis of small joints HPV is often equated to cervical cancer, well, at least in the literature for
• Chronic B19 Infection the boards. So, here’s a video that bridges this topic to pathology and
o pancytopenia in immunodeficient patients gynecology:
Dr. Calderon
B. JC POLYOMA VIRUS
• only causes disease in immunocompromised hosts
• causes progressive multifocal leukoencephalopathy (PML) in
patients with AIDS
RBC destruction in fetus leads to hydrops fetalis and death, in adults leads o demyelinating disease that affects oligodendrocytes
to pure RBC aplasia and rheumatoid arthritis–like symptoms. characterized by deficits in speech, coordination, and memory
Dr. Calderon
2. ADENOVIRIDAE
ADENOVIRUS
CHARACTERISTICS
• naked viruses with double-stranded linear DNA and an
icosahedral nucleocapsid C. BK POLYOMA VIRUS
• only virus with fibers
• only causes disease in immunocompromised hosts
• 41 antigenic types
• causes hemorrhagic cystitis and nephropathy in patients with
solid organ (kidney) and bone marrow transplants
TRANSMISSION
• aerosol droplet, fecal–oral, direct contact
ENVELOPED DNA VIRUSES
SPECTRUM OF DISEASE 1. HERPESVIRIDAE
• URT: pharyngitis, conjunctivitis, coryza PRIMARY RECURRENT
VIRUS ROUTE
• LRT: bronchitis, atypical pneumonia INFECTION INFECTION
• GIT: acute gastroenteritis Herpes
HSV-1 Secretions,
• GUT: hemorrhagic cystitis Stomatitis labialis,
(HHV-1) saliva
• histopathology encephalitis
o Cowdry type B intranuclear inclusions (intranuclear, Herpes
basophilic) HSV-2 genitalis, Herpes Sexual,
(HHV-2) perinatal genitalis perinatal
infection
VZV Varicella Respiratory
Varicella
(HHV-3) zoster secretions
Respiratory
EBV Infectious
None secretions,
(HHV-4) mononucleosis
3. PAPOVAVIRIDAE saliva
A. HUMAN PAPILLOMA VIRUS Intrauterine,
Congenital
CMV Asymptomati transfusions,
CHARACTERISTICS CMV,
(HHV-5) mononucleosis c shedding sexual,
• naked viruses with double-stranded circular DNA and an secretions
icosahedral nucleocapsid
KSHV Kaposi’s Sexual,
• least 100 types Uncertain
(HHV-8) sarcoma transplant
• More than half of cancers are due to HPV 16 (high-risk HPV)
A. HERPES SIMPLEX VIRUSES
CHARACTERISTICS
• enveloped virus with icosahedral nucleocapsid and linear
double-stranded DNA
TRANSMISSION
• HSV-1: saliva or direct
• HSV-2: sexual or transvaginal
PATHOGENESIS
• vesicle filled with virus particles and cell debris
• site of latency
o HSV-1: trigeminal ganglia
o HSV-2: lumbosacral ganglia TREATMENT
• multinucleated giant cells are seen on Tzanck smear • mild: no treatment
• large, pink to purple intranuclear inclusions (Cowdry type A) • moderate to severe: Acyclovir
o shortens the duration of the lesions
SPECTRUM OF DISEASE
• Herpes Simplex Virus Type 1
o gingivostomatitis C. CYTOMEGALOVIRUS
o herpes labialis (lips) CHARACTERISTICS
o keratoconjunctivitis • Enveloped virus with icosahedral nucleocapsid and linear ds-
o temporal lobe encephalitis DNA
o herpetic whitlow (fingers) • cultured in shell tubes
o herpes gladiatorum (trunk) • negative heterophil test
• Herpes Simplex Virus Type 2
o genital herpes TRANSMISSION
§ painful anogenital vesicles • body fluids, transplacental, organ transplantation
o neonatal herpes
§ contact within birth canal PATHOGENESIS
o aseptic meningitis • immediate early proteins
o translated from premade mRNAs
o impair assembly of the MHC class
I–viral peptide complexes
• HP: giant cells with owl's-eye
nuclear inclusions
TREATMENT SPECTRUM OF DISEASE

• DOC is Acyclovir • Congenital CMV infection
o shortens the duration of the lesions o most common cause of congenital abnormalities
o reduces the extent of shedding of the virus o microcephaly, seizures, deafness, jaundice, and purpura
o no effect on the latent state o most common when mother infected in 1st trimester
• Heterophil-negative mononucleosis
B. VARICELLA-ZOSTER VIRUS o fever, lethargy, and abnormal lymphocytes in PBS
CHARACTERISTICS • Systemic CMV infections
• Enveloped virus with icosahedral nucleocapsid and linear o pneumonitis, hepatitis, colitis, retinitis in
double-stranded DNA immunocompromised patients
TRANSMISSION CMV retinitis showing hemorrhage and

• respiratory droplets and by direct contact with lesions
retinal exudates o n fundoscopy (“pizza
PATHOGENESIS pie”,” brushfire”, “cheese and ketchup”
retinitis)
• infects URT, then spreads via the blood to the skin
• becomes latent in the dorsal root ganglia, which may reactivate
as zoster
TREATMENT
• HP: multinucleated giant cells with intranuclear inclusions
• DOC is Ganciclovir
• CMV is largely resistant to acyclovir
SPECTRUM OF DISEASE
• Varicella
D. EPSTEIN-BARR VIRUS
o incubation period of 14–21 days
o vesicular centrifugal rash • HHV-4
§ “dewdrop on a rose petal”
appearance CHARACTERISTICS
o complications: • enveloped virus with icosahedral nucleocapsid and linear ds-
§ pneumonia DNA
§ encephalitis
§ Reye syndrome TRANSMISSION
• Zoster • saliva
o painful vesicles along dermatomal distribution
o debilitating pain (postherpetic neuralgia) PATHOGENESIS
• Ramsay Hunt Syndrome • infects mainly lymphoid cells, primarily B lymphocytes
o involvement of geniculate ganglion causes facial nerve • elicits EBV-specific antibodies and nonspecific heterophil
paralysis antibodies
SPECTRUM OF DISEASE
• Infectious Mononucleosis
o “kissing disease” Smallpox is a disease of historical significance, hence, a deeper discussion
o fever, sore throat, lymphadenopathy, and splenomegaly might be necessary in a preventive medicine context. More importantly,
o splenic rupture is a rare complication the key figure you should remember here is Edward Jenner, the Father
§ rapid increase in size produces a tense, fragile splenic of Immunology.
Dr. Calderon
capsule
• Malignancies HOW WE CONQUERED

o oncogenicity associated with expression of latency-associated THE DEADLY SMALLPOX VIRUS
membrane protein 1 (LMP-1) https://qrs.ly/bmbp6g3
o Burkitt lymphoma: in African people
o B-cell lymphomas
o nasopharyngeal carcinoma: in Chinese people
B. MOLLUSCUM CONTAGIOSUM VIRUS
o hairy leukoplakia in AIDS patients
MOLLUSCUM CONTAGIOSUM
E. HUMAN HERPESVIRUS – 6 • pinkish, papular skin lesions with an umbilicated center
• HP: Henderson-Paterson bodies
• Enveloped icosahedral, double-stranded linear DNA
o intracytoplasmic eosinophilic inclusions
• ROSEOLA / EXANTHEM SUBITUM / SIXTH DISEASE
• transmission: direct contact
o rose-colored macules appear on body after several days of
• treatment: Cidofovir
high fever; can present with febrile seizures; usually affects
infants
• Nagayama spots: erythematous papules on soft palate and base
of the uvula
F. HUMAN HERPESVIRUS – 8
KAPOSI SARCOMA
• Kaposi sarcoma (KS) is a rare type of cancer that can affect both 3. HEPADNAVIRIDAE
the skin and internal organs HEPATITIS B VIRUS
• M.ost common symptoms: red or purple patches on the skin. • Enveloped virus with incomplete circular double-stranded DNA
• KS is classified into:
TRANSMISSION
o AIDS-related Kaposi sarcoma
• blood, during birth, sexual
o Endemic African Kaposi sarcoma (widespread common cancer
in parts of Africa with high levels of HIV) MEMORY AID HEPATITIDES
o Classic Kaposi sarcoma (Non-AIDS-related KS. This is rare, Hepatitis A = Asymptomatic
mostly affecting middle-aged and elderly men of Hepatitis B = Blood-borne
Mediterranean or Ashkenazi Jewish descent) Hepatitis C = Chronic, Cirrhosis, Carcinoma, Carriers
o Transplant-related Kaposi sarcoma (an uncommon side effect Hepatitis E = Enteric, Expectant mothers, Epidemics
when the immune system is weakened after a transplant)
The VOWELS (A and E) hit your BOWELS.
Hepatitis A and E cause enteric infections.
PATHOGENESIS:
Virulence
Factors
Remember that, because of similarities in terms of clinical presentation, • surface antigen
KS must be differentiated from bacillary angiomatosis (in reference to my (HBsAg)
discussion on the bacterium Bartonella). • core antigen
Dr. Calderon
(HBcAg)
• e antigen
2. POXVIRIDAE
(HBeAg)
• Largest DNA viruses
• The only DNA virus that is complex (not icosahedral) PATHOGENESIS
• The only DNA virus that replicates in the cytoplasm (not in the • only DNA virus that produces DNA by reverse transcription with
nucleus) mRNA as the template
• hepatocellular injury due to immune attack
A. VARIOLA VIRUS o HBV has NO cytopathic effect
SMALLPOX
• only disease that has been eradicated from the face of the Earth PHASES OF DAMAGE
• largest viruses • Proliferative
• brick-shaped poxvirus containing linear dsDNA o viral antigens expressed on hepatocyte surface
• HP: Guarnieri bodies o host CD8+ T cells destroy infected hepatocytes
o intracytoplasmic eosinophilic inclusions § note that the virus does not have a cytopathic effect - the host
• transmission: aerosol or contact immune system (CD8+ T cells) does the damage!
• incubation period of 7–14 days • Integrative
• prodrome of fever and malaise followed by centrifugal rash o HBV DNA integrated into host genome
o risk of HCC remains even after host mounts successful
antibody response to virus
SEROLOGICAL EVOLUTION
Surface antigen
• Describes whether the patient is diseased or immune
• HBsAg
o having this antigen means the patient has the disease (chronic,
acute, or asymptomatic carrier)
o precedes onset of symptoms and elevation of liver enzymes
• Anti-HBsAg
o presence of this antibody indicates that patient is immune
and/or cured
o NO active disease present
Core antigen
• Tells us how long the infection has been present
• HBcAg HEPATITIS B SEROLOGY
o the antigen of the core of the virus (HBsAg removed) https://qrs.ly/qdck6ox
o antibodies are not protective but yield information about the
state of infection
o positive antibodies seen during the "window period" (a period
of active infection) • The only positive during window period: Anti-HBc IgM
• The only positive among vaccinated patients: Anti-HBs
• IgM anti-HBcAg
• What can differentiate chronic active infection from chronic carrier:
o new infection is present HBeAg
o most specific marker for diagnosis of acute HBV infection • Chronic infection is characterized by the persistence of HBsAg for at
because it persists during the window period least 6 months.
• IgG anti-HBcAg • Persistence of HBsAg is the principal marker of risk for developing
o old infection is present chronic liver disease and liver cancer (hepatocellular carcinoma) later
• the soluble component of the core antigen tells us how infective in life.
Dr. Calderon
the patient is
SPECTRUM OF DISEASE
• HBeAg
• incubation period: 10–12 weeks
o a soluble component of the viral core
• fever, anorexia and jaundice
o presence connotes high infectivity
o á "e" = á "enfectivity" • dark urine, pale feces, and elevated transaminase levels
• Anti-HBeAg • cirrhosis and hepatocellular carcinoma
o presence connotes low infectivity o liver cell hyperplasia via HBc protein that interferes w/ p53
• associated with autoimmune vasculitides (polyarteritis
Anti- Anti- nodosa)
TIME PERIOD HBsAg HBeAg
HBs HBc
TREATMENT
Incubation
+ – – + • interferon-a and lamivudine
period
+ PREVENTION
Acute infection + – +
IgM • vaccination
+ o first vaccine to prevent a human cancer
Window period – – –
IgM • HBV vaccine and cancer reduction
Complete + o The first evidence of cancer prevention by vaccination in
– + –
recovery IgG humans was provided by HBV vaccination in infants
+ o Chronic HBV is related to approximately 60%-90% of
Chronic carrier + – –
IgG hepatocellular carcinomas (HCC) in adults and nearly 100% of
+ childhood HCC in areas endemic for HBV infection
Chronic active + – +
IgG o The first universal HBV vaccination program was launched in
Vaccinated – + – – Taiwan and has continued for more than 20 year
V. RNA VIRUSES
GENERALITIES ON RNA VIRUSES SPECTRUM OF DISEASE
All RNA viruses have single- Reovirus and • Herpangina
stranded RNA EXCEPT Rotavirus o fever, sore throat, and tender
All RNA viruses replicate in the Influenza and vesicles in oropharynx
cytoplasm EXCEPT Retrovirus • Hand-foot-and-mouth disease
o vesicular rash on hands and feet
NAKED RNA VIRUSES and ulcerations in the mouth
• Hemorrhagic Conjunctivitis
1. PICORNAVIRIDAE • Pleurodynia
MEMORY AID PICORNAVIRIDAE o fever and severe pleuritic-type chest pain
PERCHed on a PIC (peak). o Pleurodynia is pain due to an infection of the intercostal
Poliovirus muscles (myositis), not of the pleura
Echovirus • Myocarditis and Pericarditis
Rhinovirus o most common cause
Coxsackievirus o fever, chest pain, and signs of congestive failure.
Hepatis A virus • Aseptic Meningitis
PICornaviridae o Coxsackie virus, poliovirus and echovirus are
ENTEROVIRUSES
A. POLIOVIRUS o most common cause of aseptic meningitis
POLIOMYELITIS and MENINGITIS
• Naked nucleocapsid with single-stranded, positive-polarity RNA C. ECHOVIRUS
• oral-fecal transmission Enteric Cytopathic Human Orphan
• replicates in motor neurons in anterior horn of spinal cord, • Called "orphans" because they were not initially associated with
causing paralysis any disease
• Host range is limited to primates → limitation is due to the • Now known to cause aseptic meningitis, upper respiratory tract
binding of the viral capsid protein to a receptor found only on infection, febrile illness with and without rash, infantile
primate cell membranes. diarrhea, and hemorrhagic conjunctivitis.
• Three serologic (antigenic) types based on different antigenic • Transmitted by fecal-oral route.
determinants on the outer capsid proteins Orphan virus means a virus that is not associated with any known disease.
• Spectrum of disease Even though Echoviruses have since been identified with various diseases,
(1) inapparent, asymptomatic the original name is still used.
infection Dr. Calderon
(2) abortive poliomyelitis – most D. RHINOVIRUS

common clinical form; mild, febrile COMMON COLDS
illness with headache, sore throat, • Naked nucleocapsid viruses with single-stranded, positive-
nausea, and vomiting. polarity RNA
(3) nonparalytic poliomyelitis – • more than 100 serotypes
aseptic meningitis • transmitted by aerosol droplets and hand-to-nose contact
(4) paralytic poliomyelitis – flaccid • Replicate better at 33°C than at 37°C → they affect primarily
paralysis; permanent motor nerve damage the nose and conjunctiva rather than the lower respiratory tract.
• histopathology • Acid-labile → killed by gastric acid when swallowed → they do
o Cowdry type B intranuclear inclusions not infect the gastrointestinal tract, unlike the enteroviruses.
• prevented by vaccination • Host range is limited to humans and chimpanzees
o killed (Salk IPV) MEMORY AID RHINOVIRUS
o live, attenuated (Sabin OPV)
RHINO has a runny nose
KILLED LIVE E. HEPATITIS A VIRUS
ATTRIBUTE
(SALK) (SABIN) HEPATITIS A
Prevents disease Yes Yes • naked nucleocapsid virus with a ss-positive-RNA
Interrupts transmission No Yes • fecal–oral transmission
Secondary protection (prevents • children most frequently infected
No Yes
spread) • self-limited hepatitis
Induces humoral IgG protection Yes Yes • anti-HAV IgM is the most important test
Induces intestinal IgA protection No Yes • Also known as Enterovirus 72
Interferes with viral replication • Has one serotype
No Yes
in the gut • There is no antigenic relationship to HBV or other hepatitis
Reversion to virulence No Yes (rare) viruses.
Impaired immunization via
coinfection with other No Yes 2. CALICIVIRIDAE
enteroviruses A. HEPATITIS E VIRUS
Disease-causing in the
No Yes HEPATITIS E
immunocompromised
• fecal–oral transmission
Route Injection Oral
• no chronic carrier state
Refrigeration requirement No Yes
• no cirrhosis
Immunity duration Shorter Longer
• no hepatocellular carcinoma
• high mortality in pregnant women
B. COXSACKIE VIRUS
CHARACTERISTICS B. NORWALK VIRUS (NOROVIRUS)
• Naked nucleocapsid with single-stranded, positive-polarity RNA
VIRAL GASTROENTERITIS
• Classification based on pathogenicity in mice
• Nonenveloped virus with icosahedral nucleocapsid and one
piece of single-stranded, positive-polarity RNA
TRANSMISSION
• Oral-fecal transmission
• oral-fecal
• most common cause of nonbacterial diarrhea in adults
• sudden onset of vomiting and diarrhea accompanied by fever
and abdominal cramping
3. REOVIRIDAE
ROTAVIRUS
VIRAL GASTROENTERITIS
• Naked double-layered capsid with 10 or 11 segments of double-
stranded RNA
• most common cause of childhood diarrhea
SUPPLEMENT
HEMAGGLUTININ
• Binds to the cell surface receptor (neuraminic acid, sialic
acid) to initiate infection of the cell
• The target of neutralizing antibody
NEURAMINIDASE
• Cleaves neuraminic acid (sialic acid) to release progeny virus
from the infected cell
• Also degrades the protective layer of mucus in the respiratory
tract → enhances access to the respiratory epithelial cells.
Many species of animals (aquatic birds, chickens, swine, and horses) have
their own influenza A viruses. These animal viruses are the source of
the RNA segments that encode the antigenic shift variants that cause
epidemics among humans. For example, when avian and human influenza
A virus infect the same cell (e.g., in a farmer's respiratory tract), this leads
to genomic reassortment whereby a new variant of the human A virus,
bearing the avian virus hemagglutinin, may appear
Dr. Calderon
In this figure, note that rotaviral diarrhea occurs because the cellular
damage to the intestinal epithelium causes denudation of the mucosa.
Therefore, the diarrhea is due to malabsoprtion, and not secretory.
Dr. Calderon
MEMORY AID ROTAVIRUS

Right Out The Anus
ROTAvirus causes diarrhea!
ENVELOPED RNA VIRUSES (NEGATIVE SENSE)

1. ORTHOMYXOVIRIDAE
INFLUENZA VIRUS
CHARACTERISTICS
• Enveloped virus with a helical nucleocapsid and segmented, ss-
negative RNA
• major antigens are hemagglutinin (H) and neuraminidase (N)
• respiratory droplet transmission
• Influenza A → worldwide epidemics (pandemics)
o Each year, influenza is the most common cause of respiratory
tract infections.
• Influenza B → major outbreaks of influenza.
o Does not lead to pandemic
• Influenza C → mild respiratory tract infections but does not
• There is evidence that aquatic birds (waterfowl) are a common
cause outbreaks of influenza.
source of these new genes and that the reassortment event
leading to new human strains occurs in pigs.
PATHOGENESIS
• Pigs serve as the "mixing bowl" within which the human, avian,
• Envelope à two different types of spikes: HEMAGGLUTININ &
and swine viruses reassort.
NEURAMINIDASE
o Waterfowl: H1 to H16, N1 to N9
• Influenza A virus – has 16 antigenically distinct types of
o Humans: H1, H2, and H3, N1 and N2
hemagglutinin (HA) and 9 antigenically distinct types of
• Influenza B virus is only a human virus
neuraminidase (NA).
o There is no animal source of new RNA segments.
• Some of these types cause disease in humans, but most of the
• Influenza B virus undergoes antigenic drift that the current
types typically cause disease in other animal species such as
strain must be included in the new version of the influenza
birds, horses, and pigs.
vaccine produced each year.
• Influenza B virus has no antigens in common with influenza A
virus
• ANTIGENIC SHIFTS (pandemics)
o major changes based on the reassortment of segments of the
genome RNA
o EXAMPLE: when human flu A virus recombines with swine flu
A virus
• ANTIGENIC DRIFTS (epidemics)
o minor changes based on mutations in the genome RNA
The effects of paramyxoviruses. (A) When they infect a host cell,

paramyxoviruses induce the cell membranes of adjacent cells to fuse into
large multinucleate giant cells, or syncitia. (B) This infusion allows direct
passage of viruses from an infected cell to uninfected cell by communicating
membranes. Through this means, the virus evades antibodies.
A. MEASLES VIRUS
CHARACTERISTICS
• Enveloped virus with a helical nucleocapsid and one piece of
single-stranded, negative-polarity RNA
• Respiratory droplet transmission
PATHOGENESIS
• infects URT, then spreads to reticuloendothelial cells
MEMORY AID ANTIGENIC SHIFTS VS. DRIFTS • can transiently depress cell-mediated immunity
• HP: multinucleated giant cells (Warthin-Finkeldey bodies)
Sudden Shift is more deadly than graDual Drift.
antigenic Shifts cause PANDEMICS.
SPECTRUM OF DISEASE
antigenic Drifts cause EPIDEMICS.
• incubation period of 10–14 days
TREATMENT • pathognomonic Koplik spots
• DOC is Oseltamivir or Zanamivir o bright red lesions with a white, central dot on buccal mucosa
• Amantadine or rimantadine for influenza A only • maculopapular rash
o face - trunk - extremities - palms/soles
PREVENTION • complications
• yearly vaccination o encephalitis, pneumonia, subacute sclerosing
panencephalitis (SSPE)
THE FLU VACCINE: EXPLAINED

https://qrs.ly/17bp6ht
2. PARAMYXOVIRIDAE • Patients are contagious from 4 days before the rash to 4 days
✔GUIDE QUESTION after appearance of the rash.
A 9-month-old girl is brought to the OPD because of cough and rash.
According to her parents, the rash started on her face and neck two days
MEMORY AID CARDINAL MANIFESTATIONS OF MEASLES
ago and spread to the trunk and to the extremities. 3 Cs: Cough
PE: T 40.1C, pulse 117/min, RR 26/min, BP 92/57 mmHg. The child has Coryza
red eyes, rhinorrhea, and erythematous, maculopapular, blanching rash. Conjunctivitis
She is irritable when light is shown into her eyes. Which of the following Koplik spots
is a potential complication of this disease?
A. Diffuse coronary artery ectasia and aneurysm formation PREVENTION
B. Oophoritis and infertility • infection confers lifelong immunity
C. Progressive neurological deterioration • vitamin A reduces severity
D. Reactivation in a dermatomal distribution • prevented by giving live-attenuated vaccine
This item is asking for the clinical picture of a potential
complication of measles, which is subacute sclerosing B. MUMPS VIRUS
panencephalitis (SSPE). SSPE is a progressive neurological
disorder of children and young adults that affects the central
CHARACTERISTICS
nervous system (CNS). It is a slow, but persistent, viral infection • Enveloped virus with a helical nucleocapsid and one piece of
caused by defective measles virus. single-stranded, negative-polarity RNA
Let’s recall the other complications mentioned: • Respiratory droplet transmission
• Kawasaki disease → Diffuse coronary artery ectasia and
aneurysm formation PATHOGENESIS
• Mumps → Oophoritis and infertility • initially infects URT
• Varicella → Reactivation in a dermatomal distribution (as herpes • spreads to local lymph nodes and then via the bloodstream to
zoster) parotid glands, testes, ovaries, meninges, and pancreas
Dr. Calderon
Envelope Spikes of Paramyxoviruses

Fusion
Virus Hemagglutinin Neuraminidase
Protein
Measles + - +
Mumps + + +
RSV - - +
Parainfluenza + + +
MEMORY AID PARAMYXOVIRUSES

PaRaMyxoviruses
Parainfluenza virus
RSV
Measles virus
Mumps virus
SPECTRUM OF DISEASE
• incubation period of 18–21 days
• tender swelling of the parotid glands (parotitis)
o increase in pain when drinking citrus juices
• resolves within 1 week
• complications: orchitis, meningitis
CLINICAL MANIFESTATIONS
• The period of maximum communicability is considered to be • Prodromal period
several days before and after parotitis onset. o Symptom suggestive of rabies: paresthesia and/or
• Virus is shed in the saliva from about 3 days before to 9 days fasciculations at around the bite
after the onset of salivary gland swelling. • Encephalitic phase: excessive motor activity, excitation and
agitation
MEMORY AID MUMPS
o Periods of mental aberration are interspersed with lucid
Mumps makes your parotids and testes as big as POM-poms.
intervals
Parotitis o Prominent brainstem dysfunction
Orchitis
• Coma/ death
Meningitis (aseptic)
PREVENTION DIAGNOSIS
• infection confers lifelong immunity • Fluorescent antibody testing (direct and indirect)
• prevented by giving live-attenuated vaccine o Occurrence of rabies abs in the CSF is diagnostic for rabies
since abs from vaccination do not cross the blood-brain barrier
C. RESPIRATORY SYNCYTIAL VIRUS o Abs in serum and CSF develop late in clinical course and may
• Surface spikes are fusion proteins, not hemagglutinins or be undetectable in the acute phase
neuraminidases . • RT-PCR on fresh saliva (viral shedding precedes signs)
• The fusion protein causes cells to fuse, forming multinucleated • Skin biopsy sample (DFA or PCR)
giant cells (syncytia), which give rise to the name of the virus. • Brain is optimal sample for definitive post-mortem diagnosis &
• Humans are the natural hosts of RSV. rabies is r/o in an animal only by DFA of brain tissue
• Absence of Negri bodies does not rule out rabies
VIRAL PNEUMONIA
• most important cause of pneumonia and bronchiolitis in infants TREATMENT AND PREVENTION
• severe disease in infants due to immunologic cross-reaction • pre-exposure: vaccine
with maternal antibodies • post-exposure: vaccine and immune globulin
• treatment: Ribavirin o only vaccine that is routinely used post-exposure
Radiologic findings of Bronchiolitis: hyperinflation WHO Guidelines for Post-Exposure Prophylaxis

with increased (commonly bilateral symmetrical) Category Touching or feeding animals,
peribronchial thickening and lack focal lung No treatment
I licks on the skin
consolidative change. Nibbling of uncovered skin,
Category minor scratches without
Vaccine
II bleeding, licks on broken
D. PARAINFLUENZA VIRUS 1 AND 2 skin
LARYNGOTRACHEOBRONCHITIS Single or multiple
(CROUP) transdermal bites or
• characterized by inspiratory stridor, Category scratches, contamination of Vaccine +
cough, and hoarseness III mucus membrane with saliva immunoglobulin
• steeple sign on x-ray from licks, exposure to bat
bites or scratches
The steeple sign, also called the wine bottle
sign, refers to the tapering of the upper ✔GUIDE QUESTION
trachea on a frontal chest radiograph A 29/M PhD student is brought to the ER for fever, severe agitation, and
reminiscent of a church steeple. disorientation. According to Airbnb hosts, he has been acting strangely
and seeing and hearing things that do not exist. He is sensitive to light
and develops occasional episodes of severe pharyngo-spasm during
3. RHABDOVIRIDAE which he feels that he is choking and cannot speak. He also refuses to
RABIES VIRUS eat and has excessive salivation. Several days later, he lapses into a
CHARACTERISTICS coma and dies. The virulence of this infection is due to its ability to bind
• Bullet-shaped enveloped virus with a helical nucleocapsid and to which of the following receptors?
A. Acetylcholine receptors
one piece of single-stranded, negative-polarity RNA
B. CD4 receptors
TRANSMISSION C. ICAM 1
• animal reservoir: dogs, cats, skunks, raccoons, and bats. D. Cellular integrins
• transmission by animal bite
PATHOGENESIS GUIDE QUESTION 17
• multiplies locally at bite site, infects sensory neurons, and https://qrs.ly/lfck6pf
moves by axonal transport to CNS
• HP: Negri body
Receptors used by viruses
VIRUS RECEPTORS
CMV • Integrins (heparan sulfate)
EBV • CD21
HIV • CD4, CXCR4, CCR5
Parvovirus B19 • P antigen on RBCs
Rabies • Nicotinic AChR
Rhinovirus • ICAM-1
ENVELOPED RNA VIRUSES (POSITIVE SENSE) § Corticosteroids x 3-5 days

§ Antivirals:
1. CORONAVIRIDAE - Remdesivir: inhibits viral RNA-dependent RNA
CORONAVIRUS polymerase
CHARACTERISTICS - Favipravir: conversion into the ribofuranosyl
• Enveloped virus with helical nucleocapsid and one piece of triphosphate derivative by host enzymes, then inhibits
single-stranded, positive-polarity RNA viral RNA-dependent RNA polymerase
• prominent club-shaped spikes form a "corona“ § Immunomodulatory drugs:
• displays high frequency of recombination - Tocilizumab: humanised IgG1 monoclonal antibody,
• four main sub-groupings of coronaviruses: alpha, beta, gamma, directed against the IL-6 receptor
and delta § Plasma exchange
§ Prophylactic anticoagulation
STRUCTURE
• Made up of 4 structural proteins: spike (S), membrane (M), 2. FLAVIVIRIDAE
envelope (E) and nucleocapsid (N) proteins A. DENGUE VIRUS
• S protein: important for host attachment and penetration CHARACTERISTICS
o composed of two functional subunits: • Flavivirus family
§ S1: for binding to host cell receptor • Enveloped virus with icosahedral nucleocapsid and one piece
§ S2: for fusion of viral and host cellular membranes of single-stranded, positive-polarity RNA
• 4 serotypes
TRANSMISSION
• respiratory droplet and aerosol transmission TRANSMISSION and DIAGNOSIS
• virus binds to ACE-2 receptor (highly expressed on pulmonary • transmitted by Aedes aegypti mosquito
epithelial cells) • diagnosed using dengue IgM
• enters host through endocytosis or membrane fusion • positive tourniquet test, but is nonspecific
SPECTRUM OF DISEASE • TOURNIQUET TEST
• common colds
o 229E (alpha coronavirus)
o NL63 (alpha coronavirus) • Inflate the BP cuff between
o OC43 (beta coronavirus) systolic and diastolic blood
o HKU1 (beta coronavirus) pressure.
• Severe Acute Respiratory Syndrome (SARS) • Keep cuff inflated for 5 minutes
o Emerged in 2002 in China • > 20 petechiae in a one-inch
o Most likely originated in horseshoe bats, amplified in palm square indicates capillary
civets then transmitted to humans fragility
o incubation period 2-10 days
o atypical pneumonia rapidly progressing to ARDS
o chest x-ray: non-cavitary “ground-glass” infiltrates
• Middle East Respiratory Syndrome (MERS)
o A Betacoronavirus
o originated in bats, became widespread in dromedary camels,
then transmitted to humans
o Emerged in 2012 in Arabian Peninsula
o Causes severe pneumonia and respiratory failure
• Coronavirus disease-2019 (COVID-19)
o “Severe acute respiratory syndrome CoV-2 (SARS-CoV-2)”
o A novel Betacoronavirus belonging to the subgenus
Sarbecovirus
o Emerged in Wuhan in late 2019
o Clinical presentation:
§ Incubation period: 5–6 days, but can be up to 14 days
§ may be asymptomatic; fever, body aches, breathlessness,
malaise and dry cough, GI Sx (abdominal pain, vomiting and
loose stools)
§ The complications mostly due to cytokine storm:
- Acute respiratory distress syndrome
- Acute respiratory failure
- Sepsis
- Disseminated intravascular coagulation
- Acute liver and kidney injury
- Pulmonary embolism
o Diagnostics: Molecular RT-PCR
o Lab findings:
§ normal or decreased WBC count (lymphopenia)
§ Increased LDH, CRP, creatine kinase (CK MB and CK MM),
AST ALT, D-dimer
§ Coagulation abnormalities can be observed in severe cases
(increased prothrombin time, increased INR)
o Radiologic findings:
§ High-resolution CT (HRCT): multifocal bilateral ‘ground- PATHOPHYSIOLOGY OF DENGUE HEMORRHAGIC FEVER
glass’ areas associated with consolidation and a patchy Dengue generally produces a self-febrile illness that lasts between 2 and 7
peripheral distribution, with greater involvement of the days. Most of the patients are able to fully recover after the febrile period,
lower lobes however, some patients are unfortunate and enter the critical stages of
§ ‘reversed halo sign’: focal area of patchy opacities dengue. The critical stage of dengue can lead to mortality if not treated
properly in time. While the exact reason for the severity is still unknown,
surrounded by a peripheral ring with consolidation
studies have linked the severity to antibody-dependent enhancement
o Management (currently undergoing many changes): (ADE). This theory was first described in 1964, when it was observed that
§ Oxygen support serious dengue infection was linked to secondary infection.
After a primary infection with one dengue virus serotype, the immune system • Congenital Rubella
produces antibodies that bind and neutralize secondary infection with the Syndrome
same serotype, however, a secondary heterotypic infection may lead to o infected during the 1st
enhance severity. The antibodies produced from the primary infection
have the ability to bind to the virus but lack the ability to neutralize.
trimester
These cross-reactive antibodies form infectious virus-antibody complexes are o associated
able to bind and enter in cells that present the Fc-receptors such as, abnormalities:
monocytes, macrophages, and dendritic cells, therefore, enhancing viral § patent ductus
production leading to higher viral loads. arteriosus
§ congenital cataracts
SPECTRUM OF DISEASE § sensorineural
• influenza-like syndrome with maculopapular rash and severe deafness
pains in muscles and joints (Breakbone fever) § mental retardation
• labs: leukopenia, thrombocytopenia, increased hematocrit
count MEMORY AID CONGENITAL RUBELLA SYNDROME
• hemorrhagic shock due to cross-reacting antibody during 2nd 5 Bs of Congenital Rubella Syndrome
dengue infection Bulag (cataracts)
Bingi (sensorineural deafness)
PREVENTION Bobo (mental retardation)
• insecticides Butas ng puso (PDA)
• draining stagnant water Blueberry muffin baby
• mosquito repellent
PREVENTION
B. HEPATITIS C VIRUS • infection confers lifelong immunity
CHARACTERISTICS • prevented by giving live-attenuated vaccine
• Enveloped virus with one piece of single-stranded, positive- o should not be given to immunocompromised patients or to
polarity RNA pregnant women
• hypervariable region in envelope glycoprotein
• 6 serotypes 4. RETROVIRIDAE
• diagnosis by anti-HCV or HCV RNA • Distinguished from all other RNA viruses by the presence of an
unusual enzyme, reverse transcriptase → which converts a
TRANSMISSION single-stranded RNA viral genome into double-stranded viral
• most prevalent blood-borne pathogen DNA.
• major mode: blood-borne ✔GUIDE QUESTION
o setting: IV drug abusers Lamivudine is an anti-retroviral drug which acts as an inhibitor of
• minor modes: needle-stick injury, vertical transmission, sexual reverse transcriptase. Hence, this drug may be useful in the treatment of
which of the following infections?
PATHOGENESIS A. HIV and Hepatitis B
B. HIV and Hepatitis D
• replication in liver enhanced by liver-specific micro-RNA C. Hepatitis B and Hepatitis C
• hepatocellular injury due to immune attack D. Hepatitis B and Hepatitis D
• alcoholism greatly enhances rate of hepatocellular CA
• chronic carriage of HCV is much higher than HBV
GUIDE QUESTION 18
SPECTRUM OF DISEASE https://qrs.ly/1pck6pn
• incubation: 8 weeks
• clinical presentation resembles hepatitis B
• autoimmune reactions
o thyroiditis, autoantibodies, MPGN, PORPHYRIA CUTANEA
TARDA, DM
• main cause of essential mixed cryoglobulinemia
TREATMENT
• acute hepatitis C: interferon
• chronic hepatitis: peginterferon and ribavirin
• liver transplantation for severe cirrhosis
o most common indication for liver transplantation
• New antivirals against Hepatitis C:
o Simeprevir, Sofosbuvir, Lepidasvir
3. TOGAVIRIDAE
RUBELLA VIRUS
CHARACTERISTICS
• Enveloped virus with an icosahedral nucleocapsid and one ss-
positive-RNA
• Transmission: respiratory droplet, transplacental
SPECTRUM OF DISEASE
• German Measles
o incubation period 14–21 days
o prodrome followed by 3-day
maculopapular rash and
posterior auricular LAD
o face - trunk - arms/legs
o immune-complex
polyarthritis in adults
HUMAN IMMUNODEFICIENCY VIRUS • The RNA is tightly complexed with a basic protein, NC (p7), in a
CHARACTERISTICS nucleocapsid structure that differs in morphology among the
• Enveloped virus with two copies (diploid) of a single-stranded, different retrovirus genera.
positive-polarity RNA genome
• most complex of the known retroviruses
• many serotypes
THIS IS VERY IMPORTANT!

HIV & AIDS – SIGNS,
SYMPTOMS, TRANSMISSION,
CAUSES & PATHOLOGY
https://qrs.ly/iibp6ie
STRUCTURE
• Transmembrane protein, TM (fusion protein, also called gp41),
which is linked to a surface protein, and SU (attachment protein,
gp120)
• Cone-shaped, icosahedral core containing the major capsid
protein (CA also called p24)
• MA (p17)-- directs entry of the double-stranded DNA provirus
into the nucleus, and is later essential for the process of virus
assembly. STRUCTURE OF THE HUMAN IMMUNODEFICIENCY VIRUS
Figure 28.2. Lippincott’s Illustrated Reviews: Microbiology. 3 ed. 2013 rd
• There are two identical copies of the positive sense, single-

stranded RNA genome in the capsid (that is, unlike other viruses,
retroviruses are diploid).
HIV Proviral Genome
HIV Viral Structure HIV viral genes and the proteins they code
GENOME: Structural Genes gp120 and gp41: Type-specific envelope glycoproteins

GENE PROTEINS FUNCTION gp120 – interacts with the CD4 receptor
p24, p7 • Nucleocapsid • Gene mutates rapidly → many antigenic variants.
gag • V3 loop – most immunogenic region of gp120
p17 • Matrix
reverse • Antibody neutralizes HIV infectivity, but the rapid appearance of
• Transcribes RNA genome into DNA variants → difficult to prepare vaccine.
transcriptase
• High mutation rate may be due to lack of an editing function in
pol protease • Cleaves precursor polypeptides the reverse transcriptase.
• Integrates viral DNA into host cell
integrase
DNA gp41 – mediates the fusion of the viral envelope with the cell
• Attachment to CD4 protein membrane at the time of infection.
gp120
env • Antigenicity changes rapidly GENOME: Regulatory Genes
gp41 • Fusion with host cell GENE PROTEINS FUNCTION
p24 • Activation of transcription of viral
tat tat
• Group-specific antigen genes
• Located in the core • Transport of late mRNAs to
rev rev
• Not known to vary cytoplasm
• Antibodies against p24 do not neutralize HIV infectivity but nef nef • ↓CD4 and class I MHC proteins
serve as important serologic markers of infection. vif vif • Enhances hypermutation
vpr vpr • Transport in nondividing cells
vpu vpu • Enhances virion release
TRANSMISSION HIV timeline of symptoms

• original source: chimpanzees
• transfer of body fluids
• transplacental and perinatal
• needlestick
PATHOGENESIS
• preferentially infects and kills helper (CD4+) T lymphocytes
o loss of cell-mediated immunity
o high probability of opportunistic infections
• main immune response consists of cytotoxic (CD8+)
lymphocytes
STAGES OF INFECTION
✔GUIDE QUESTION
According to the WHO, which is the most common life-threatening
Review of Medical Microbiology and Immunology
opportunistic infection affecting people living with HIV?
A. Atypical mycobacteria (MAC)
• PHASE 0 – INFECTION B. Cryptococcosis
o HIV acquired through sexual intercourse, blood, or perinatally C. Systemic CMV
• PHASE 1 – WINDOW PERIOD D. Tuberculosis
o rapid viral replication but HIV test is negative TB is the most common illness among people living with HIV. Fatal
• PHASE 2 – SEROCONVERSION if undetected or untreated, TB is the leading cause of death among
o peak of viral load, positive HIV test, mild flu-like illness, lasting people with HIV, responsible for nearly 1 in 3 HIV-associated
1-2 weeks deaths. Early detection of TB and prompt linkage to TB treatment
and ART can prevent these deaths.
• PHASE 3 – LATENT PERIOD
o asymptomatic, CD4 goes down, lasts 1-15 years Here’s an interesting feature about TB as a killer disease:
• PHASE 4 – EARLY SYMPTOMATIC WHAT MAKES
o CD4 500 to 200, lasts 5 years, mild mucocutaneous, TUBERCULOSIS (TB)
dermatologic and hematologic illnesses THE WORLD'S
• PHASE 5 – AIDS MOST INFECTIOUS KILLER?
o CD4 <200, lasts 2 years, AIDS-defining illnesses develop https://qrs.ly/tqbpd08
Dr. Author
AIDS-DEFINING ILLNESSES
CD4 count ETIOLOGY CLINICAL SYNDROME DIAGNOSIS
M. tuberculosis Disseminated tuberculosis • Presumptive diagnosis → detection of antibodies by ELISA
o There are some false-positive results with this test
HSV HSV esophagitis
< 500 • Definitive diagnosis → Western blot analysis
C. albicans Esophageal candidiasis
o If antibodies are present, they will bind to the viral proteins
HHV-8 Kaposi’s sarcoma
(predominantly to the gp41 or p24 protein).
P. jiroveci PCP pneumonia
T. gondii Cerebral toxoplasmosis ELISA WESTERN BLOT
< 200 C. neoformans Meningoencephalitis • Presumptive diagnosis • Definitive diagnosis
C. immitis Coccidioidomycosis • sensitive • specific
C. parvum Chronic diarrhea • high false positive rate • low false positive rate
M. avium Invasive pulmonary disease • low threshold • high threshold
<50 H. capsulatum Histoplasmosis • rule out test • rule in test
CMV CMV retinitis HIV can be grown in culture from clinical specimens, but this procedure is
available only at a few medical centers.
• Polymerase chain reaction (PCR) → very sensitive and specific Dr. Banzuela: Remember what I’ve told you during my physio lecture -
o To detect HIV DNA within infected cells. The Rule of “Compensation”? Where we are never given everything, but
o Some individuals who do not have detectable antibodies have our always given something, and it’s all up to us make it work and
maximize it our entire lives. Here’s one of the best stories I’ve ever read,
been shown by this test to be infected.
and it’s not even a story about a Doctor. It’s a story of a High School
o Amount of viral RNA in the plasma (i.e., the viral load) can also Teacher. During those quiet moments in your preparation for the med
be determined using PCR-based assays. boards, when you feel miserable because you still have to deal with other
TREATMENT non-academic problems - financial, family, relationship problems, etc. -
• highly active antiretroviral therapy (HAART) remember: there are still a lot of things to be thankful for. And you are
o Often initiated at the time of HIV diagnosis still showered with blessings. Read the article, and learn from it.
o Strongest indication for patients presenting with AIDS-
defining illness, low CD4+ cell counts (< 500 cells/mm3), or "A WALK TO REMEMBER"
high viral load Jeff Joseph Alicante
https://www.facebook.com/Tambalan/photos/this-is-not-a-love-story-that-nicholas-sparks-has-written-but-i-used-his-
o Regimen consists of 3 drugs to prevent resistance: 2 NRTIs story-t/10154260579183363/
(zidovudine and lamivudine) and protease inhibitor

(indinavir) This is not a love story that Nicholas Sparks has written, but I used
Immune reconstitution inflammatory syndrome (IRIS) describes a
his story title, to describe my journey in school.
collection of inflammatory disorders associated with paradoxical Pumasok ako ng PUP na hindi alam ng pamilya ko, kasi ayaw nila
worsening of preexisting infectious processes (HBV, HCV, MAC, MAI, etc.) akong mag-aral dun dahil malayo sa bahay namin at delikado daw
following the initiation HAART in HIV-infected individuals sa Maynila. Pero nagpumilit ako at tinustusan ko ang mga gastos
Dr. Calderon
mula PUPCET, xray, medical at kung anu-ano pa para makapasok
lang ng PUP, gamit ang mga ipon kong pera from being a service
WHY IT’S SO HARD crew ng Jollibee, sweldo ko yun. Naalala ko pa nun, puro pan de
TO CURE HIV/AIDS coco, cupcakes, at tubigan ang laman ng bag ko, para hindi ako
https://qrs.ly/dvbpd5o gutumin sa pagaantay ng proseso ng enrolment at para hindi na ko
aalis sa pilang pagkahaba haba.
Wala na silang nagawa kung hindi ang pag-aralin ako sa PUP.

MISCELLANEOUS VIRUSES Mahirap ang buhay namin noon dahil wala kaming kabuhayan
HUMAN T-CELL LYMPHOTROPIC VIRUS (HTLV) mula nang namatay ang papa namin nung 2004. Nakatapos si ate
• retrovirus causing adult T-cell leukemia and a HTLV- at nagtrabaho pero mababa pa lang ang sweldo niya noon (siya pa
associated myelopathy lang ang nagtatrabaho nung taong 2010) at si mama naman ay
• HP: malignant T cells with flower-shaped nucleus mananahi (kaya kapag walang nagpatahi, wala ding kita) si Ditse
ay nasa 3rd year college naman)
EBOLA VIRUS
EBOLA HEMORRHAGIC FEVER So ayun na nga, alam kong magiging mahirap ang journey ko sa
• "thread-like" viruses PUP dahil nga medyo taghirap kami, at 70 pesos ang pamasahe ko
• longest viruses back and forth. Pero sa kabila ng aming mahirap na buhay, simula
• outbreak of hemorrhagic fever in Zaire (1976) ng namatay ang papa ko, ay nagpatuloy pa din ako. Binibigyan ako
ng 80 pesos ng mama ko araw-araw, sobrang maswerte na kapag
• 100% mortality rate
isang daan. Natural kulang dahil 70 nga ang pamasahe ko balikan,
WHAT WE KNOW pero ang nasa isip ko noon, kahit pamasahe lang ang dala ko, ang
(AND DON'T KNOW) mahalaga ay makapasok ako. Diskarte talagang maituturing. At
ABOUT EBOLA nagkaroon ako ng mga kaibigan na SOBRANG BLESSING SA
https://qrs.ly/ldbp6ik KABAITAN, pinapautang/nililibre ako kapag wala akong perang
pangkain o kaya ay pambayad sa mga kailangang bayaran. Kahit
P2 na photocopy hirap akong bayaran. Pero hindi ko yun
JAPANESE B VIRUS sinukuan. Mapalad ako at may mga kaibigan akong nililibre ako, at
tinatanaw ko yung malaking utang na loob.
JAPANESE B ENCEPHALITIS
• member of flavivirus family 2010, first year kami, pag kauwi ko nun sa bahay, sinabi na ni
• most common cause of epidemic encephalitis mama na wala na syang pera na pambaon ko kinabukasan,
• most prevalent in SEA tinanong ko sya kung meron kahit 35 lang, pamasahe papunta
• transmitted by Culex tritaeniorhynchus mosquitoes (Jeep to baclaran: 12, LRT Baclaran to D.Jose: 15 at jeep to Sta.
• thalamic infarcts on CT scan mesa: 8, student fare kasi) pero wala daw talaga. May very long
exam pa naman kami nun sa Statistics at hindi nagbibigay ng
special exam yung prof namin dun lalo na kung ang dahilan ko ay
END OF MICROBIOLOGY wala akong pamasahe. Hindi naman kami makautang sa mga
kapitbahay namin, dahil bukod sa gabi na, eh malaki na ang utang
namin dun sa may-ari ng bakery na malapit sa amin. Buti na lang
at may tira pa kong kinse sa wallet ko, ipon ko yun ng tatlong araw
Important Legal Information mula sa mga baon ko, sabi ko, pwede na tong pang LRT.
Preparation Incorporated are duly protected by RA 8293 otherwise known as the
Intellectual Property Code of the Philippines, and shall only be for the sole use of the person: Nagplano ako kinagabihan. Ayun, natulog agad ako at gumising
a) whose name appear on the handout or review material, b) person subscribed to Topnotch bandang 3am. Buti na lang kahit papano ay may pagkain, binusog
Medical Board Preparation Incorporated Program or c) is the recipient of this electronic
ko na yung sarili ko nung umagang yun kasi alam kong
shared, sold and distributed through any printed form, audio or video recording, electronic mapapasabak ako eh, puno din yung lagayan ko ng tubig. Alas
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para malibang, nagbibilang ng mga kotseng magaganda, at
DISCLOSURE kinakausap ang sarili ko at sinasabihan ng "kaya mo to, Jeff, ikaw
The handouts/review materials must be treated with utmost confidentiality. It shall be the pa ba." At iniisip ko din na makakarating din ako sa school, dahil
materials are not photocopied or in any way reproduced, shared or lent to any person or 9am pa naman ang Statistics Class ko. Kapag sumakay ka, in 45
disposed in any manner. Any handout/review material found in the possession of another minutes nasa Baclaran ka na, pero since naglalakad ako, dumating
person whose name does not appear therein shall be prima facie evidence of violation of RA
ako dun ng 6:30am (or so).
trends and feedback. Please buy all recommended review books and other materials listed
below. Uminom ako ng baon kong tubig saka bumili ng ticket sa LRT. 22
minutes ang byahe sa tren, kaya kahit papano ay napahinga ko ang
mga paa ko. 7:00am (or so) nakarating ako ng D.Jose station.
Mula dun ay nilakad ko hanggang Sta. Mesa. Iniisip ko na, malapit At sa mga tumulong sa akin noon, medyo malayo na po ang
lang ang Avenida sa Mendiola, (madalas sinasabayan ko ang mga narating ng mga barya ninyo. Utang na loob ko yun sa inyo, sa mga
estudyanteng naglalakad din papasok ng FEU, UE, San Beda etc..) kaklase, kaibigan at mga propesor ko, tulad ni Ma'am Junie at Sir
tapos mula Mendiola ay ilang hakbang lang ay Legarda na, tapos Gepila at marami pang iba, at sa pamilya ko syempre. Hinding
Nagtahan na, tapos Pureza na at ayun Sta. Mesa na. Lagi kong hindi ako makakalimot, sa lahat-lahat.
iniisip na, malapit lang at kayang kaya ko yun. hindi ko
Sabi ko na nga ba eh, Success is the product of man's perseverance
namamalayan na nandun na pala ako sa may riles ng PNR, sa may
and will only be achieved if you will put hard work on your dreams.
malapit sa Puregold. Hindi po ako magpapakamatay, don't worry.
hehe. Ayun na nga, pawisan ako kaya naman basa na yung tatlong
Pag may tyaga, may itlog na nilaga.=)
bimpong dala ko. Ang ipinagtataka ko lang din nun, hindi ko pa din
Hanggang sa muli,
matapos yung kinakanta ko, sa dami ng iniisip ko. hehe
Finally, dumating ako ng PUP campus bandang 8:30am. Wala pa Ako po si Jeff Joseph M. Alicante, BSEd English Major, PUP College
kong pakialam kung paano ako makakauwi, ang iniisip ko lang ay of Education
ang makapasok at makapagtake ng exam, lalo pa't alanganin talaga
ako sa subject na yun. Pagdating ko ng N317 Room, nakaayos na And that was the walk, that I will always remember. A walk
yung mga upuan, yung mga kaklase ko ay nakapwesto na at naupo towards my dream, a walk to remember
ako sa labas. Pagkaupo ko, di ako nagsasalita, which was really
odd kasi maingay talaga ako. Nung lumapit yung classmates ko,
tinanong nila kung bakit ako tahimik, napaiyak na lang ako,
marahil ay sa sobrang pagod. Naiyak na ko ng tuluyan. Hindi ko
akalaing makakaya ko yun.
Bago dumating si Ma'am, nanghiram pa ko ng Statistics Book sa
ibang section, di kasi ako bumili ng book, ang mahal eh.
Pinagalitan pa ko ni Ma'am kasi di ako bumili nung book at
namimihasa daw ako sa kakahiram.
Matapos ang exam, nagulat ako nung nag-ambagan ang mga
kaklase ko ng pera para may pamasahe ako pauwi at nagulat talaga
ako, pamasahe ko ng tatlong araw ang naipon nila. Binigay nila
yun sa akin, tulong kumbaga. Nahihiya akong tanggapin pero
nilunok ko na ang pride ko, wala naman mawawala eh. Saka,
kailangan ko naman talaga ng pera nun. Maraming beses na yung
naulit, at binigyan din nila ako ng pandagdag sa tuition fee ko.
nakapasa ako ng 1st year, salamat sa Diyos.
Problemado na naman sa next school year dahil sa tuition fee, kaya
namasukan ako bilang kasambahay, ng tatlong buwan lang, kapalit
ng pang tuition ko. Ang pang araw-araw ko, nakakayanan na nila
mama at ate. 90php na ang baon ko, minsan wala, pero madalas
meron na. Pag wala akong pera, nakikikain na lang ako sa mga
kaibigan ko. Madalas libre nila.
Bago naman ako mag 3rd year, naging tindero naman ako sa
Tiangge Store ng tita ko, at nag-ipon din ng pang tuition.
Nung 4th year na ko ay kaklase at kaibigan ko pa din sila. Sa ngayon
okay na yung buhay namin, Public School teacher na yung
panganay kong Ate at sa isang kumpanya ng gamot naman
nagtatrabaho yung pangalawa kong Ate. Si mama naman, ayun
busy na sa candy crush sa tablet niya.
Nagsimula akong tumanaw ng utang na loob mula 3rd year kami.
it's payback time kumbaga. minsan nililibre ko na sila, kahit mga
tusuk-tusok lang, coke float, tortillos at kung anu-ano pa.
Makabawi man lang.
Salamat sa propesor ko sa Statistics, dahil nasubok ang kasipagan
ko nang dahil na din sa kanya. Naging instrumento sya para
makamit ko ito.
Sobrang saya ko lalo na’t hindi ako bumagsak sa Statistics, okay na
kahit TRES, at okay na kahit hindi ako Honor Student, dahil ang
mahalaga, isa na ko sa PUP Batch 2014 at ang mas mahalaga, high
school teacher na po ako ngayon, natupad na ang pangarap ko, ang
pangarap ko mula Grade 2 ako. Ang bait ni Lord sobraaaaa =)
I shared my experience kasi hindi ako nahihiya. Proud ako at
nakayanan ko ang mga pagsubok. Sapat na din na nakatanggap
ako ng una't huling medalya ko sa buong College life ko, bilang Best
Thesis Presenter ng CoEd noong 2013 para sa Undergraduare
Research namin ng mga kaibigan ko.
Alam ko na marami din sa mga kapwa ko ISKOLAR NG BAYAN ang
naghirap at naghihirap, mas naghirap pa nga upang makamit ang
mga pangarap nila, at isa na nga ako dun. Ang swerte ko pa din
pala dahil kinaya ko yun. Hindi man ako ang may pinakamahirap
na buhay sa buong mundo, masasabi kong pinagsumikapan ko din
naman ang lugar ko ngayon. Sana ay nakapagbigay ako ng
inspirasyon sa mga estudyanteng katulad ko.
Imagine how happy I was during our Graduation. Sabi nga nila,
kitang kita daw sa aking mga mata ang sayang nadarama ko.
Natural daw na nakangiti ang mga mata ko. Naiyak pa nga ako sa
bus pag-uwi kasi, may Mother's Day gift na ko kay Mama.
TOPNOTCH MEDICAL BOARD PREP MICRO PHASE 0 HANDOUT CLARIFICATIONS BY TOPNOTCH MICRO TEAM
This handout is only valid for September 2021 PLE batch. This will be rendered obsolete for the next batch since we update our handouts regularly.
INSTRUCTIONS
For those who have printed the initial handout:
Please use this handout as a guide to correct the initial handout.
Page guides are available to assist you in doing so.
MICRO CORRECTIONS
• Page 2, RLQ, Guide Question, Correct answer is D.
• Page 78, RLQ, HBc à HBx
END OF MICROBIOLOGY PHASE 0 CORRECTIONS
TOPNOTCH MEDICAL BOARD PREP MICRO PHASE 0 HANDOUT CLARIFICATIONS BY TOPNOTCH MICRO TEAM Page 1 of 1
TOPNOTCH MEDICAL BOARD PREP MICROBIOLOGY PHASE X DIGITAL HANDOUT BY DR. TIFFANY GRACE UY

Intellectual Property Code of the Philippines, and shall only be for the sole use of the person:
medium or machine-readable form, in whole or in part without the written consent of
extent guaranteed by law.
DISCLOSURE Capsule
The handouts/review materials must be treated with utmost confidentiality. It shall be the
materials are not photocopied or in any way reproduced, shared or lent to any person or
disposed in any manner. Any handout/review material found in the possession of another
person whose name does not appear therein shall be prima facie evidence of violation of RA
below.
REMINDERS
1. Phase X lectures are bonus lectures and may follow any format selected
by the lecturer. It is expected that you have finished Phase 0, 1, and 2
before watching the Phase X video.
IgA Protease
This handout is only valid for the September 2021 PLE batch.
This will be rendered obsolete for the next batch • N. gonorrhoeae—pili and outer membrane
since we update our handouts regularly. proteins
• Trypanosoma brucei rhodesiense and T. b.
ANTIGENIC
gambiense—phase variation
MICROBIOLOGY – PHASE X VARIATION
• Enterobacteriaceae: capsular and flagellar
By Tiffany Grace Uy, MD antigens may or may not be expressed
• HIV, influenza—antigenic drift
GENERAL MICROBIOLOGY
MAJOR MECHANISMS OF PATHOGENICITY
• Teichoic acids: primary mechanism of
gram-positive cells
• Pili/fimbriae: primary mechanism in
most gram-negative cells
• Adhesins: colonizing factor adhesins,
COLONIZATION/
pertussis toxin, and hemagglutinins
ADHERENCE
• IgA proteases: make it easier for
pathogens to colonize
• Biofilms: Staph. epidermidis,
Streptococcus mutans, Pseudomonas
aeruginosa
N. gonorrhoeae pili
Teichoic acid
Antigenic drift
MECHANISM DESCRIPTION
• M. tuberculosis survives by
inhibiting phagosome-lysosome
SURVIVING fusion.
INTRACELLULARLY • Listeria quickly escapes the
phagosome into the cytoplasm
Pili/fimbriae Biofilm
before phagosome-lysosome fusion.
GATHERING • Siderophores: chelate and import
• Capsules/slime layers:
NUTRIENTS iron
o Staphylococcus aureus A protein
o Streptococcus pyogenes M protein
ANTI-
o Neisseria gonorrhoeae pili
PHAGOCYTOSIS
• IgA proteases, destruction of mucosal
IgA: Neisseria, Haemophilus, S.
pneumoniae
TOPNOTCH MEDICAL BOARD PREP MICROBIOLOGY PHASE X DIGITAL HANDOUT BY DR. TIFFANY GRACE UY Page 1 of 39
ENDOTOXIN
(LPS = lipopolysaccharide)
Inhibiting phagosome-lysosome fusion
• LPS is part of the gram-negative outer membrane.
• Toxic portion is lipid A: generally not released (and toxic)
EXOTOXIN
until death of cell. Exception: N. meningitidis, which over-
• protein toxins, secreted by bacterial cells (some gram +,
produces outer membrane fragments.
some gram –)
• LPS is heat stable and not strongly immunogenic so it cannot
• Can be modified by chemicals or heat to produce a toxoid that
be converted to a toxoid.
still is immunogenic, but no longer toxic so can be used as a
• LPS activates macrophages, leading to release of TNF-alpha,
vaccine
IL-1, and IL-6 and tissue damage.
A-B (or “two”) component protein toxins
• Damage to the endothelium from bradykinin-induced
• B component binds to specific cell receptors to facilitate the
vasodilation leads to shock .
internalization of A.
• Coagulation (DIC) is mediated through the activation of
• A component is the active (toxic) component (often an
Hageman factor .
enzyme such as an ADP ribosyl transferase).
• Exotoxins may be subclassed as enterotoxins, neurotoxins, or
cytotoxins.
Cytolysins: lyse cells from outside by damaging membrane.

• C. perfringens alpha toxin is a lecithinase.
• Staphylococcus aureus alpha toxin inserts itself to form pores
in the membrane.
CULTURE OF MICROORGANISMS
Culture mediua
• Selective Medium (S)
o Medium that selects for certain bacteria by inclusion of special
nutrients and/or antibiotics
• Differential Medium (D)
o Medium on which different bacteria can be distinguished by
differences in colonial morphology or color.
REAGENT SAMPLE STAIN DESCRIPTION

1. Crystal violet
2. Grams Iodine
Gram Stain
3. Acetone/ Alcohol
4. Safranin (pink)
1. Carbol fuchsin with heat

2. Acid alcohol
Ziehl-Neelsen
3. Methylene blue
Acid fast
stain
Mycobacterium
(Kinyoun)
Nocardia
Some protozoa
1. Silver seeds
2. Reducing agent*
Silver
(methen-
Listeria monocytogenes
amine) stain
Pneumocystis jirovecii
Fungi (Pneumocystis, Cryptococcus, and Candida)
Wright/ Borrelia recurrentis

Giemsa Blood parasites (Plasmodium spp., Trypanosoma spp. and Babesia microti)
(PBS stain) Chlamydia and Rickettsia
KOH Fungi
Darkfield
Spirochetes
microscopy
Iron
hematoxylin
Protozoa
and
trichrome
Fecal wet
Protozoa, helminth eggs
mount
BACTERIA
GRAM-POSITIVE BACTERIA
STAPHYLOCOCCUS
STREPTOCOCCUS
GRAM-POSITIVE BACILLI
GRAM-POSITIVE WITH BRANCHING FILAMENTS
GRAM-NEGATIVE BACTERIA
Gram Negative (Pink)
Diplococci Coccobacilli Comma-shaped rods
Aerobic Haemophilus influenzae Oxidase +

(requires factors V and X)
Pasteurella
Maltose utilization Brucella
Bordetella pertussis Grows in 42oC Grows alkaline media Produces urease
Francisella tularensis
N. gonorrhoeae N. meningitidis Campylobacter jejuni Vibrio cholerae Helicobacter pylori
Moraxella
Bacilli
Lactose fermentation
- +
Fast Slow
Oxidase
Klebsiella Citrobacter
E. Coli
- +
Enterobacter
Serratia
H2S Production Pseudomonas

on TSI agar
- +
Shigella Salmonella
Yersinia Proteus
DIPLOCOCCI
NEISSERIA
GRAM NEGATIVE RODS
E. coli strains
• Klebsiella pneumoniae
• Shigella
• Salmonella
• Proteus • Pseudomonas
COCCOBACILLI Legionella pneumophila

ANIMAL ASSOCIATED COCCOBACILLI
Related
Organism Disease
Animal
Brucella
B. mellitensis Brucellosis/ Undulant
(goat), fever/ Malta fever
B. abortus (cattle)
Tularemia
(Ulceroglandular,
Francisella
Pneumonic,
F. tularensis
Oculoglandular,
Glandular, Typhoidal)
Yersinia
Y. pestis (plague), Pandemics of "black
Y. enterocolotica death”
(gastroenteritis)
Human wounds
Pasteurella
inflicted by cat/dog
P. multocida
bites
RESPIRATORY COCCOBACILLI
ORGANISM DESCRIPTION
Haemophilus
• Virulent factor: polyribose capsule type B
• H. influenzae type B: pneumonia,
meningitis, epiglottitis GRAM NEGATIVE COMMA-SHAPED
• Chocolate agar with NAD and Heme ORGANISM MORPHOLOGY DISEASE
Bordetella Cholera : rice

• Pertussis toxin Vibrio
water stools
• Whooping cough (coughing, marked
lymphocytosis)
Acute
• Bordet Gengou, Regan-Lowe medium
Gastroenteritis,
Campylobacter
Legionella Guillain Barre
• Mip protein (invade macrophages) syndrome
• Pontiac fever, Legionnaire’s disease Antral gastritis,
• Buffered charcoal yeast extract agar (w/ a- Duodenal/peptic
ketoglutarate, L-cysteine, iron) ulcer, Gastric
ulcer,
Helicobacter
Gastric
Haemophilus adenocarcinoma,
Gastric MALT
lymphomas
SPIROCHETES
ORGANISM MORPHOLOGY DISEASE
Primary,
Secondary,
Treponema
Tertiary,
pallidum
Congenital
Syphilis
Borrelia
Lyme disease
burgdorferi
Borrelia Louse-born
recurrentis relapsing fever
Leptospira
Leptospirosis
interrogans
MYCOBACTERIA
ORGANISM MORPHOLOGY DISEASE

Mycobacterium
tuberculosis
Mycobacterium
avium-
intercellulare
Mycobacterium
leprae
INTRACELLULAR BACTERIA
CHLAMYDIA
RICKETTSIA
VIRUSES
CLASSIFICATION OF VIRUSES
NAKED DNA VIRUSES

PARVOVIRUS B19
Erythema infectiosum Hydrops fetalis
ADENOVIRIDAE
Pharyngoconjunctival fever
PAPILLOMAVIRIDAE
Warts Condyloma acuminata Cervical cancer
POLYOMAVIRIDAE
JC virus BK virus
PML Hemorrhagic cystitis
DNA VIRUSES
HEPADNAVIRIDAE
HERPESVIRIDAE
POXVIRIDAE
Smallpox Cowpox Molluscum contagiosum
NAKED RNA VIRUSES

CALICIVIRIDAE
Norovirus outbreak
PICORNAVIRIDAE
RNA VIRUSES
CORONAVIRIDAE
COVID-19
• Mode of transmission: direct person-to-person
(via respiratory particles)
• Incubation period (from the time of exposure until
the onset of symptoms): 4-5 days on average but
may be as long as 14 days.
• Period of Infectiousness: starting a few days prior
to the development of symptoms; Transmission
after 7 to 10 days of illness is unlikely
• Quarantine: preferred period is 14 days
• Symptoms: anosmia/ageusia, fever/chills, nasal
congestion, cough, dyspnea, sore throat,
nausea/vomiting, headache, myalgia
• Diagnostics:
o RT-PCR is preferred
o Antigen testing (lower sensitivity)
o Antibody tests (detects past infection, low utility)
• Other lab features associated with severe
COVID-19: lymphopenia, elevated D-dimer, and
elevated inflammatory markers
COVID-19 DISEASE SEVERITY
DISEASE SEVERITY DESCRIPTION
Symptomatic patients meeting the case definition for COVID-19 without evidence of viral
Mild
pneumonia or hypoxia.
Adolescent or adult with clinical signs of pneumonia (fever, cough, dyspnea, fast
breathing) but no signs of severe pneumonia, including SpO2 ≥ 90% on room air.
Child with clinical signs of non-severe pneumonia (cough or difficulty breathing +
fast breathing and/or chest indrawing) and no signs of severe pneumonia. Fast
breathing (in breaths/min): < 2 months: ≥ 60; 2–11 months: ≥ 50; 1–5 years: ≥ 40.
While the diagnosis can be made on clinical grounds; chest imaging (radiograph, CT scan, ultrasound)
Moderate Pneumonia may assist in diagnosis and identify or exclude pulmonary complications. Caution: The oxygen saturation
threshold of 90% to define severe COVID-19 was arbitrary and should be interpreted cautiously. For
example, clinicians must use their judgment to determine whether a low oxygen saturation is a sign of
severity or is normal for a given patient with chronic lung disease. Similarly, a saturation >90–94% on
room air is abnormal (in patient with normal lungs) and can be an early sign of severe disease, if patient
is on a downward trend. Generally, if there is any doubt, the panel suggested erring on the side of
considering the illness as severe.
Adolescent or adult with clinical signs of pneumonia (fever, cough, dyspnoea, fast
breathing) plus one of the following: respiratory rate > 30 breaths/min; severe
respiratory distress; or SpO2 < 90% on room air.
Child with clinical signs of pneumonia (cough or difficulty in breathing) + at least one of
the following:
Severe Severe pneumonia • Central cyanosis or SpO2 < 90%; severe respiratory distress (e.g. fast breathing,
grunting, very severe chest indrawing); general danger sign: inability to breastfeed or
drink, lethargy or unconsciousness, or convulsions.
• Fast breathing (in breaths/min): < 2 months: ≥ 60; 2–11 months: ≥ 50; 1–5 years: ≥
40.
While the diagnosis can be made on clinical grounds; chest imaging (radiograph, CT scan, ultrasound)
may assist in diagnosis and identify or exclude pulmonary complications.
Onset: within 1 week of a known clinical insult (i.e. pneumonia) or new or worsening
respiratory symptoms. Chest imaging: (radiograph, CT scan, or lung ultrasound): bilateral
opacities, not fully explained by volume overload, lobar or lung collapse, or nodules.
Origin of pulmonary infiltrates: respiratory failure not fully explained by cardiac failure
or fluid overload. Need objective assessment (e.g. echocardiography) to exclude
hydrostatic cause of infiltrates/oedema if no risk factor present.
Oxygenation impairment in adults:
• Mild ARDS: 200 mmHg < PaO2/FiO2a ≤ 300 mmHg (with PEEP or CPAP ≥ 5 cmH2O).
Critical ARDS • Moderate ARDS: 100 mmHg < PaO2/FiO2 ≤ 200 mmHg (with PEEP ≥ 5 cmH2O).
• Severe ARDS: PaO2/FiO2 ≤ 100 mmHg (with PEEP ≥ 5 cmH2O).
Oxygenation impairment in children: note OI and OSI. Use OI when available. If PaO2
not available, wean FiO2 to maintain SpO2 ≤ 97% to calculate OSI or SpO2/FiO2 ratio:
• Bilevel (NIV or CPAP) ≥ 5 cmH2O via full face mask: PaO2/FiO2 ≤ 300 mmHg or
SpO2/FiO2 ≤ 264.
• Mild ARDS (invasively ventilated): 4 ≤ OI < 8 or 5 ≤ OSI < 7.5.
• Moderate ARDS (invasively ventilated): 8 ≤ OI < 16 or 7.5 ≤ OSI < 12.3.
• Severe ARDS (invasively ventilated): OI ≥ 16 or OSI ≥ 12.3.
DISEASE SEVERITY DESCRIPTION
Adults: acute life-threatening organ dysfunction caused by a dysregulated host
response to suspected or proven infection.
Signs of organ dysfunction include: altered mental status (delirium), difficult or fast
breathing, low oxygen saturation, reduced urine output, fast heart rate, weak pulse, cold
Sepsis extremities or low blood pressure, skin mottling, laboratory evidence of coagulopathy,
thrombocytopenia, acidosis, high lactate, or hyperbilirubinemia.
Children: suspected or proven infection and ≥ 2 age-based systemic inflammatory
response syndrome (SIRS) criteria, of which one must be abnormal temperature or white
blood cell count.
Adults: persistent hypotension despite volume resuscitation, requiring vasopressors to
maintain MAP ≥ 65 mmHg and serum lactate level > 2 mmol/L.
Children: any hypotension (SBP < 5th centile or > 2 SD below normal for age) or two or
Septic shock three of the following: altered mental status; bradycardia or tachycardia (HR < 90 bpm or
> 160 bpm in infants and heart rate < 70 bpm or > 150 bpm in children); prolonged
capillary refill (> 2 sec) or weak pulse; fast breathing; mottled or cool skin or petechial or
purpuric rash; high lactate; reduced urine output; hyperthermia or hypothermia
Acute venous thromboembolism (i.e. pulmonary embolism), acute coronary syndrome,
Acute thrombosis
acute stroke
Preliminary case definition: children and adolescents 0–19 years of age with fever > 3
days
AND two of the following: rash or bilateral non-purulent conjunctivitis or muco-
cutaneous inflammation signs (oral, hands or feet); hypotension or shock; features of
Multisystemic Inflammatory myocardial dysfunction, pericarditis, valvulitis, or coronary abnormalities (including
syndrome - in children and ECHO findings or elevated troponin/NT-proBNP); evidence of coagulopathy (by PT, PTT,
Critical adolescents, temporarily elevated D-dimers), acute gastrointestinal problems (diarrhoea, vomiting, or abdominal
related to COVID-19 pain);
(MIS-C) AND elevated markers of inflammation such as ESR, C-reactive protein, or procalcitonin.
AND no other obvious microbial cause of inflammation, including bacterial sepsis,
staphylococcal or streptococcal shock syndromes.
AND evidence of COVID-19 (RT-PCR, antigen test or serology positive), or likely contact
with patients with COVID-19.
WHO. COVID-19 Clinical management. Living guidance. Jan 25, 2021
Management: depends on severity of disease
• Work-up for features of severe illness, comorbid, organ Vaccination:
dysfunction • Primary antigenic target: surface spike protein, which binds to
• Antipyretics (Paracetamol preferred) the ACE-2 receptor on host cells and induces membrane fusion
• Oxygen support and/ ventilation • Platforms: inactivated, live attenuated, recombinant proteins,
• Glucocorticoids (Dexamethasone) mRNA, vector vaccines
• Antiviral (Remdesivir) • Contraindications: The only contraindications to COVID-19
• Monoclonal antibody (IL-6 inhibitor: Tocilizumab) vaccination are allergic reactions to the COVID-19 vaccines or
• VTE prophylaxis their components.
• Continue ACE/ARBs, statins, aspirin as needed
• Infection control, Contact tracing
TOGAVIRIDAE
German measles/rubella Congenital rubella syndrome
FLAVIVIRIDAE
RETROVIRIDAE
Adult T-cell leukemia

HIV-ASSOCIATED INFECTIONS
AIDS-DEFINING CONDITIONS
• Bacterial infections, multiple or recurrent • Lymphoid interstitial pneumonia or pulmonary lymphoid
• Candidiasis of bronchi, trachea, or lungs hyperplasia complex
• Candidiasis of esophagus • Lymphoma, Burkitt (or equivalent term)
• Cervical cancer, invasive • Lymphoma, immunoblastic (or equivalent term)
• Coccidioidomycosis, disseminated or extrapulmonary • Lymphoma, primary, of brain
• Cryptococcosis, extrapulmonary • Mycobacterium avium complex or Mycobacterium
• Cryptosporidiosis, chronic intestinal (>1 month's duration) kansasii, disseminated or extrapulmonary
• Cytomegalovirus disease (other than liver, spleen, or nodes), • Mycobacterium tuberculosis of any site, pulmonary,
onset at age >1 month disseminated, or extrapulmonary
• Cytomegalovirus retinitis (with loss of vision) • Mycobacterium, other species or unidentified species,
• Encephalopathy, HIV related disseminated† or extrapulmonary
• Herpes simplex: chronic ulcers (>1 month's duration) or • Pneumocystis jirovecii pneumonia
bronchitis, pneumonitis, or esophagitis (onset at age >1 month) • Pneumonia, recurrent
• Histoplasmosis, disseminated or extrapulmonary • Progressive multifocal leukoencephalopathy
• Isosporiasis, chronic intestinal (>1 month's duration) • Salmonella septicemia, recurrent
• Kaposi sarcoma • Toxoplasmosis of brain, onset at age >1 month
• Wasting syndrome attributed to HIV
CDC. Retrieved from http://www.cdc.gov/mmwr
PARAMYXOVIRIDAE
Measles SSPE
Mumps
ORTHOMYXOVIRIDAE
Influenza
RHABDOVIRIDAE
Rabies
RED RASHES OF CHILDHOOD
FUNGI
CUTANEOUS FUNGI
o Malassezia furfur
§ Pityriasis versicolor
• Dermatophyes
o Wood’s lamp test
o Trichophyton mentagrophytes
o Epidermophyton
• Blastomyces dermatitidis
• Coccidioides immitus
o Cladosporium werneckii
§ Tinea nigra
§ Treat with salicylic acid
o Trichosporon beigelii (white Piedra)
§ Mycosis of hair
§ Hyphae, arthroconidia, blastoconidia
• Paracoccidioides
SUBCUTANEOUS FUNGI
• Sporothrix schenckii
ENDEMIC FUNGI
• Histoplasma capsulatum
OPPORTUNISTIC FUNGI
Candida Cryptococcus P. jirovecii Aspergillus Mucor and Rhizopus
PARASITES
PROTOZOA
AMEBAE (SARCODINA)
ENTAMOEBA
FREE-LIVING AMOEBA
CILIATES (CILIOPHORA)
FLAGELLATES MASTIGOPHORA
GIARDIA
TRICHOMONAS
LEISHMANIA
TRYPANOSOMA
AMPICOMPLEXA (SPOROZOA)
PLASMODIUM
BABESIA
TOXOPLASMA
METAZOA
NEMATODES
NEMATODES: TRANSMITTED BY EGGS
NEMATODES: TRANSMITTED BY LARVAE
NEMATODES: FILARIAL
WUCHERERIA BANCROFTI BRUGIA MALAYI
• Transmitted by mosquito bite (third stage larvae) -> adult worms in the lymph nodes, inflammation, lymphatic obstruction and edema
o Acute disease: acute adenolymphangitis
o Chronic disease: hydrocele, elephantiasis
• Mazotti reaction: DEC treatment causes fever/rash/pruritus/edema
Loa loa Onchocerca volvulus

African eye worm River blindness
CESTODES (TAPEWORMS)
TREMATODES (FLUKES)
SEXUALLY TRANSMITTED DISEASES

• Syphilis SYPHILIS
• Gonorrhea
• Caused by Treponema pallidum
• Nongonococcal urethritis
• 3 stages:
• Lymphogranuloma venereum o Primary syphilis
• Chancroid (Soft Chancre) o Secondary syphilis
• Granuloma inguinale o Tertiary syphilis
• Trichomoniasis • Congenital syphilis
• Genital Herpes Simplex • Lesions: proliferative endarteritis and a plasma cell rich
• Human Papillomavirus Infection inflammatory infiltrate
• Dx: Serologic testing
o Nontreponemal antibody tests (VDRL, RPR):
o Treponeme specific antibody test
• Dx: identification of H. ducreyi on special culture media (not
widely available, low sensitivity)
o Usually diagnosed on clinical grounds alone
GONORRHEA
• Caused by Neisseria gonorrhoeae, Gram-negative
GRANULOMA INGUINALE
• Sx:
o High frequency of cases are asymptomatic • Caused by Calymmatobacterium granulomatis (Klebsiella
o Male: dysuria and purulent urethral discharge; prostatitis, granulomatis), an encapsuled coccobacillus
epididymitis, orchitis • Clinical features
o Female: urethral and endocervical exudates; salpingitis, o Initial papular lesion expands into a Painless, ulcerative lesions
tuboovarian abscess, PID on the genitals or perineum, without regional
• Usually also infected with Chlamydia trachomatis lymphadenopathy
• Dx: GS of purulent exudate (Gram negative diplococci), NAATs o The lesions are highly vascular (i.e., beefy red appearance) and
bleed.
o May cause formation of urethral, vulvar, or anal strictures in
some cases
• Lesions show granulation tissue and intense epithelial
hyperplasia (pseudoepitheliomatous hyperplasia), that can
mimic squamous cell carcinoma
• Dx: Giemsa smear of exudate (Donovan bodies, small
intracellular coccobacilli within vacuolated macrophages)
NONGONOCOCCAL URETHRITIS AND CERVICITIS

• Caused by Chlamydia trachomatis; also Mycoplasma
genitalium, Trichomonas vaginalis, Ureaplasma urealyticum
• Wide range of clinical features
o indistinguishable from gonorrhea
o may cause Reactive arthritis (Reiter syndrome TRICHOMONIASIS
• Dx: sensitive NAATs in urine sample or vaginal swabs • Caused by protozoan Trichomonas vaginalis
o Organisms not visible in Gram-stained sections • Clinical features
o May be asymptomatic
o Vaginal colonization: Pruritus and profuse, frothy, yellow
vaginal discharge, Strawberry cervix
o Urethral colonization: Urinary frequency and dysuria
• Dx: smears of vaginal scrapings
LYMPHOGRANULOMA VENEREUM
• Caused by Chlamydia trachomatis serovar L1, L2 and L3
• Stages
o 1st stage (small short-lived ulcer; UL tender enlarged matted
inguinal/femoral lymphadenopathy; proctocolitis)
o 2nd stage (fever, malaise; lymphatic dissemination, bubos;
painful anal cramps, constipation)
o 3rd stage (structures, fistulas, elephantiasis, anorectal GENITAL HERPES SIMPLEX
syndrome)
• Caused by HSV-2, less commonly HSV-1
• Lesions: mixed granulomatous and neutrophilic inflammatory
• Clinical manifestation: primary or recurrent mucocutaneous
response
lesions (genital or oral)
• Dx: NAATs and serology
o Painful, erythematous, intraepithelial vesicles on the mucosa
and skin of external genitalia
o Painful regional lymph node enlargement
• Neonatal herpes (generalized herpes, encephalitis)
• Histology: fused multinucleate giant cells with intranuclear
inclusions (Cowdry type A)
• Dx: Viral culture or NAAT testing of fluid after unroofing the
vesicular lesion
CHANCROID
• Caused by Haemophilus ducreyi (small gram-negative
coccobacillus)
• Clinical features:
o Acute painful ulcerative genital lesion (chancroid)
o Regional inguinal LN become enlarged and tender
HUMAN PAPILLOMAVIRUS INFECTION

• HPV 1,2,3,7,10: cutaneous warts (plantar, common, flat wart)
• HPV 6, 11: condyloma acuminata, respiratory papillomatosis
(transmitted from mother to baby)
o Do not confuse with condyloma lata of secondary syphilis!
• HPV 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68: high risk
for cervical cancer
ANTIMICROBIALS
CELL WALL SYNTHESIS INHIBITORS
PENICILLINS
CEPHALOSPORINS
CARBAPENEMS, MONOBACTAMS, BETA LACTAM INHIBITORS
GLYCOPEPTIDES, PEPTIDE ANTIBIOTICS, CYCLOSERINE, DAPTOMYCIN, FOSFOMYCIN
PROTEIN SYNTHESIS INHIBITORS
AMINOGLYCOSIDES AND TETRACYCLINE
OTHER PROTEIN SYNTHESIS INHIBITORS
NUCLEIC ACID SYNTHESIS INHIBITORS SULFONAMIDE AND TRIMETHOPRIM
FLUOROQUINOLONES
MISCELLANEOUS ANTIBIOTICS
ANTIVIRALS
ANTIFUNGALS
END OF MICROBIOLOGY PHASE X
TOPNOTCH MEDICAL BOARD PREP MICROBIOLOGY PHASE 2 HANDOUT BY DR. FRINZ MOEY C. RUBIO
A 24/M developed diplopia, difficulty in swallowing
The handouts, videos and other review materials, provided by Topnotch Medical Board and speech production, and dyspnea after ingestion
Preparation Incorporated are duly protected by RA 8293 otherwise known as the of bulged canned goods. What is the incubation
Intellectual Property Code of the Philippines, and shall only be for the sole use of the person: period of the condition of the patient?
a) whose name appear on the handout or review material, b) person subscribed to Topnotch 4.
Medical Board Preparation Incorporated Program or c) is the recipient of this electronic A. 18-24 hours
communication. No part of the handout, video or other review material may be reproduced, B. 15-18 hours
medium or machine-readable form, in whole or in part without the written consent of C. 24-36 hours
Topnotch Medical Board Preparation Incorporated. Any violation and or infringement, D. 6-10 hours
whether intended or otherwise shall be subject to legal action and prosecution to the full A 10/M presented with paroxysms of intense cough
followed by inspiratory “whoops.” What is the
DISCLOSURE culture medium recommended for the isolation of
The handouts/review materials must be treated with utmost confidentiality. It shall be the the etiologic agent of the condition of the patient?
5.
responsibility of the person, whose name appears therein, that the handouts/review A. Buffered charcoal yeast extract agar
disposed in any manner. Any handout/review material found in the possession of another B. Cystine-tellurite blood agar
person whose name does not appear therein shall be prima facie evidence of violation of RA C. Eaton agar
8293. Topnotch review materials are updated every six (6) months based on the current D. Regan-Lowe agar
below. A 24/M patient presented with tender, enlarged
THIS HANDOUT IS NOT FOR SALE! lymph nodes at the right axilla. Microbiological
examination of the infected nodes revealed Gram-
REMINDERS negative rods exhibiting bipolar staining. What is
1. Finish the Phase 0 handout and Phase 1 video before proceeding to the 6. the primary vector of the etiologic agent?
Phase 2 handout and video. A. Rats
2. Phase 2 handouts are based on commonly used review books and B. Cows
previous question feedback from students. C. Rabbits
3. Answer the Pre-Test (Guide Questions) first prior to watching the video D. Fleas
lectures.
What virulence factor of Neisseria gonorrhoeae is
4. The guided content of the video lectures are in the 2nd part of the Phase
2 handouts and are meant to complement the video lecture. NOT involved in the process of antigenic variation?
A. Pili or fimbriae
7.
B. Por protein
This handout is only valid for the September 2021 PLE batch. C. Opa Protein
This will be rendered obsolete for the next batch D. Lipooligosaccharide (LOS)
since we update our handouts regularly. What is the most sensitive and specific diagnostic
tool for identifying gonorrheal infections in women?
MICROBIOLOGY AND 8.
A. Nucleic acid amplification testing (NAAT)
B. Culture
PARASITOLOGY – PHASE 2 C. Gram stain
D. Enzyme-linked immunosorbent assay (ELISA)
By Frinz Moey C. Rubio, MD Cat-scratch disease is a non-caseating
granulomatous disease with neutrophilic
predominance in histopathology results. What is the
QUESTIONNAIRE etiologic agent of this condition?
9.
A 45/F woolsorter presented with flu-like A. Eikenella corrodens
symptoms that rapidly progressed to fever, and B. Pasteurella multocida
difficulty of breathing. Chest radiograph presented C. Streptobacillus moniliformis
with widening of the mediastinum. Culture of D. Bartonella henselae
sputum specimen revealed Gram-positive, aerobic, What staining technique is used to stain the
1. spore-forming bacteria. What is the most likely etiologic agent of Whipple disease?
etiologic agent causing the condition of the patient? A. Feulgen technique
10.
A. Bacillus anthracis B. Malachite green stain
B. Corynebacterium diphtheriae C. Tannic acid stain
C. Clostridium perfringens D. Periodic acid-Schiff stain
D. Mycobacterium tuberculosis What is the definition of multiple drug-resistant
A 22/F developed high fever, vomiting, diarrhea, (MDR) tuberculosis?
myalgias, and hypotension five days after using i. Resistance to both isoniazid and rifampicin
high-absorbency tampons during the onset of her ii. Resistance to both pyrazinamide and ethambutol
menses. What is the mechanism of the virulence iii. Resistance to any fluoroquinolone
factor associated with this condition? 11. iv. Resistance to at least one of the 3 injectable second-
2.
A. Stimulation of T cells to produce massive line drugs
quantities of cytokines A. i only
B. Degradation of hyaluronic acid B. i, ii
C. Destruction of white blood cells C. i, ii, iii, iv
D. Destruction of red blood cells D. i, iii, iv
A 34/M developed rapid rise of fever hours after What diagnostic test is the gold standard in
ingestion of water from an unreliable source. There establishing the diagnosis of tuberculous
were no gastrointestinal symptoms. Blood culture meningitis?
yielded positive for salmonellae when specimen A. Nucleic acid amplification test (Xpert
12.
was collected during high fever. What is the most MTB/RIF assay)
3. commonly associated etiologic agent to the B. CSF culture
condition of the patient? C. CSF analysis
A. Salmonella typhi D. Blood culture
B. Salmonella choleraesuis
C. Salmonella typhimurium
D. Salmonella enteritidis
TOPNOTCH MEDICAL BOARD PREP MICROBIOLOGY PHASE 2 HANDOUT BY DR. FRINZ MOEY C. RUBIO Page 1 of 19
Which of the following serologic tests for syphilis A 25-day-old neonate developed severe diarrhea
can be used to monitor response to antibiotic necessitating hospitalization. What is the property
treatment? of the most likely viral etiologic agent causing the
A. Venereal Disease Research Laboratory (VDRL) presentation of the patient?
test A. Naked, single-stranded, negative-sense RNA
13. 22.
B. Microhemagglutination T pallidum (MHA-TP) virus
test B. Enveloped, single-stranded, positive-sense
C. T pallidum hemagglutination (TPHA) test RNA virus
D. Fluorescent treponemal antibody absorbed C. Enveloped, double-stranded RNA virus
(FTA-ABS) test D. Naked, double-stranded RNA virus
What is the etiologic agent of Buruli ulcer, a A 27/M developed symptoms of orthopnea, severe
Neglected Tropical Disease (NTD) designated by the dyspnea and swelling of the legs for the past 2
World Health Organization (WHO)? weeks. Echocardiography of the heart showed right
14. A. Mycobacterium ulcerans and left ventricular dilation, but no valvular
B. Chlamydia trachomatis deformities. An endomyocardial biopsy was done
C. Dracunculus medinensis and yielded focal myocyte necrosis and lymphocytic
23.
D. Treponema pallidum pertenue infiltrate. Which of the following etiologic agents
A 11/M developed sepsis, thrombophlebitis of the most likely caused the condition of the patient?
internal jugular vein, and pulmonary abscesses A. Trypanosoma cruzi
after two weeks of having untreated sore throat B. Coxsackievirus A
infection. What is the etiologic agent of the C. Coxsackievirus B
15. condition? D. Toxoplasma gondii
A. Corynebacterium diphtheriae A 25/M noted a 1 x 1 cm flesh-colored nodule on the
B. Fusobacterium necrophorum lower trunk. The dome-shaped lesion is umbilicated
C. Streptococcus pyogenes and a curd-like material can be expressed from the
D. Francisella tularensis center. Smear of the material revealed cytoplasmic
A 6/F was brought to the emergency room due to Henderson-Patterson inclusions under the
difficulty of breathing. She was seen drooling, with 24. microscope. What is the etiologic agent of this
hyperextended neck, and at tripod position. condition?
Laryngoscopy was performed wherein a large A. Molluscum contagiosum virus
cherry red, swollen epiglottis was observed. What B. Varicella-zoster virus
16.
are the growth requirements of the etiologic agent? C. Human papillomavirus
A. Factor X, Factor V D. Measles virus
B. Factor V only What is the virus used in the worldwide vaccination
C. Factor X only of the first and only human disease to be eradicated
D. No specific growth requirements globally?
A 3-week-old, male patient developed a striking 25. A. Cowpox virus
tachypnea, paroxysmal staccato cough, and B. Variola virus
eosinophilia. Chest radiograph was performed and C. Pseudocowpox virus
it revealed interstitial infiltrates and hyperinflation. D. Vaccinia virus
17. What is the etiologic agent of the condition? What etiologic agent is mostly associated with head
A. Chlamydia trachomatis types A, B, C and neck cancers?
B. Chlamydia trachomatis types D-K A. Epstein-Barr virus
26.
C. Chlamydophila pneumoniae B. Herpes simplex virus 1
D. Chlamydophila psittaci C. Human papillomavirus
A 34/M went to the clinic with the chief complaint of D. Cytomegalovirus
gross hematuria. Imaging revealed staghorn calculi Which of the following viral family - viral disease
occupying the renal calyces. What etiologic agent is pairings is CORRECTLY matched?
mostly associated with this condition? A. Influenza virus – Paramyxovirus family
18. 27.
A. Escherichia coli B. Hepatitis E virus – Calicivirus family
B. Proteus mirabilis C. Chikungunya virus – Flavivirus family
C. Staphylococcus epidermidis D. Marburg virus – Filovirus family
D. Klebsiella pneumoniae Which of the following statements about Parvovirus
What is the most common cause of community- B19 is FALSE?
acquired pneumonia among patients more than 5 A. It can cause arthralgia-arthritis syndrome
years of age? among affected adults
19. A. Group B Streptococcus B. It is the smallest DNA animal virus
28.
B. Respiratory syncytial virus C. The site of viral shedding of Parvovirus B19 is
C. Mycoplasma pneumoniae the salivary glands
D. Streptococcus pneumoniae D. The most likely route of transmission of
A 33/M presented with headache, fever, and rashes. Parvovirus B19 is via contact with respiratory
Rashes started on the wrists and ankles, and secretions or droplets
progressed to the trunk, palms and soles. What is Which of the following diseases is least likely to be
the vector of the etiologic agent causing the clinical caused by adenoviruses?
20. presentation? A. Keratoconjunctivitis
29.
A. Tick B. Acute respiratory diseases
B. Flea C. Hemorrhagic cystitis
C. Human body louse D. Glomerulonephritis
D. Mites What is the complication of measles infection that
A neonate born at 35 weeks AOG manifested with may appear 1-10 months after the appearance of
blueberry muffin rash, chorioretinitis, viral exanthem?
hydrocephalus, and periventricular calcifications. 30. A. Otitis media
What is the etiologic agent of the abovementioned B. Postinfectious encephalomyelitis
21. condition? C. Measles inclusion body encephalitis
A. Cytomegalovirus D. Subacute sclerosing panencephalitis
B. Toxoplasma gondii
C. Rubella virus
D. Herpes simplex virus 2
A 9/M developed fever, hepatosplenomegaly, A 33/M Filipino residing in California developed
pharyngitis and posterior cervical erythema nodosum, and arthralgia. What is the
lymphadenopathy. Histopathology revealed expected finding in the tissue biopsy of the skin
infected cells with nuclear and cytoplasmic lesion of the patient?
inclusions. Which of the following is TRUE about the 40. A. “captain's wheel"-formation of budding yeast
etiologic agent of the condition? cells
31.
A. The etiologic agent is positive for heterophile B. Broad-based budding of yeast cells
antibodies (Monospot test) C. Ovoid yeast cells within macrophages
B. It is also known as human herpesvirus 4 D. Spherules
C. Has resistance against acyclovir, famciclovir Which of the following soil-transmitted helminths
and valacyclovir does NOT cause Loeffler pneumonitis?
D. It is associated with Burkitt lymphoma A. Ascaris lumbricoides
41.
Histopathologic analysis of lung tissue done in a few B. Trichuris trichiura
COVID-19 patients revealed _____. C. Necator americanus
A. Diffuse alveolar damage only D. Strongyloides stercoralis
B. Diffuse alveolar damage and inflammation A 44/M farmer presented with elephantiasis and
32. with mainly mononuclear cells scrotal enlargement. Peripheral blood examination
C. Diffuse alveolar damage and inflammation taken at 1AM revealed microfilariae with kinky
with mainly polymorphonuclear cells appearance, distinct terminal nuclei. What is the
D. Diffuse alveolar damage with inflammation primary vector of the etiologic agent of the
42.
with mainly eosinophils condition?
A 9/M presented with low-grade fever, and A. Culex
morbilliform rash appearing on the same day. The B. Aedes
rash started on the face and extended to the trunk C. Anopheles
and extremities. Postauricular lymphadenopathy D. Mansonia
and Forchheimer spots on the soft palate were also A 10/M presents with serpiginous rash located on
33. present. The clinical presentation of the patient is the dorsal aspect of his right foot. According to
expected to last not more than ____. medical history, he is fond of playing on sandy soil
A. 3 days barefooted. What is the most likely etiologic agent of
B. 5 days 43. the condition of the patient?
C. 7 days A. Necator americanus
D. 10 days B. Ancylostoma duodenale
Which of the following HIV structural protein – C. Ancylostoma braziliense
corresponding function pairings is CORRECTLY D. Strongyloides stercoralis
matched? A 36/M developed cough of more than 8 weeks with
34. A. p17 : capsid protein blood-tinged sputum. Sputum and stool examination
B. p24 : allows fusion and entry revealed an egg with thickened abopercular portion.
C. gp120 : attachment to host CD4+ T cell What is the 2nd intermediate host of the etiologic
D. gp41 : matrix protein 44. agent in the Philippines?
Which viral agent can present as hemorrhagic A. Snail
necrotizing temporal lobe encephalitis? B. Freshwater crab
A. Human simplex virus C. Freshwater fish
35.
B. Cytomegalovirus D. Pigs
C. Rabies virus What is the infective stage of dwarf tapeworm?
D. Poliovirus A. Cysticercus cellulosae
Pathogenic fungi are generally not contagious hence 45. B. Cysticercus bovis
transmission among humans is extremely rare C. Sparganum
EXCEPT for cases of ____. D. Cysticercoid
36. A. Superficial mycoses A 33/M presented with dysentery for the past 7
B. Cutaneous mycoses weeks. Colonoscopy and eventual biopsy of the
C. Subcutaneous mycoses colonic epithelium was performed, which revealed
D. Systemic mycoses flask-shaped ulcer with a narrow neck and broad
A 32/M farmer developed a 5 x 3 x 4 cm verrucous base. What part of the GI tract is mostly affected by
46.
mass on his right foot. Upon biopsy of this lesion, this etiologic agent?
draining sinuses containing sulfur granules were A. Cecum
identified. What is the diagnosis? B. Sigmoid colon
37.
A. Sporotrichosis C. Rectum
B. Mycetoma D. Duodenum
C. Chromoblastomycosis A 19/F went to Palawan during her summer break.
D. Phaeohyphomycosis When she went back to Manila, she developed
A 44/F presented with soft, yellowish nodules on the paroxysms of fever every 48 hours, which is
hair shafts of her scalp. What is the etiologic agent of accompanied by body aches. A few days later, she
this condition? went into delirium, coma, and eventually death.
38. A. Malassezia furfur Biopsy revealed Dürck granulomata and ring
47.
B. Hortaea (Exophiala) werneckii hemorrhages surrounding her cerebral vessels.
C. Trichosporon sp. What is the etiologic agent?
D. Piedraia hortae A. Plasmodium vivax
A 54/M with a history of cavitary form of pulmonary B. Plasmodium ovale
tuberculosis, developed cough and hemoptysis. C. Plasmodium malariae
Chest imaging revealed Monod sign. What is the D. Plasmodium falciparum
expected finding in the sputum examination of the
patient?
39.
A. Heavily encapsulated yeast
B. Broad, nonseptate hyphae, branching at wide
angles
C. Septate hyphae, branching at acute angles
D. Pseudohyphae at 25°C
A 34/M hiker presented at the clinic with history of Bacillus anthracis PEARLS
excessive flatus, and chronic diarrhea of rotten-egg Parameter Diagnostic Features
smelling, fatty stools. Fecalysis revealed organisms Most common • Cutaneous anthrax
exhibiting falling leaf motility. What is/are the form of anthrax • (+) black necrotic eschar
diagnostic stage(s) of the etiologic agent causing the Most life- • Pulmonary anthrax
48.
condition? threatening • (+) mediastinitis
A. Cyst form of anthrax • (+) can be up to 6 weeks
B. Trophozoite Rarest form of
C. Both A and B • Gastrointestinal anthrax
anthrax
D. Clinical diagnosis is sufficient
• (+) Medusa head pattern
A 46/F presented with severe but intermittent Culture
• Comma-shaped out-growths from colony
itching of her wrists, breasts, and buttocks. Upon
• PA (protective antigen)
physical examination, burrows were identified at Mechanism of
the interdigitations. What is the drug of choice • EF (edema factor) – adenylate cyclase
anthrax toxins
recommended by CDC for treating the condition of • LF (lethal factor)
49.
the patient?
A. Lindane 1% A 22/F developed high fever, vomiting, diarrhea,
B. Permethrin cream myalgias, and hypotension five days after using high-
C. Malathion 0.5% absorbency tampons during the onset of her menses.
D. Pyrethrins with piperonyl butoxide What is the mechanism of the virulence factor
What is the etiologic agent of granulomatous amebic associated with this condition?
2.
encephalitis? A. Stimulation of T cells to produce massive
A. Acanthamoeba sp. quantities of cytokines
50. B. Degradation of hyaluronic acid
B. Naegleria fowleri
C. Entamoeba histolytica C. Destruction of white blood cells
D. Toxoplasma gondii D. Destruction of red blood cells
(+) young female, tampon user

DISCUSSION (+) fever, hypotension
Toxic shock syndrome (TSS)
MEDICAL BACTERIOLOGY Staphylococcus aureus
TIPS FOR MEDICAL BACTERIOLOGY
• Expect a lot of questions on bacteriology (more than 50%) VIRULENCE FACTORS OF STAPHYLOCOCCUS AUREUS
• Recognize the distinguishing laboratory parameters Virulence Factor Remarks
• Determine the salient features of the distinct diseases Converts H2O2 → H2O
• Know the epidemiology of the bacterial diseases Catalase
(+) Staphylococcus - positive
Allows adherence of agent to fibrinogen
A 45/F woolsorter presented with flu-like symptoms and fibrin
that rapidly progressed to fever, and difficulty of Clumping factor
Clumping factor – target for
breathing. Chest radiograph presented with widening vaccination
of the mediastinum. Culture of sputum specimen Hyaluronidase Spreading factor
revealed Gram-positive, aerobic, spore-forming Responsible for necrosis and severe
1. bacteria. What is the most likely etiologic agent causing Hemolysins
inflammation
the condition of the patient? Panton-Valentine Important virulence factor in CA-MRSA
A. Bacillus anthracis Leukocidin infections
B. Corynebacterium diphtheriae
C. Clostridium perfringens Exfoliative toxins Superantigens
D. Mycobacterium tuberculosis A and B Responsible for Ritter disease
TSST toxin Superantigen
HOW TO ATTACK QUESTION #1 (Exotoxin F) Associated with tampon use
Prioritization of Data for Diagnosis of Infectious Diseases Enterotoxins A-E, Superantigen (heat-stable)
G-P Staphylococcal food poisoning
Culture / Biopsy / Direct Observation of
HIGHEST
the Organism
A 34/M developed rapid rise of fever hours after
INTERMEDIATE Clinical Presentation ingestion of water from an unreliable source. There
LOWEST Risk Factors / Epidemiologic Data were no gastrointestinal symptoms. Blood culture
yielded positive for salmonellae when specimen was
collected during high fever. What is the most commonly
3. associated etiologic agent to the condition of the
patient?
A. Salmonella typhi
B. Salmonella choleraesuis
C. Salmonella typhimurium
(+) woolsorter D. Salmonella enteritidis
(+) widened mediastinum
(+) Gram-positive, aerobic, spore-forming (+) rapid rise of fever
(-) GI symptoms
CLOSTRIDIUM VS. BACILLUS (+) blood culture-positive
Clostridium Bacillus Septicemia form of salmonellosis
Gram-positive
Spore-forming
Anaerobe Aerobe
Gram-negative bacteria exhibiting “spore-like” formation?

• Coxiella burnetii
CLINICAL SYNDROMES OF SALMONELLOSIS (JAWETZ)
Parameter Enteric fever (typhoid fever) Septicemia Enterocolitis
Incubation period 7-20 days (insidious) Variable (abrupt) 8-48 hours (abrupt)
Fever Gradual increase Rapid rise Low
Disease duration Weeks Variable 2-5 days
GI symptoms Constipation → bloody diarrhea -- Nausea/vomiting, diarrhea
Blood culture (+) 1st – 2nd weeks of disease (+) in high fever --
Stool culture (+) 2nd week onwards -- (+) after onset
S typhimurium
Associated pathogens S typhi S choleraesuis
S enteritidis
A 24/M developed diplopia, difficulty in swallowing A 24/M patient presented with tender, enlarged lymph
and speech production, and dyspnea after ingestion of nodes at the right axilla. Microbiological examination
bulged canned goods. What is the incubation period of of the infected nodes revealed Gram-negative rods
the condition of the patient? exhibiting bipolar staining. What is the primary vector
4.
A. 18-24 hours 6. of the etiologic agent?
B. 15-18 hours A. Rats
C. 24-36 hours B. Cows
D. 6-10 hours C. Rabbits
D. Fleas
(+) ingestion of bulged canned goods
(+) 4 Ds (+) bubo formation
Botulism (+) bipolar staining
Yersinia pestis
INCUBATION PERIODS OF SELECTED BACTERIAL DISEASES
(JAWETZ)
Disease Incubation Period
Botulism 18-24 hours
Tetanus 4 to 5 days (up to 3 weeks)
Emetic form: 1-5 hours
B cereus food poisoning
Diarrheal form: 1-24 hours
S aureus food poisoning 1-8 hours
V cholerae 12 hours – 3 days YERSINIA PESTIS PEARLS
S aureus TSS 5 days Parameter Remarks
Primary syphilis 2-10 weeks Oriental rat flea
Primary vector
Xenopsylla cheopis
A 10/M presented with paroxysms of intense cough Bubonic plague (+) bubo formation
followed by inspiratory “whoops.” What is the culture Buboes → septicemia
medium recommended for the isolation of the etiologic (+) septic shock
Septicemic plague
agent of the condition of the patient? (+) disseminated intravascular
5. coagulation
A. Buffered charcoal yeast extract agar
B. Cystine-tellurite blood agar Primary
(+) chest pain, cough, hemoptysis
C. Eaton agar pneumonic plague
D. Regan-Lowe agar
What virulence factor of Neisseria gonorrhoeae is NOT
(+) whooping cough involved in the process of antigenic variation?
Bordetella pertussis A. Pili or fimbriae
7.
B. Por protein
CULTURE MEDIA USED FOR INFECTIOUS DISEASES (JAWETZ) C. Opa Protein
Culture Medium Etiologic Agent D. Lipooligosaccharide (LOS)
Barbour-Stoenner-Kelly
Borrelia burgdorferi
(BSK) agar
Bordet-Gengou agar
Regan-Lowe agar
Buffered Charcoal Yeast
Legionella spp.
Extract (BCYE)
Campy-Blood agar Campylobacter spp.
Chocolate agar Haemophilus spp.
CHROMagar Candida sp.
Cystine-Tellurite Blood agar
C diphtheriae
Loeffler’s agar
Eaton agar M pneumoniae
Lowenstein-Jensen agar
M tuberculosis
Middlebrook media
MacConkey agar Enterobacteriaceae family
MacConkey agar with sorbitol E coli O157:H7
Mannitol salt agar S aureus From Jawetz, Melnick, Adelbergs Medical Microbiology, 27th Edition
Martin-Lewis agar Antigenic variation:

Modified Thayer-Martin agar Neisseriae • Mechanism by which an infectious agent alters its surface
New York City agar molecules to avoid host immune response
Skirrow agar C jejuni
Stuart agar H pylori
NEISSERIA MENINGITIDIS VS. NEISSERIA GONORRHOEAE What staining technique is used to stain the etiologic
Meningococci GoNOcocci agent of Whipple disease?
Gram-negative diplococci A. Feulgen technique
10.
Oxidizes glucose B. Malachite green stain
(+) lipooligosaccharides (LOS) C. Tannic acid stain
(+) polysaccharide capsule NO polysaccharide capsule D. Periodic acid-Schiff stain
(+) maltose oxidation NO maltose oxidation
NO vaccine due to antigenic (+) malabsorption syndrome
(+) vaccine is available (+) Gram-positive actinomycete
variation of pilus proteins
Tropheryma whipplei
VIRULENCE FACTORS OF NEISSERIA GONORRHOEAE
(JAWETZ) COMMONLY USED STAINS IN MICROBIOLOGY
Virulence Factor Remarks Stain Significance
Mediates attachment to host cells Gram stain General distinction of bacteria
Pili Resists phagocytosis Ziehl-Neelsen stain Acid-fast organisms:
(+) antigenic variation (MAIN) (hot method) Mycobacteria, Nocardia
Functions in adhesion of gonococci Acid-fast organisms (coccidian
within colonies (makes colonies K(C)inyoun stain parasites)
Opa proteins
opaque) (Cold method) Cryptosporidium, Cyclospora,
(+) antigenic variation Cytoisospora
Mimics human cell membrane Periodic acid-Schiff Tropheryma whipplei
Ligooligosaccharide glycosphingolipids → immune stain PASS the sugar!
(LOS) response evasion
(+) antigenic variation
Por protein Forms pores in the surface of host
Rmp (Protein III) cells
Inactivates IgA1
IgA1 protease
Present in SHiN organisms
What is the most sensitive and specific diagnostic tool
for identifying gonorrheal infections in women?
A. Nucleic acid amplification testing (NAAT)
8.
B. Culture
C. Gram stain
D. Enzyme-linked immunosorbent assay (ELISA)
LABORATORY DIAGNOSIS OF NEISSERIA GONORRHOEAE https://www.researchgate.net/figure/Histologic-examination-using-PAS-staining-revealed-massive-infiltration-by-
Tropheryma_fig3_23301122
(JAWETZ, HARRISON’S, LENTZ)
COMMONLY USED STAINS IN MICROBIOLOGY
Parameter Test
Stain Significance
Establishment of presumptive Gram stain of urethral or
For negative staining
diagnosis in WOMEN endocervical exudates India Ink stain
Cryptococcus neoformans
Establishment of definitive Nucleic acid amplification
Stains red for
diagnosis in WOMEN tests (NAAT) Mucicarmine stain
Cryptococcus neoformans
Establishment of definitive Gram stain of urethral
diagnosis in MEN exudates
Establishment of gonococcal Gram stain of conjunctival
conjunctivitis exudates
Standardized culture of
Preferred method for urethral or endocervical
establishing definitive exudates
diagnosis in children (because of legal
implications)
Specimens that are generally https://microbewiki.kenyon.edu/index.php/ https://commons.wikimedia.org/wiki/File:Cryptococcosis_
Throat or rectum Cryptococcus_neoformans of_lung_in_patient_with_AIDS._Mucicarmine_stain_962_lores.jpg
NOT HELPFUL in establishing
specimens
diagnosis
COMMONLY USED STAINS IN MICROBIOLOGY
Cat-scratch disease is a non-caseating granulomatous Stain Significance
disease with neutrophilic predominance in Feulgen method For nucleoid
histopathology results. What is the etiologic agent of Malachite green stain For bacterial endospore
this condition?
9.
A. Eikenella corrodens
B. Pasteurella multocida
C. Streptobacillus moniliformis
D. Bartonella henselae
(+) human bites
(+) animal bites
(+) rat bites
DISEASES WITH NON-CASEATING GRANULOMAS (ROBBINS) https://www.sciencedirect.com https://chromoscience.com/2020/03/14/the-endospore-staining/
Disease Feature /science/article/abs/pii/
S0065128117301617
Leprosy Acid-fast bacilli macrophages
Tertiary syphilis Gumma - “rubbery-like” gross lesion Stain Significance
Cat-scratch Caused by Bartonella henselae Welch method For negative stain of bacterial capsule
disease Neutrophilic predominance Tannic acid stain For flagella
Unknown cause
Sarcoidosis “well-formed non-necrotizing
granulomas”
Transmural granulomatous lesion of
Crohn disease
the GI tract
SEROLOGIC TESTS FOR SYPHILIS
Non-treponemal Tests
Antigen – cardiolipin Treponemal Tests
Antibody – reagin
VDRL TP-PA
USR TPHA
RPR MHA-TP
TRUST FTA-ABS
https://www.slideserve.com/daktari https://chromoscience.com/2020/03/14/the-flagella-staining/ For screening testing For confirmatory testing
/clinical-microbiology
(universal) (universal)
What is the definition of multiple drug-resistant For monitoring antibiotic
(MDR) tuberculosis? response
i. Resistance to both isoniazid and rifampicin
ii. Resistance to both pyrazinamide and ethambutol Significance
iii. Resistance to any fluoroquinolone VDRL Standardized serologic diagnosis of neurosyphilis
11. iv. Resistance to at least one of the 3 injectable second-
line drugs
A. i only What is the etiologic agent of Buruli ulcer, a Neglected
B. i, ii Tropical Disease (NTD) designated by the World Health
C. i, ii, iii, iv Organization (WHO)?
D. i, iii, iv 14. A. Mycobacterium ulcerans
B. Chlamydia trachomatis
DRUG RESISTANCE TO MYCOBACTERIUM TUBERCULOSIS C. Dracunculus medinensis
Terminology Definition D. Treponema pallidum pertenue
Drug-resistant • Chlamydia trachomatis – Trachoma
Resistance to a single anti-TB drug • Dracunculus medinensis – Guinea worm disease
TB
Multiple drug- • Treponema pallidum pertenue – Yaws
Resistance to BOTH ISONIAZID (H) AND
resistant TB
RIFAMPICIN (R) NEGLECTED TROPICAL DISEASES (WHO) – 20 DISEASE
(MDR-TB)
(1) Resistance to BOTH H AND R CATEGORIES
From https://www.who.int/teams/control-of-neglected-tropical-diseases
(2) Resistance to any • Buruli ulcer
Extensively
fluoroquinolone
drug-resistant • Chagas disease (American trypanosomiasis)
AND
TB • Dengue and Chikungunya
(3) Resistance to at least 1 of the 3
(XDR-TB) • Dracunculiasis (Guinea-worm disease)
injectable 2nd-line drugs – amikacin,
capreomycin, kanamycin • Echinococcosis
• Food-borne trematode infection
Significance • Human African trypanosomiasis (sleeping sickness)
Isoniazid Most common drug resistance to M tuberculosis • Leishmaniasis
Drug resistance that can be detected by Xpert • Leprosy (Hansen’s disease)
Rifampicin • Lymphatic filariasis (Elephantiasis)
MTB/RIF assay
• Mycetoma, chromoblastomycosis and other deep mycoses
What diagnostic test is the gold standard in • Onchocerciasis (river blindness)
establishing the diagnosis of tuberculous meningitis? • Rabies
A. Nucleic acid amplification test (Xpert • Scabies and other ectoparasites
12. MTB/RIF assay) • Schistosomiasis (Bilharzia)
B. CSF culture
C. CSF analysis TREPONEMA PALLIDUM SUBSPECIES
D. Blood culture Subspecies Associated condition
Epidemic syphilis /
T pallidum pallidum
DIAGNOSIS OF EXTRAPULMONARY TUBERCULOSIS Venereal syphilis
(HARRISON’S) Bejel
Disease Diagnosis T pallidum endemicum Endemic syphilis
TB Fine-needle biopsy or Nonvenereal syphilis
lymphadenitis Surgical excision biopsy T pallidum pertenue Yaws
Screening test: Adenosine deaminase T pallidum carateum Pinta
Pleural TB Definitive diagnosis: Needle biopsy of the
pleura
Genitourinary Biopsy or culture of specimens obtained by A 11/M developed sepsis, thrombophlebitis of the
TB D&C internal jugular vein, and pulmonary abscesses after
Presumptive diagnosis: CT or MRI two weeks of having untreated sore throat infection.
Skeletal TB What is the etiologic agent of the condition?
Definitive diagnosis: Skeletal biopsy 15.
Initial diagnosis: Xpert MTB/RIF assay A. Corynebacterium diphtheriae
TB meningitis B. Fusobacterium necrophorum
Definitive diagnosis: CSF culture
GI TB Peritoneal biopsy C. Streptococcus pyogenes
Pericardial Pericardial biopsy via pericardiocentesis D. Francisella tularensis
TB (under echocardiographic guidance)
(+) sepsis
Which of the following serologic tests for syphilis can be (+) thrombophlebitis of IJV
used to monitor response to antibiotic treatment? (+) pulmonary abscesses
A. Venereal Disease Research Laboratory Lemierre syndrome
(VDRL) test
13. B. Microhemagglutination T pallidum (MHA-TP)
test
C. T pallidum hemagglutination (TPHA) test
D. Fluorescent treponemal antibody absorbed
(FTA-ABS) test
A 6/F was brought to the emergency room due to (+) new-onset tachypnea in neonate
difficulty of breathing. She was seen drooling, with (+) staccato cough
hyperextended neck, and at tripod position. (+) eosinophilia
Laryngoscopy was performed wherein a large cherry Neonatal pneumonia
red, swollen epiglottis was observed. What are the CHLAMYDIA TRACHOMATIS SEROTYPES
16.
growth requirements of the etiologic agent?
Agent Associated Conditions
A. Factor X, Factor V
Types A, B, C Trachoma → blindness
B. Factor V only
Urethritis/PID
C. Factor X only
Ectopic pregnancy
D. No specific growth requirements Types D-K
Neonatal cough
Neonatal pneumonia (staccato cough)
(+) drooling, hyperextended neck
Types L1, L2, L3 LGV (lymphogranuloma venereum)
(+) large cherry red, swollen epiglottis
Epiglottitis (Haemophilus influenzae) CHLAMYDOPHILA SP INFECTIONS
Agent Associated Conditions
HAEMOPHILUS GROWTH REQUIREMENTS C pneumoniae Atypical pneumonia in adults
Psittacosis – form of pneumonia associated
C psittaci
with handling of birds (parrots)
A 34/M went to the clinic with the chief complaint of

gross hematuria. Imaging revealed staghorn calculi
occupying the renal calyces. What etiologic agent is
mostly associated with this condition?
18.
A. Escherichia coli
B. Proteus mirabilis
C. Staphylococcus epidermidis
D. Klebsiella pneumoniae
(+) staghorn calculi
Magnesium AMMONIUM phosphate (struvite stones)
URINARY TRACT INFECTION PEARLS
Agent Features
Escherichia coli Leading cause of UTI
Staphylococcus 2nd leading cause of UTI
saprophyticus Common in young women
3rd leading cause of UTI
Klebsiella pneumoniae
From Jawetz Melnick & Adelbergs Medical Microbiology, 27th edition
(+) mucoid encapsulation
Associated with struvite stones
Factor V Factor X Proteus mirabilis
(+) swarming motility
NAD Heme
Produces red pigmentation
REMEMBER: H. ducreyi (an STD) needs the XXX factor! Serratia marcescens
Nosocomial, drug resistant
Produces blue-green
A 3-week-old, male patient developed a striking Pseudomonas
pigmentation and fruity odor
tachypnea, paroxysmal staccato cough, and aeruginosa
Nosocomial, drug resistant
eosinophilia. Chest radiograph was performed and it
revealed interstitial infiltrates and hyperinflation.
What is the most common cause of community-acquired
17. What is the etiologic agent of the condition?
pneumonia among patients more than 5 years of age?
A. Chlamydia trachomatis types A, B, C
A. Group B Streptococcus
B. Chlamydia trachomatis types D-K 19.
B. Respiratory syncytial virus
C. Chlamydophila pneumoniae
C. Mycoplasma pneumoniae
D. Chlamydophila psittaci
D. Streptococcus pneumoniae
From Nelsons Textbook of Pediatrics, 21st edition
A 33/M presented with headache, fever, and rashes. (+) headache, fever, rashes
Rashes started on the wrists and ankles, and (+) started on the wrists and ankles → trunks, palms, soles
progressed to the trunk, palms and soles. What is the Rocky Mountain spotted fever
vector of the etiologic agent causing the clinical Rickettsia rickettsii
20. presentation?
A. Tick
B. Flea
C. Human body louse
D. Mites
Common Rickettsial Diseases Congenital Infections
Diseases Agent Clinical Presentation
Features Vector
(Agent) Chorioretinitis
Rocky Mountain Blueberry muffin rash
Wrists, ankles → trunk,
spotted fever Ticks Toxoplasma gondii Hydrocephalus
palms, soles
R rickettsii Intracranial (cerebral)
Endemic typhus calcifications
Trunks → spreads to Fleas Chorioretinitis
R typhi
other parts (spares palms Cytomegalovirus Blueberry muffin rash
Epidemic typhus and soles) Human Periventricular calcifications
R prowazekii body louse Rubella virus Cataracts (eye)
Eye Love (heart) ruby Congenital heart disease (PDA)
Rickettsii on the wRists (rubella) earrings Sensorineural deafness (ear)
Typhus on the Trunks Herpes simplex virus- Meningoencephalitis
2 Herpetic (vesicular) lesions
Saddle nose, saber shins
MEDICAL VIROLOGY Syphilis
Eight nerve deafness
Tips for Medical Virology
• Know the general classification of the different viruses A 25-day-old neonate developed severe diarrhea
• Determine the salient features of the distinct diseases necessitating hospitalization. What is the property of
• Know the epidemiology of the viral diseases the most likely viral etiologic agent causing the
• Have a good background on the properties of the different presentation of the patient?
viruses A. Naked, single-stranded, negative-sense RNA
22.
virus
A neonate born at 35 weeks AOG manifested with B. Enveloped, single-stranded, positive-sense
blueberry muffin rash, chorioretinitis, RNA virus
hydrocephalus, and periventricular calcifications. C. Enveloped, double-stranded RNA virus
What is the etiologic agent of the abovementioned D. Naked, double-stranded RNA virus
21. condition?
A. Cytomegalovirus (+) diarrhea in infant
B. Toxoplasma gondii Rotavirus (Reovirus)
C. Rubella virus
D. Herpes simplex virus 2
Most common cause of congenital infection which can lead to

severe abnormalities
From Jawetz, Melnick, Adelbergs Medical Microbiology, 27th Edition
Classification Scheme for RNA Viruses
From Review of Medical Microbiology and Immunology, 15th edition

Always Bring Polymerase Or Fail Replication:
Replication in Except Retroviruses, influenza
cytoplasm viruses (Orthomyxovirus) Arenavirus, Bunyavirus, Paramyxovirus, Orthomyxovirus, Filovirus,
Rhabdovirus
Health Care Providers are Raw

and NAKED:
Hepevirus, Calicivirus, Picornavirus, Reovirus
(+) sense (-) sense

Readily Needs RNA-dependent RNA polymerase
infectious to be infectious
Viruses Associated with Acute Gastroenteritis in Humans
From Jawetz, Melnick & Adelbergs Medical Microbiology, 27th edition
A 27/M developed symptoms of orthopnea, severe

dyspnea and swelling of the legs for the past 2 weeks. A 25/M noted a 1 x 1 cm flesh-colored nodule on the
Echocardiography of the heart showed right and left lower trunk. The dome-shaped lesion is umbilicated
ventricular dilation, but no valvular deformities. An and a curd-like material can be expressed from the
endomyocardial biopsy was done and yielded focal center. Smear of the material revealed cytoplasmic
myocyte necrosis and lymphocytic infiltrate. Which of Henderson-Patterson inclusions under the
23.
the following etiologic agents most likely caused the 24. microscope. What is the etiologic agent of this
condition of the patient? condition?
A. Trypanosoma cruzi A. Molluscum contagiosum virus
B. Coxsackievirus A B. Varicella-zoster virus
C. Coxsackievirus B C. Human papillomavirus
D. Toxoplasma gondii D. Measles virus
(+) congestive heart failure (+) umbilicated nodule

(+) secondary to viral myocarditis (+) cytoplasmic inclusions
Molluscum contagiosum
Clinical Presentation of Coxsackieviruses (Jawetz)
Coxsackie A Coxsackie B
Herpangina
Pleurodynia
(+) vesicles on posterior
(+) stabbing chest pain
pharynx
Aseptic meningitis (B > A)
Myocarditis (B > A)
Hand-foot-and-mouth disease (A > B)
Classification Scheme of DNA Viruses
DNA viruses HHAPPPPy viruses

Replication
Except Poxviruses
in nucleus
Icosahedral Except Poxviruses
dsDNA Except Parvoviruses
Except Papilloma,
Linear
Polyoma, Hepadna
genomes
(circular)
Source: Review of Medical Microbiology and Immunology, 15th edition
Some Viruses and their Associated Inclusion Bodies Infections and Carcinogenesis
Viral infection Inclusion bodies Location Etiologic Agent Associated Cancer
Rabies virus Negri bodies Cytoplasm Gastric adenocarcinoma
H pylori
Guarnieri bodies, Gastric MALT lymphoma
Smallpox Cytoplasm
Paschen bodies C jejuni Small intestinal MALT lymphoma
Molluscum Henderson- Borrelia sp. Skin MALT lymphoma
Cytoplasm
contagiosum Paterson bodies Chlamydophila
Ocular MALT lymphoma
HSV, VZV Cowdry type A Nucleus psittaci
Poliovirus Schistosoma
Cowdry type B Nucleus Squamous cell carcinoma
Adenovirus haematobium
Yellow fever Torres bodies Nucleus Clonorchis,
Cholangiocarcinoma
Owl’s eye Both nucleus and Opistorchis
CMV
appearance cytoplasm Hepatitis C virus >
Hepatocellular carcinoma (HCC)
Warthin-Finkeldey Both nucleus and Hepatitis B virus
Measles
bodies cytoplasm HTLV-1 (not HTLV-2) Adult T-cell leukemia/lymphoma
Burkitt lymphoma
What is the virus used in the worldwide vaccination of Epstein-Barr virus
Hodgkin/Non-Hodgkin lymphomas
the first and only human disease to be eradicated (EBV)
Nasopharyngeal carcinoma (NPCA)
globally? Head and neck cancers
25. A. Cowpox virus HPV
Anogenital warts and cancers
B. Variola virus
C. Pseudocowpox virus
Which of the following viral family - viral disease
D. Vaccinia virus
pairings is CORRECTLY matched?
A. Influenza virus – Paramyxovirus family
27.
B. Hepatitis E virus – Calicivirus family
C. Chikungunya virus – Flavivirus family
D. Marburg virus – Filovirus family
Selected RNA Viral Families

Viral Family Viruses
Polioviruses
Echoviruses
Picornavirus
Rhinoviruses
(PERCH)
Coxsackieviruses
Hepatitis A virus
Hepevirus Hepatitis E
Calicivirus Norovirus
Hepatitis C virus
SMALLPOX
From Jawetz, Melnick & Adelbergs Medical Microbiology, 27th edition Yellow fever
Dengue fever
Flavivirus
Eradication VS. Elimination St. Louis Encephalitis
Term Definition West Nile Virus
Refers to the reduction to zero (or a very low Zika Virus
Elimination defined target rate) of new cases of a disease Chikungunya virus
in a defined geographical area Togavirus CREW Rubella
Refers to the permanent reduction to zero of Eastern and Western equine
Eradication the worldwide incidence of an infectious Orthomyxovirus Influenza viruses
disease as a result of deliberate efforts Parainfluenza
PaRaMxyovirus RSV
Eradication of Smallpox PEARLS (Jawetz) Measles, Mumps
Parameter Information Filoviruses Ebola, Marburg viruses
Etiologic agent of Delta virus Hepatitis D virus
Variola virus
smallpox
Original agent Which of the following statements about Parvovirus B19
Cowpox virus
Edward Jenner used is FALSE?
Agent used in the A. It can cause arthralgia-arthritis syndrome
WHO campaign to Vaccinia virus among affected adults
eradicate smallpox B. It is the smallest DNA animal virus
28.
Year of eradication 1980 C. The site of viral shedding of Parvovirus B19
1. Single serotype of the virus is the salivary glands
2. Most infections are clinically D. The most likely route of transmission of
apparent Parvovirus B19 is via contact with respiratory
Several reasons for 3. Vaccine was easily prepared, secretions or droplets
the successful stable and safe
eradication 4. Vaccine can be easily given by a Parvovirus B19 PEARLS
field personnel
5. Mass vaccination was not
necessary
What etiologic agent is mostly associated with head

and neck cancers?
A. Epstein-Barr virus
26.
B. Herpes simplex virus 1
C. Human papillomavirus
D. Cytomegalovirus
Parameter Viruses (+) pharyngitis
Site of viral shedding Pharynx (+) hepatosplenomegaly
Viral tropism Erythroid progenitor cells (+) lymphadenopathy
Receptor for viral tropism P antigen (+) nuclear & cytoplasmic inclusions
Cytomegalovirus
Which of the following diseases is least likely to be
caused by adenoviruses? EBV VS. CMV
A. Keratoconjunctivitis EBV CMV
29. (Human herpesvirus 4) (Human herpesvirus 5)
B. Acute respiratory diseases
C. Hemorrhagic cystitis (+) hepatosplenomegaly
D. Glomerulonephritis (+) lymphadenopathy
(+) pharyngitis
Diseases Associated with Adenoviruses (Jawetz) (+) heterophile antibodies (-) heterophile antibodies
(+) atypical lymphocytosis (-) atypical lymphocytosis
Disease Associated Adenoviruses
Nuclear AND cytoplasmic
Gastroenteritis Type 40, 41 Nuclear inclusions ONLY
inclusions
Epidemic
Types 8, 19, 37 Resistant to acyclovir,
keratoconjunctivitis Sensitive to acyclovir,
famciclovir, valacyclovir
Swimming pool famciclovir, valacyclovir
Types 3, 7 (sensitive to ganciclovir)
conjunctivitis
Respiratory diseases
Types 1-7
(pharyngitis, pneumonia)
Hemorrhagic cystitis Types 11, 21
What is the complication of measles infection that may

appear 1-10 months after the appearance of viral
exanthem?
30. A. Otitis media
B. Postinfectious encephalomyelitis
C. Measles inclusion body encephalitis
D. Subacute sclerosing panencephalitis
From https://ppdictionary.com/viruses/cytomegalovirus.htm
Histopathologic analysis of lung tissue done in a few

COVID-19 patients revealed _____.
A. Diffuse alveolar damage only
B. Diffuse alveolar damage and inflammation
32. with mainly mononuclear cells
C. Diffuse alveolar damage and inflammation
with mainly polymorphonuclear cells
D. Diffuse alveolar damage with inflammation
Measles Virus Infection PEARLS with mainly eosinophils
Parameter Remarks
Most common COVID-19 PEARLS
Otitis media Parameter Remarks
complication
Most common life- Secondary bacterial Diffuse alveolar damage and
Histopathology
threatening complication pneumonia mononuclear inflammation
Warthin-Finkeldey cells First detected in Wuhan, China
Pathognomonic cells found First reported to
(nuclear and cytoplasmic December 2019
in lungs, lymphoid organs WHO in
inclusions)
Koplik spots Declared as a global
March 11, 2020
(near the opening of the pandemic
Pathognomonic enanthem Seafood and animal market in
Stensen duct – opposite the Origin
1st/2nd molars Wuhan
Chest imaging Bilateral ground-glass opacities
Coronaviruses and Receptors for Viral Tropism (Jawetz)

Virus Receptor for Viral Tropism
SARS-CoV-1 and Angiotensin converting
SARS-CoV-2 enzyme 2
MERS-CoV CD26 (dipeptyl peptidase 4)
CEA antigen-related
Mouse coronavirus
glycoprotein
Human coronavirus
Aminopeptidase N
From Robbins and Cotran Pathologic Basis of Disease, 10th edition 229E
A 9/M developed fever, hepatosplenomegaly, A 9/M presented with low-grade fever, and
pharyngitis and posterior cervical lymphadenopathy. morbilliform rash appearing on the same day. The
Histopathology revealed infected cells with nuclear and rash started on the face and extended to the trunk and
cytoplasmic inclusions. Which of the following is TRUE extremities. Postauricular lymphadenopathy and
about the etiologic agent of the condition? Forchheimer spots on the soft palate were also
31. A. The etiologic agent is positive for heterophile 33. present. The clinical presentation of the patient is
antibodies (Monospot test) expected to last not more than ____.
B. It is also known as human herpesvirus 4 A. 3 days
C. Has resistance against acyclovir, B. 5 days
famciclovir and valacyclovir C. 7 days
D. It is associated with Burkitt lymphoma D. 10 days
(+) morbilliform rash and fever on same day Structural gene Product(s)
(+) cephalocaudad migration env gp120, gp41(from gp160)
(+) postauricular lymphadenopathy gag p24, p17
(+) Forchheimer spots Reverse transcriptase, integrase,
Rubella (German measles) or 3-day measles pol
protease
Salient Features of Childhood Rashes Which viral agent can present as hemorrhagic
Disease Pattern of Rash Other Features necrotizing temporal lobe encephalitis?
(+) Forchheimer spots A. Human simplex virus
Rubella 35.
(soft palate) – B. Cytomegalovirus
German
Morbilliform rash accompanies rash C. Rabies virus
measles
(cephalocaudad) (+) postauricular D. Poliovirus
3-day
lymphadenopathy –
measles • Cytomegalovirus – Paraventricular subependymal region
occurs 1 day before rash
Maculopapular • Rabies virus – Brainstem
(+) Koplik spots – • Poliovirus – anterior horn cells of the spinal cord
Measles rash → brawny
occurs before rash
Rubeola desquamation Herpes Simplex Virus PEARLS
(+) photophobia
(cephalocaudad) Virus Receptor for Viral Tropism
Roseola Classically associated with oropharyngeal lesions
High fever → rash (+) Nagayama spots
infantum Leading viral cause of sporadic encephalitis
appearance (after (uvulopalatoglossal HSV-1
(HHV-6, Most common cause of sporadic, fatal
fever resolution) junction)
HHV-7) encephalitis in the US
Dew on rose petal HSV-2 Classically associated with genital herpes
Can cause Reye
→ lesions in
syndrome (also in flu)
Varicella different stages
(centrifugal from the
Associated with aspirin MEDICAL MYCOLOGY
intake Tips for Medical Mycology
trunk)
• Know the major classifications of fungal diseases
Which of the following HIV structural protein - • Master the distinguishing clinical and diagnostic features of
corresponding function pairings is CORRECTLY fungal diseases
matched?
34. A. p17 : capsid protein Pathogenic fungi are generally not contagious hence
B. p24 : allows fusion and entry transmission among humans is extremely rare EXCEPT
C. gp120 : attachment to host CD4+ T cell for cases of ____.
D. gp41 : matrix protein 36. A. Superficial mycoses
B. Cutaneous mycoses
HIV Virion Structure C. Subcutaneous mycoses
D. Systemic mycoses
• Cutaneous mycoses – Microsporum, Trichophyton,

Epidermophyton
Anthropophilic species
• Residence in humans
• Causes the greatest number of human infections
• Hardest group of dermatophytes to treat
Geophilic species
• Residence in soil
Zoophilic species
• Residence in animals
From First Aid for the USMLE STEP 1 (2020), 30th edition
Medically Important Fungi
From Jawetz, Melnick, Adelbergs Medical Microbiology, 27th Edition
A 32/M farmer developed a 5 x 3 x 4 cm verrucous mass Superficial Mycoses
on his right foot. Upon biopsy of this lesion, draining Mycosis Diagnostic Features
sinuses containing sulfur granules were identified. Pityriasis (+) hypo/hyperpigmented macule
What is the diagnosis? versicolor (+) “spaghetti and meatballs”
37.
A. Sporotrichosis Malassezia furfur morphology
B. Mycetoma Tinea nigra (+) dark discoloration of palms
C. Chromoblastomycosis Hortaea werneckii (+) dematiaceous fungi
D. Phaeohyphomycosis White Piedra
Trichosporon (+) soft, white nodules on hair shaft
(+) farmer species
(+) verrucous lesion on lower extremity Black Piedra
(+) draining sinuses with sulfur granules (+) hard, dark nodules on hair shaft
Piedraia hortae
From https://upload.wikimedia.org/wikipedia/commons/thumb/5/59/Madura_foot..JPG/1200px-Madura_foot..JPG
https://i0.wp.com/cdn-prod.medicalnewstoday.com/content/images/articles/282/282844/cauliflower-is-rich-in-
nutrients-and-fiber.jpg?w=1155&h=1541
Subcutaneous Mycoses
A 54/M with a history of cavitary form of pulmonary
Diagnostic
Mycosis Etiologic Agent tuberculosis, developed cough and hemoptysis. Chest
Features
imaging revealed Monod sign. What is the expected
(+) cigar-
finding in the sputum examination of the patient?
shaped
39. A. Heavily encapsulated yeast
Sporotrichosis yeasts Sporothrix schenckii
B. Broad, nonseptate hyphae, branching at wide
(+) asteroid
angles
bodies C. Septate hyphae, branching at acute angles
Phialophora verrucosa D. Pseudohyphae at 25°C
(+) sclerotic Fonsecaea pedrosoi
bodies / Fonsecaea compacta
Chromoblasto- (+) history of lung cavitation
copper Rhinocladiella
mycosis (CMB) (+) Monod sign
penny aquaspersa
bodies Cladophialophora
carrionii
Pseudallescheria boydii
Madurella mycetomatis
Mycetoma (+) sulfur
Madurella grisea
(Madura foot) granules
Exophiala jeanselmei
Acremonium falciforme
Phialophora richardsiae
(+) darkly Exophiala jeanselmei
Opportunistic Mycoses
pigmented Bipolaris spicifera
Phaeohypho- Mycosis Diagnostic Features
septate Wangiella dermatitidis
mycosis (+) germ tubes at 37°C
hyphae in Exserohilum rostratum Candidiasis
(+) pseudohyphae, blastoconidia
tissue Alternaria Candida sp.
(budding yeast cells) at 25°C
Curvularia
(+) septate hyphae branching at
Key Fungal Structures Observed in Clinical Specimens acute angles
Etiologic Agent Diagnostic Features Aspergillosis
(+) Monod sign – aspergilloma
Cryptococcus Aspergillus sp.
(+) encapsulated yeasts (+) air crescent sign – invasive
neoformans aspergilloma
Coccidioides sp. (+) spherules Mucormycosis
(+) cysts (or asci) (+) nonseptate hyphae branching at
Pneumocystis sp. Rhizopus sp.
(+) immunocompromised state wide angles (obtuse)
Mucor sp.
A 44/F presented with soft, yellowish nodules on the Cryptococcosis
hair shafts of her scalp. What is the etiologic agent of Cryptococcus (+) heavily encapsulated yeast
this condition? neoformans
38. A. Malassezia furfur
B. Hortaea (Exophiala) werneckii
C. Trichosporon sp.
D. Piedraia hortae
Monod sign VS. Air crescent sign (+) residence in California
(+) erythema nodosum
(+) arthralgias
Desert rheumatism
Coccidioides immitis
Systemic Mycoses
A 33/M Filipino residing in California developed

erythema nodosum, and arthralgia. What is the
expected finding in the tissue biopsy of the skin lesion of
the patient?
40. A. “captain's wheel"-formation of budding yeast
cells
B. Broad-based budding of yeast cells
C. Ovoid yeast cells within macrophages From First Aid for the USMLE STEP 1 (2020), 30th edition
D. Spherules • Where is paracoccidioidomycosis prevalent? Latin America

• What ethnicity has the highest risk for acquiring
coccidioidomycosis? Filipino
Histoplasmosis Blastomycosis Coccidioidomycosis Paracoccidioidomycosis
Mississippi and Ohio River Eastern and Central US, Great
Southwestern US, California Latin America
Valleys Lakes
Pancytopenia Squamous cell carcinoma
Desert rheumatism
→ oral ulcers, splenomegaly mimicker
(+) Macrophage filled with (+) Broad-based budding of (+) Spherule (filled with
(+) Captain’s wheel formation
Histoplasma yeasts endospores)
From First Aid for the USMLE STEP 1 (2020), 30th edition
MEDICAL PARASITOLOGY AND ENTOMOLOGY Life Cycle of Trichuris trichiura

Tips for Medical Parasitology and Entomology
• Recognize the generalities and exemptions to the rule (e.g. all
trematodes are hermaphroditic except for Schistosoma)
• Determine the salient features of the distinct diseases
• Review the life cycles every now and then (they can ask
questions on infective stages and diagnostic stages of the
different parasites)
• Master the vectors of diseases
Which of the following soil-transmitted helminths does
NOT cause Loeffler pneumonitis?
A. Ascaris lumbricoides
41.
B. Trichuris trichiura
C. Necator americanus
D. Strongyloides stercoralis
Loeffler pnuemonitis
(+) respiratory symptoms
(+) peripheral eosinophilia
Secondary to larval migration to the lungs
Nematode PEARLS
Parameter Remarks
Ascaris lumbricoides
Necator americanus
Soil-transmitted
Ancylostoma duodenale From https://www.cdc.gov/parasites/whipworm/biology.html
helminth (STH)
Trichuris trichiura
Strongyloides stercoralis A 44/M farmer presented with elephantiasis and
STH with NO LUNG scrotal enlargement. Peripheral blood examination
Trichuris trichiura taken at 1AM revealed microfilariae with kinky
MIGRATION
Hookworm infection appearance, distinct terminal nuclei. What is the
Unholy trinity Ascaris lumbricoides 42. primary vector of the etiologic agent of the condition?
Trichuris trichiura A. Culex
Etiologic agent of B. Aedes
tropical pulmonary Filarial worms C. Anopheles
eosinophilia D. Mansonia
(+) kinky appearance
(+) distinct terminal nuclei
Brugia malayi
Lymphatic Filariasis
Wuchereria bancrofti Brugia malayi
Smoothly curved (graceful)
Kinky microfilariae
microfilariae
(+) confluent nuclei
(+) distinct nuclei
(+) terminal nuclei
(-) terminal nuclei
Best time for collection of microfilariae:
Between 8 PM and 4 AM
Aedes
Anopheles Mansonia Hookworm PEARLS
Culex Parameter Remarks
Widespread prevalence Limited in Southeast Asia Most common human hookworm
Necator americanus
infection in the Philippines
Human hookworm causing more
Ancylostoma duodenale
blood loss
Animal hookworms causing
Ancylostoma braziliense,
cutaneous larva migrans
Ancylostoma caninum
(creeping eruptions)
A 36/M developed cough of more than 8 weeks with

blood-tinged sputum. Sputum and stool examination
revealed an egg with thickened abopercular portion.
What is the 2nd intermediate host of the etiologic agent
44. in the Philippines?
Vectors of Medically Important Parasites A. Snail
Disease Vector B. Freshwater crab
Wuchereria bancrofti Aedes, Anopheles, Culex C. Freshwater fish
Brugia malayi Mansonia D. Pigs
Onchocerciasis
River blindness Simulium (blackfly) (+) hemoptysis
Onchocerca volvulus (+) chronic cough
Pulmonary tuberculosis?
Loiasis Chrysops (deer fly, horse fly, mango
Loa loa fly)
Malaria Anopheles minimus flavirostris
Plasmodium sp. (primary vector)
Babesiosis
Ixodes tick
Babesia microti
African
trypanosomiasis Glossina (tsetse fly)
Trypanosoma brucei
Leishmaniasis Phlebotomus, Lutzomyia (sand
Leishmania sp. flies)
American
Reduviid bugs (assassin
trypanosomiasis
bugs/kissing bugs/triatomine bugs)
Trypanosoma cruzi
A 10/M presents with serpiginous rash located on the

dorsal aspect of his right foot. According to medical Life Cycle of Paragonimus westermani
history, he is fond of playing on sandy soil barefooted.
What is the most likely etiologic agent of the condition
43. of the patient?
A. Necator americanus
B. Ancylostoma duodenale
C. Ancylostoma braziliense
D. Strongyloides stercoralis
(+) serpiginous rash

(+) barefooted
Cutaneous larva migrans
Miracidium is released from the egg Entamoeba histolytica PEARLS (Belizario, Robbins, Schwartz)
1st intermediate host Antemalania snails Parameter Information
Releases cercaria into the water Most common affected site Cecum and Ascending colon
2nd intermediate Crayfish and Freshwater crabs Invasion of the mucosa →
host (Sundathelphusa philippina) Pathogenesis burrows laterally into the
2nd intermediate host harbors lamina propria
metacercaria (infective stage) Flask-shaped ulcer
Definitive host Pathology (vs wide-necked ulcers of B.
Mammals coli)
(adult form)
Paratenic host Wild pigs/boar Presentation Dysentery
Amebic liver abscess
What is the infective stage of dwarf tapeworm? Most common (anchovy-like aspirate)
A. Cysticercus cellulosae extraintestinal form Anterosuperior aspect of liver
45. B. Cysticercus bovis (Schwartz)
C. Sparganum Gold standard for
Direct microscopy
D. Cysticercoid diagnosing amebic colitis
Serologic test
Gold standard for
Pork tapeworm Taenia solium (indirect fluorescent
diagnosing ALA
Beef tapeworm Taenia saginata antibody test)
Rat tapeworm Hymenolepis diminuta Gold standard in
Dwarf tapeworm Hymenolepis nana differentiating E
PCR
Broad tapeworm/ histolytica from
Diphyllobothrium latum commensal Entamoeba
Fish tapeworm
Dog tapeworm/ Warrants treatment in the Hemophagocytosis
Dipylidium caninum absence of PCR (under direct microscopy)
Double-pored tapeworm
Infective Stages of Cestodes
Disease Infective Stage
Cysticercus cellulosae (pork
Taeniasis tapeworm)
Cysticercus bovis (beef tapeworm)
Cysticercosis Cestode egg of pork tapeworm
Hymenolepiasis
Cysticercoid
(H diminuta)
Cysticercoid (indirect cycle) OR
Cestode egg of dwarf tapeworm
Hymenolepiasis (direct cycle) A 19/F went to Palawan during her summer break.
(H nana) The only human cestode capable of When she went back to Manila, she developed
completing its entire life cycle in a paroxysms of fever every 48 hours, which is
single host accompanied by body aches. A few days later, she went
Plerocercoid larva into delirium, coma, and eventually death. Biopsy
Diphyllobothriasis
(aka sparganum) revealed Dürck granulomata and ring hemorrhages
47.
surrounding her cerebral vessels. What is the etiologic
agent?
A. Plasmodium vivax
B. Plasmodium ovale
C. Plasmodium malariae
D. Plasmodium falciparum
(+) Palawan
(+) tertian fever pattern (every 48 hours)
(+) Dürck granulomata
Cerebral malaria
Types of Intermittent Fever (Plasmodium spp.)

Type of
Interval Between Associated
Intermittent
Febrile Episodes Malarial Parasite
Fever
Quotidian fever 24 hours (1 day) P. knowlesi
P. vivax
P. ovale
Tertian fever 48 hours (2 days)
P. falciparum –
Life cycle of Hymenolepis nana malignant
From https://www.cdc.gov/dpdx/hymenolepiasis/index.html
Quartan fever 72 hours (3 days) P. malariae
A 33/M presented with dysentery for the past 7 weeks.
Colonoscopy and eventual biopsy of the colonic
epithelium was performed, which revealed flask-
shaped ulcer with a narrow neck and broad base.
What part of the GI tract is mostly affected by this
46.
etiologic agent?
A. Cecum
B. Sigmoid colon
C. Rectum
D. Duodenum
(+) dysentery https://twitter.com/nursingahead/status/1005029543164473345
(+) flask-shaped ulcer • What is the etiologic agent of undulant fever? Brucellosis
(vs wide-necked ulcers of Balantidium coli)
Entamoeba histolytica
Species differentiation of Plasmodium
P. falciparum P. vivax P. ovale P. malariae P. knowlesi
Malignant tertian Benign tertian Benign tertian Benign quartan Quotidian
(+) large round
(+) banana-shaped gametocytes (+) small round
gametocyte (+) rosette formation of schizont
(+) multiple trophozoites in a red cell gametocyte
“Vi-gatin”
Maurer dots Schuffner dots SOVrang daming dots! Ziemann dots
--
Ferdinand Marcos *James dots (P. ovale) Orange Juice Manila Zoo
All RBCs
All RBCs regardless of age Infects young RBCs Infects old RBCs
regardless of age
-- (+) relapse due to hypnozoites in liver --
A 34/M hiker presented at the clinic with history of A 46/F presented with severe but intermittent itching
excessive flatus, and chronic diarrhea of rotten-egg of her wrists, breasts, and buttocks. Upon physical
smelling, fatty stools. Fecalysis revealed organisms examination, burrows were identified at the
exhibiting falling leaf motility. What is/are the interdigitations. What is the drug of choice
diagnostic stage(s) of the etiologic agent causing the recommended by CDC for treating the condition of the
48. 49.
condition? patient?
A. Cyst A. Lindane 1%
B. Trophozoite B. Permethrin cream
C. Both A and B C. Malathion 0.5%
D. Clinical diagnosis is sufficient D. Pyrethrins with piperonyl butoxide
(+) hiker (+) severe, but intermittent itching of non-hairy parts

(+) rotten-egg odor stools (+) burrows
(+) steatorrhea Scabies
(+) falling leaf motility (Sarcoptes scabiei var. hominis)
Giardiasis
Giardia duodenalis PEARLS (Belizario)

Parameter Information
Infective stage Cyst only
Trophozoite
Diagnostic stages From https://www.cdc.gov/parasites/scabies/index.html
Cyst
Trophozoite 2 nuclei
Pediculosis pubis VS. Scabies
4 nuclei
Cysts Scabies
Dormant stage
Pediculosis pubis “great dermatologic
Rotten-egg odor imitator”
Presentation
Steatorrhea Phthirus pubis Sarcoptes scabiei var.
Direct microscopy “crab louse” hominis
(+) falling leaf motility
Diagnostic tests With predilection to pubic Widespread
Duodenal string test
hair (-) hair predilection
Also used for S stercoralis
Presence of nits Burrows
Drug of choice: permethrin cream
Applied to all areas of the
Applied to affected areas → body (from neck down) →
washed off after 10 minutes washed off after 8 to 14
hours
What is the etiologic agent of granulomatous amebic

encephalitis?
A. Acanthamoeba sp.
50.
C. Entamoeba histolytica
D. Toxoplasma gondii
From https://www.cdc.gov/parasites/acanthamoeba/index.html
Life cycle of Giardia duodenalis

From https://www.cdc.gov/dpdx/giardiasis/index.html
From https://www.cdc.gov/parasites/acanthamoeba/pathogen.html
Free-living Amebas
Etiologic Agent Disease Presentation
Granulomatous amebic encephalitis
Acanthamoeba
(GAE)
sp.
Acanthamoeba keratitis
Primary amebic meningoencephalitis
Naegleria (vs secondary amebic
fowleri meningoencephalitis caused by E
histolytica)
END OF MICRO/PARA PHASE 2
TOPNOTCH MEDICAL BOARD PREP MICROBIOLOGY PHASE 3 HANDOUT BY DR. JAN BENDRIC BORBE

The handouts, videos and other review materials, provided by Topnotch Medical Board Gram Stain Procedure
Intellectual Property Code of the Philippines, and shall only be for the sole use of the person:
medium or machine-readable form, in whole or in part without the written consent of
DISCLOSURE
The handouts/review materials must be treated with utmost confidentiality. It shall be the
disposed in any manner. Any handout/review material found in the possession of another Which of the following is not an acid fast organism?
person whose name does not appear therein shall be prima facie evidence of violation of RA A. Cryptosporidium
trends and feedback. Please buy all recommended review books and other materials listed 2. B. Nocardia
below. C. Rhodococcus
THIS HANDOUT IS NOT FOR SALE! D. None of the above
REMINDERS Acid Fast Procedure

1. Phase 3 serves as the final coaching. It is expected that you have finished
at least the Phase 1 videos prior to watching the Phase 3 videos
2. The guided content of the video lectures are seen within the handout.
Answers to questions / blanks will be seen in the Phase 3 video.
This handout is only valid for the September 2021 PLE batch.
This will be rendered obsolete for the next batch
since we update our handouts regularly.
MICROBIOLOGY – PHASE 3
By Jan Bendric C. Borbe, RMT, MLS(ASCPi), MD
Which of the following is correct with regards to

Which of the following is unique to the gram positive
gram staining?
cell wall?
A. Gram positive bacteria appear colorless after
A. Teichoic Acid
the addition of the decolorizer 3.
B. Lipopolysaccharide
1. B. Safranin functions as the mordant
C. Muramyl dipeptide
C. Gram negative organisms appear purple after
D. Peptidoglycan
the addition of iodine
D. Gram negative organism turn red upon
decolorization
Which drug inhibits bacterial DNA synthesis by PROPERTY EXOTOXIN ENDOTOXIN

blocking DNA gyrase? Gram Positive and Outer membrane
Source
A. Spectinomycin Negative of Gram Negative
4.
B. Oritavancin Secreted from
C. Quinupristin-Dalfopristin Yes No
cell
D. Fluoroquinolones Lipid A component of
Endotoxins are best characterized as? Chemistry Polypeptide
LPS
A. Polypeptides Low (fatal dose
5. B. Secreted by gram positive bacteria Adverse High (fatal dose
hundreds of
C. Highly antigenic Effects 1ug)
micrograms)
D. Lipid A component of the LPS Highly antigenic Antigenicity Poorly antigenic
Toxoids used as
Vaccines None
vaccines
Destroyed Rapidly Stable at 100 degrees
Heat Stability
at 60 degrees for 1 hr
TOPNOTCH MEDICAL BOARD PREP MICROBIOLOGY PHASE 3 HANDOUT BY DR. JAN BENDRIC BORBE Page 1 of 19
What are highly mobile segments of DNA that can

move from one part of the DNA to another? This can
result in recombination between extra-
chromosomal DNA and the chromosome.
6.
A. Plasmids
B. Bacteriophages
C. Transposons
D. Conjugation
TRANSFORMATION
• involves recipient cell uptake of free DNA when another
bacterial cell dies
TRANSDUCTION
• mediated through bacteriophages (viruses capable of infecting
bacteria )
CONJUGATION
• cell to cell contact through a sex pilus, a conjugative bridge that
serves as the conduit for DNA transfer
MRSA (Methicillin-Resistant Staphylococcus aureus)

• Hospitalization is a risk factor
• Causes serious infections: septicemia, pneumonia, infection of
surgical wounds
• Due to mecAgene → PBP2a
• Drug of choice: _____________________________________
Staphylococcus epidermidis
• Normal flora of the skin and mucous membrane
• Ability to produce biofilms promote adherence
• Poly-D-glutamic acid involved in adherence
• Associated with: _____________________________________________________
A 16/F presents in the ER with abrupt onset fever,

hypotension and scarlatiniform rash. She then
develops abdominal pain, vomiting, and diarrhea.
Past medical history is unremarkable. She also tells Staphylococcus saprophyticus
you her menses started 3 days ago and is trying out • Important cause of UTI in sexually active young women
tampons as suggested by her classmate. She • Resistant to Novobiocin
eventually improved and was discharged stable. 1
7.
week later, the patient came back to you with A 66/M tricycle driver was brought to the
generalized desquamation. What is the most emergency room for difficulty of breathing. Patient
appropriate diagnosis given this clinical scenario? claims to be coughing for the past week with note of
A. Reiter’s disease rust colored sputum. Past medical history revealed
B. Staphylococcal scalded skin syndrome that he had underwent splenectomy following a
C. Toxic shock syndrome road accident 10 years ago. Chest X-ray reveals
10.
D. Scarlet fever consolidation of the left lower lobe. Which organism
What mechanism is involved in the patient's case? is the most likely etiology of this infection?
A. Presence of exfoliatin toxin leading to A. Viridans streptococci
desquamation B. Streptococcus pneumoniae
8. B. Ingestion of preformed enterotoxins C. Legionella pneumophila
C. Release of TSST-1 into the bloodstream D. Mycoplasma pneumoniae
D. Cell lysis secondary to panton valentine
leukocidin
Should the causative agent be isolated, which of the
following is the expected finding?
A. Coagulase positive
9.
B. Gram positive cocci in chains
C. Novobiocin resistant
D. Catalase negative
Streptococcus Viridans
Test The causative agent above is best characterized as?
pneumoniae Streptococci
A. Part of the oropharyngeal flora
Optochin 11. B. Optochin sensitive
C. Bile Insoluble
Inulin
D. Devoid of cell wall
fermentation
A baby boy developed high fever, lethargy, poor
Bile solubility suck, and poor cry on the 3rd day of life. The mother
revealed that she delivered the baby via VBAC at
Neufeld Quellung home. A lumbar tap was performed which
test subsequently revealed numerous gram (+) cocci.
Upon inoculation perpendicular to a Staphylococcal
12.
streak, the cultures showed an arrow head zone of
hemolysis. The most likely organism is?
A. Streptococcus pyogenes
B. Streptococcus agalactiae
C. Viridans Streptococci
D. Escherichia coli
6 years later, the boy went to your clinic due to C. Anti-streptococcal chemoprophylaxis is
erythematous papules appearing in the perioral recommended in glomerulonephritis patients
area. His mother tells you that the papules became D. Antibiotic treatment does not prevent post-
pustules and vesicles with honey colored crusting. streptococcal disease
How should you advice the mother?
A. Her son may present with tea colored urine as Post-Streptococcal Disease
13.
a result of this infection • Follows a latent period of 1-4 weeks
B. Acute rheumatic fever is a common sequala of • Rheumatic fever has a marked tendency to be reactivated by
this infection recurrent streptococcal infection while nephritis does not
C. She should expect frothy urine due to massive • Rheumatic fever is not associated with cutaneous streptococcal
loss of proteins in the urine infections
D. All of the above • Antimicrobial drugs have no effect on established
True of the sequela caused by this organism glomerulonephritis and rheumatic fever
A. Aschoff bodies may be found in the heart • Acute streptococcal infection require treatment (penicillin,
14.
B. Rheumatic fever is not typically reactivated by erythromycin)
repeated streptococcal infection
A. Dengue Hemorrhagic Fever
B. Fitz-Hugh-Curtis Syndrome
C. Waterhouse-Friderichsen syndrome
D. Disseminated Gonococcal Infection
A 25 year old post-graduate intern complains of

dysuria with profuse and purulent penile discharge
staining his underwear. He recalls having
unprotected sex with a commercial sex worker.
Gram stain of the discharge showed gram negative
diplococci within PMNs. The most likely organism
15. Which of the following conditions may increase the
would have all of the following surface structures
except? risk of the above infection by 6000-fold?
A. Opa A. Bruton’s agammaglobulinemia
18.
B. Rmp B. Chronic granulomatous disease
C. Lipooligosaccharide C. Deficiency in late-acting complement
D. W-135 D. Chediak-Higashi disease
In order to prevent developing subsequent
infection, which regimen must be given to
household members and healthcare workers that
have been directly exposed to this patient?
19.
A. Doxycycline 100mg 2 tabs
B. Cefuroxime per orem
C. Ceftriaxone single IM injection
D. Vancomycin
A 7/M patient came in with sore throat and nasal
discharge. On PE, you were able to note a thick
grayish membrane over the throat and tonsils
accompanied by enlarged cervical lymph nodes. He
has no history of prior hospitalizations or
20. vaccinations. Which organism is the most likely
etiology of the case above?
A. Moraxella catarrhalis
B. Corynebacterium diphtheriae
C. Chlamydophila pneumoniae
D. Neisseria meningitides
The primary mechanism behind this patient’s
condition is?
A. T cell activation and release of cytokines
21.
B. Release of endotoxins
C. Inactivation of elongation factor 2 (EF-2)
D. None of the above
Possible treatment options for the above case
includes?
A. Immediate administration of anti-toxin
22.
B. Procaine penicillin G, 600,000 IU IM q12
C. Erythromycin, 500mg IV q6h
D. All of the above
Corynebacterium diphtheriae
• Gram (+) bacilli exhibiting X, L V, Y

forms resembling Chinese
characters
• Metachromatic granules/ Babes
Ernst Granules
• Cultured with: Cystine tellurite
agar, Loeffler’s serum slant
In order to isolate the organism above, the specimen

must be plated on which culture media?
A. Buffered Charcoal Yeast Extract Agar (BCYE) Pharyngeal diphtheria
16. B. Thiosulfate Citrate Bile Salt Sucrose Agar
(TCBS)
C. Mannitol Salt Agar (MSA)
D. Thayer Martin Agar
A 12/F was brought to the emergency room for
decrease in sensorium. On examination, she was
febrile, tachypneic, and had a BP of 70/40. On
examination, you noted multiple large purpuric
17.
lesions all over the body. CBC showed mild
leukocytosis and thrombocytopenia. Blood
chemistry revealed low glucose and sodium with
high potassium. Your most likely diagnosis is?
Cutaneous diphtheria
Which statement about gas gangrene is false?
A. Debridement of the affected site is needed
B. Hyperbaric oxygen therapy is one of the
27.
mainstays of therapy
C. Antitoxins have no evidence of efficacy
D. Mixed infection is the rule
An elderly paraplegic patient was being treated with
Clindamycin for an infected sacral ulcer. He then
developed bloody diarrhea associated with crampy
abdominal pain and fever. Stool guiac test came
back positive. Endoscopic evaluation revealed the
presence of erythema and raised white to yellowish
The lymph nodes of a 45/M shepherd who died of an 28.
plaques 4-8mm in diameter. What is the most likely
unknown disease showed extensive necrosis and cause of this patient’s condition?
hemorrhage with the presence of gram-positive, A. Corynebacterium diphtheria
boxcar-shaped, and encapsulated bacteria. Which is B. Bacillus cereus enterotoxin
23. the most likely diagnosis? C. Clostridium difficile toxin
A. Anthrax D. Enteroinvasive E. coli
B. Bacillary angiomatosis Which of the following treatment regimens may be
C. Scrofula used for the infection above?
D. Infectious mononucleosis A. Oral Metronidazole
The most common form of anthrax in humans is? 29. B. IV Vancomycin
A. Mediastinal C. Fidaxomicin
24. B. Woolsorter's disease D. A & C
C. Cutaneous E. A & B
D. Gastrointestinal A young man from Cavite sustains multiple injuries
due to a motorcycle accident. He opted to see a faith
Bacillus anthracis healer who applied macerated leaves on his
• poly-D-glutamic acid capsule wounds. 1 week later, the patient started having
painful muscle spasms in his legs and in his jaw. He
Anthrax proteins then went to the emergency room due to difficulty
30.
• Protective antigen (PA) opening his mouth. The following describes possible
• Edema factor (EF) – adenylate mechanisms of the infection except?
cyclase A. Proteolysis of the VAMPs
• Lethal factor (LF) B. Inhibition of the release of acetylcholine
C. Inhibition of the release of glycine
D. Cleavage of synaptobrevin and syntaxin
A 30/M from a nearby town was brought to the

emergency room after sustaining multiple injuries
and open fractures. Days after accepting this
uncoordinated transfer, the patient complained of
excruciating pain in the affected site with foul
smelling thin serosanguinous discharge and gas
25. bubbles. The cutaneous blisters appeared to contain
bluish to maroon colored fluid. Which of the ff.
organisms is the most likely cause of this infection?
A. Clostridium difficile
B. Clostridium perfringens
C. Clostridium botulinum
D. Clostridium novyi
Which virulence factor is associated with the
causative agent above?
A. Lecithinase
26.
B. Opa
C. Internalin
D. Porin
A 26/M ordered a plate of oysters at a bar in Makati.

Days later, he was admitted for fever and chills. He
was hypotensive on admission. On examination, the
patient had hemorrhagic bullous skin lesions with
evident necrosis and sloughing. History taking
revealed that the he started drinking a bottle of
whiskey every day after a break up. Cultures
31.
revealed gram negative organisms with single polar
flagellum. A microorganism of major concern for
this patient is? A 9/M came to the emergency department due to
A. Vibrio parahaemolyticus fever of 7 days duration. The child was complaining
B. Vibrio alginolyticus of abdominal pain and has had multiple episodes of
C. Vibrio cholerae loose stools. The mother tells you that her son has
D. Vibrio vulnificus been picking on the bed sheets and appears to be
All are true of Vibrio cholerae except? 34. talking to somebody. What is the most likely
A. Increased levels of cAMP results in organism implicated in this case?
hypersecretion A. EHEC
B. Infected individuals have profuse diarrhea B. Salmonella typhi
32. amounting to 20-30L/day C. Shigella dysenteriae
C. Analysis of rice water stools reveal numerous D. Entamoeba histolytica
RBCs and PMNs In relation to the case above, what is the most
D. Oral doxycycline is indicated as it reduces appropriate sample to be collected during the first
stool output and excretion of Vibrio week of illness?
Which culture media is useful in the isolation of 35. A. Blood
Vibrio species because of its high pH that enhances B. Urine
its growth? C. Bone marrow
33. A. Lowenstein Jensen D. Stool
B. Thiosulfate citrate bile sucrose agar (TCBS) The most prominent symptom in patients with the
C. Buffered charcoal yeast extract agar (BCYE) above condition is?
D. Cycloserine cefoxitin fructose agar (CCFA) A. Intestinal perforation and bleeding
36.
B. Diarrhea
C. Rose spots
D. Prolonged fever
If this were a case of Salmonella infection, which of STRAIN PRESENTATION
the following will be seen upon biochemical testing?
A. Lactose negative, H2S positive, Glucose • Traveler’s diarrhea, No inflammation or
positive invasion
B. Lactose positive, Glucose positive, greenish
37. • Diarrhea in children, adheres to the apical
metallic sheen on EMB
surface, flattens the villi and prevents
C. Urease positive, Phenylalanine deaminase
absorption
positive
D. Lactose negative, Mannitol negative, H2S • Bloody diarrhea, invades the mucosa and
negative causes necrosis and inflammation
• Dysentery, Shiga like toxin causes HUS

Rapid lactose Unable to ferment sorbitol
fermenters
The organism above causes disease by which
mechanism?
A. Attachment and effacement
Non-lactose
41. B. Activation of adenylyl cyclase
fermenters
C. Invasion of the intestinal mucosal epithelial
cells
D. Production of cytotoxic shiga-like toxins
Late lactose Shigella sonnei An 18-year-old student presented with high fever
fermenters Salmonella arizonae with painful, enlarged nodes (buboes) in the neck,
groin and axilla. Aspirate from the enlarged nodes
revealed bipolar staining organisms. Which of the
following is responsible for transmitting the
42.
infection to man?
A. Rodents
B. Fleas
C. Ticks
D. Sandfly
A 65/M, alcoholic, presented with high fever,

dyspnea, and cough with currant jelly sputum.
Auscultation revealed crackles on the left lower
lung fields. Sputum examination showed gram
negative coccobacilli. Pending culture results, the
38.
most likely pathogen in this case is?
A. Klebsiella pneumoniae
B. Legionella pneumophila
C. Mycoplasma pneumoniae
D. Streptococcus pneumoniae
Which of the following is true of the pathogen
above?
A. Slow urease producer
39. B. Has a large capsule with mucoid colonies on
culture
C. Rapid lactose fermenter
D. All of the above
A 9 year old boy developed abdominal pain, low
grade fever, and five episodes of bloody stools days
after eating undercooked hamburger at a local fast
food chain. Persistence of diarrhea prompted
admission. On initial examination, patient was
febrile, hypotensive, tachycardic, and weak looking.
Abdominal examination revealed tenderness in the Which organism is most commonly isolated in
40. lower quadrant. CBC showed: Hgb 8 mg/dL, Hct lesions involving human bite wounds and fistfight
24%, WBC 12,000/cumm, and Platelets injuries?
95,000/cumm. What is the most likely pathogen 43. A. Eikenella corrodens
causing this child’s illness? B. Kingella kingae
A. ETEC C. Moraxella catarrhalis
B. VTEC D. Erysipelothrix rhusiopathiae
C. EPEC
D. EIEC
A 30y/o firefighter was admitted to the ICU after A 24-year-old patient recently underwent
sustaining burn injuries while on duty. Several days endoscopy following recurrent bouts of epigastric
later, the patient developed high fever and went into pain that awakens him at night. Gastric biopsy
shock. On examination, his wounds had greenish material was tested in a urea containing medium
discharge and a fruity odor. There were also black which turned positive within 2 hours. This organism
49.
and necrotic lesions noted which were surrounded is associated with which of the following conditions?
44. by erythema with no pus. The exotoxin A produced A. Duodenal ulcers
by this organism mainly acts by which mechanism? B. Gastric adenocarcinoma
A. Splitting of lecithin into phosphorylcholine C. MALT lymphoma
and diacylglycerol D. All of the above
B. Blockade of Elongation factor 2 Following treatment, which of the following may be
C. Production of hyaluronidase used to assess treatment success?
D. Formation of pores in white blood cells A. 13C Urea breath test
50.
Which of the following statements correctly B. Repeat stool culture
describe the causative agent above? C. Detection of Shiga-like toxin
A. Rapidly ferments lactose D. Cytotoxin assay
B. Not able to grow at 42 degrees Celsius All are true about this patient’s condition except?
45.
C. Neutropenia is a risk factor for developing A. Eradication of the organism is needed to
bacteremia prevent recurrent disease
D. CFTR gene mutation is protective against the B. Race is an important risk factor
51.
infection C. More common in the lower socioeconomic
strata
D. Treatment may require a combination of
antibiotics
A 6-year-old girl was brought to the emergency
room for respiratory distress. Her mother tells you
that she declined vaccination as it would cause
autism. The child is not able to lie down flat and
prefers to lean forward with chin lifted. On
examination, patient was febrile. Lateral
52.
radiography revealed thumb sign. The most likely
organism is?
A. Bordetella pertussis
B. Parainfluenzae
C. Staphylococcus
D. Haemophilus influenzae
The most common serotype is?
A. D
53. B. C
C. B
D. A
A major virulence factor of this case is
A. Pili
54. B. Endotoxins
C. Polyribitol phosphate
D. Slime layer
Haemophilus
• tiny gram-negative coccobacilli
• very sensitive to drying and chilling
• exhibit satellite phenomenon
• requires horse blood/ chocolate agar for
growth
• special growth requirements:
o X factor
o V factor
The most appropriate drug to give this patient is?

A. Benzathine Penicillin G
46. B. Cefoxitin
C. Ertapenem
D. Ceftazidime
Campylobacter jejuni is one of the most common
causes of bacterial gastroenteritis. All of the
following are true of C. jejuni except?
A. Unable to grow at 42 degrees Celsius
47. B. Microaerophilic Haemophilus ducreyi
C. Very common cause of bacterial
gastroenteritis in humans
D. Organisms are motile, gram negative, gullwing
shaped rods
The above infection is associated with which of the
following sequela?
A. Guillain-Barré Syndrome
48.
B. Reiter’s Syndrome
C. Reactive arthritis
D. All of the above
This organism is best cultured using?

A. Foot pad of mice or armadillo
60. B. Ellinghausen McCullough Johnson Harris
C. McCoy
D. Organism cannot be cultured
Urine antigen test is useful in the diagnosis of

infections caused by which organism?
A. Viridans streptococci
55.
B. Streptococcus pneumoniae
C. Legionella pneumophila
D. Mycoplasma pneumoniae
A 40-year-old construction worker was admitted for
decrease in sensorium. Patient has been
complaining of cough for the past 3 months, weight
loss, night sweats, and malaise. Imaging of the chest If a lepromin test is to be done in this patient, the
revealed numerous nodules that resemble millet expected result would be?
seeds. Lumbar tap revealed elevated proteins, A. Positive
decreased glucose, numerous lymphocytes, and 61.
B. Negative
elevated adenosine deaminase. Which of the C. Indeterminate
56. following is not a characteristic of the organism? D. Non-reactive
A. The organism is a thin slender acid-fast
obligate aerobe
OTHER MYCOBACTERIA
B. Contains numerous lipids (ex. Muramyl
Scrofula; cervical
dipeptide) that can trigger granuloma Mycobacterium scrofulaceum
lymphadenitis in children
formation
Mycobacterium Avium
C. The organism cannot be cultured in vitro Common in HIV/AIDS
Intracellulare complex
D. Virulent strains are known to produce
serpentine cord formation Tapwater bacillus, generally
Mycobacterium gordonae
nonpathogenic
Mycobacterium marinum Swimming pool granuloma
Mycobacterium kansasii Pulmonary infection
A suspected case of Mycoplasma pneumonia was

empirically treated with Co-amoxiclav. Patient was
shifted to Meropenem after 3 days of therapy.
However, there was still no response after 1 week of
therapy. If this was indeed a case of atypical
pneumonia, what is the most likely cause for the
62. lack of response?
A. The organism has sterols in its cell membrane
B. The organism is known to produce beta-
lactamases
C. The organism lacks the target of the antibiotics
D. The organism requires longer duration of
treatment
Pulmonary disease caused by the above infection is Which of the following diseases is associated with
indistinguishable from which organism? the organism above?
A. Mycobacterium chelonae A. Cold Agglutinin Disease
57. 63.
B. Mycobacterium kansasii B. Paroxysmal nocturnal hemoglobinuria
C. Nocardia asteroides C. Warm autoimmune hemolytic anemia
D. Aspergillus D. Paroxysmal cold hemoglobinuria
If this patient had HIV, which of the following drugs A 21/F G2P2(2002) presents with vaginal discharge
may significantly increase the metabolism of anti- and lower abdominal pain. On examination, patient
retrovirals? was febrile and tachycardic. IE: Cervix is firm, long,
58. A. Isoniazid closed, (+) cervical motion tenderness. Gram stain
B. Rifampicin of the endocervical smear revealed numerous PMNs
64.
C. Ethambutol without bacteria. The most likely cause is?
D. Pyrazinamide A. Neisseria gonorrhoeae
A 30-year-old vagrant has shortening of the toes and B. Chlamydia trachomatis
fingers, loss of eyebrows, and disfigurement of the C. Listeria monocytogenes
nose. He also has painless lumps in the face and D. Group B Streptococci
earlobes. What is the most appropriate diagnostic A possible sequela of the above infection is?
59. tool for this particular case? A. Cervical Cancer
A. Slit smear microscopy 65. B. Uterine fibroid
B. Gram stain and culture on routine media C. Rectovaginal fistula
C. Anti-leprosy IgG and IgM D. Infertility
D. Dark field microscopy
The test of choice for your diagnosis above is?
A. KOH smear
66. B. Culture with routine media
C. NAATs
D. Electron microscopy
RETICULATE BODY (RB) ELEMENTARY BODY (EB)

Intracellular Extracellular
Replicative form Infective form
Metabolically active Metabolically Inert
The patient came back to you presenting with joint

pains. Yellow brown vesiculopustular waxy lesions
were seen in the palms and soles. These lesions are
suggestive of?
67.
A. Pityriasis rosea
B. Dermatitis herpetiformis
C. Keratoderma blennorrhagica
D. Shagreen patches
CLINICAL ROUTE OF
SEROVAR
SYNDROME TRANSMISSION
A, B, Ba, C • Hand to eye Fomites
L1, L2,
• Sexual contact
L2a, L3
• Sexual contact
• Hand to eye by
D-K
autoinoculation of
genital secretions
A health care worker is suspected of having

psittacosis. In history taking, which data should be
elicited to support the diagnosis?
A. Do you have any history of travel to Africa?
B. Are you exposed to birds, such as parrots,
68. parakeets, macaws or cockatiels?
C. Do you use protective masks when
administering treatment to patients with Which of the following techniques may be used to
respiratory infections? visualize the organism during the early stage of the
D. Do you have any history of coronary heart disease?
disease and atherosclerosis? 71. A. Gram stain smear
An African man was suspected of having chlamydial B. Giemsa stained smear
keratoconjunctivitis. Purulent ocular discharge was C. Dark Field microscopy
obtained for examination. Which microscopic D. Phase contrast microscopy
finding will most likely confirm the diagnosis?
69.
A. Warthin-Finkeldey cells
B. Councilman bodies
C. Henderson-Patterson bodies
D. Halberstadter-Prowazek inclusion bodies
Rickettsia
• fastidious bacteria that are obligate intracellular
• multiply by binary fission
• transmitted by bite of an infected arthropod vector
• Triad of fever, headache, and rash
An 18/M comes to your clinic because of
maculopapular rash on the palms and soles. On Patient suddenly developed neurologic symptoms.
further probing, he claims he had a painless "ulcer" Which of the following is the most ideal test to
at the tip of his penis which spontaneously confirm your diagnosis of neurosyphilis?
disappeared after 6 weeks. He goes on to tell you 72. A. RPR
that he engages in unprotected sex with multiple B. VDRL
70. C. FTA-ABS
male and female partners. The most likely organism
implicated in this case is? D. MHA-TP
A. Klebsiella granulomatis A test result of RPR (+) VDRL (+)
B. Haemophilus ducreyi FTA-ABS (-) is suggestive of?
C. Treponema pallidum A. Biological false positive
73.
D. Herpes simplex virus B. True positive
C. Tertiary syphilis
D. Secondary syphilis
Biological false positive results on VDRL

V - Viral infections (EBV, hepatitis)
D - Drugs
R - Rheumatic fever, Rheumatoid arthritis
L - Lupus, Leprosy
You decided to treat this patient with Penicillin G. 24
hours after treatment, patient suddenly developed
tachycardia, fever, chills, rigors, hypotension and
diaphoresis. What could be a possible explanation?
74. A. Patient is having Stevens Johnson syndrome
B. Patient is experiencing a Jarisch-Herxheimer
reaction
C. Anaphylaxis
D. Tachyphylaxis
A 24/M sought consult due to circular bald patches
with short hair stubs. If you are considering black
dot tinea capitis, which of the following tests should
you perform to support your diagnosis?
78.
A. Wood’s lamp
B. Measurement of fungal antigens in blood
C. Microscopic examination with KOH
D. Culture on CHROMagar
The most likely cause of this patient’s condition is?
A. Epidermophyton floccosum
79. B. Trichophyton mentagrophytes
C. Microsporum canis
D. Trichophyton tonsurans
A 35-year-old man went camping in the mountains.
Several days later, he developed fever with a Tmax Tinea Barbae • Beard and mustache
of 38.5°C accompanied by chills and headache Tinea Capitis • Scalp
lasting for 5 days. Ten days later, he had another
similar episode of fever. He claims to feel well in _______________ The hair follicle is the initial site of infection,
75. between episodes. What laboratory test will you and fungal growth continues within the hair
request for your patient above? shaft, causing it to weaken. The brittle, infected
A. Dark Field Microscopy
hair shafts break off at the scalp, leaving the
B. Fluorescent microscopy
black stubs.
C. Peripheral blood smear
D. Latex Agglutination _______________Primarily involves the outer portion of hair
shafts. The lesions are seldom inflamed, but
luster and color of the hair shaft may be lost
• Infection of the hair follicle at its base.
Tinea favosa
Crusty, cup-shaped flakes called scutula are
formed.
Caused by:
• Hair loss and scar tissue formation
T. schoenleinii
commonly follow.
Tinea cruris • Groin
Tinea
• Body or trunk
corporis
Which is true of the above case? Tinea • Hands, palms, bet fingers (frequently T.
A. Repeated febrile episodes are associated with manuum rubrum)
reinfection
B. Febrile episodes coincide with lysis of RBCs • Sole of feet and in between toes
76. and release of merozoites Tinea pedis “athlete’s foot” progress around the sides of
C. Each relapse is associated with an the foot from the sole
antigenically distinct variant Tinea
D. Relapses are associated with presence of imbricata
• Distinct lesion. Involved portions of the trunk
hypnozoites in the liver develop diagnostically distinctive concentric
Caused by:
rings of scaling tissue.
T.
FUNGI concentricum
Dimorphic fungi are best described as?
A. Fungi that have a mold phase and a yeast phase WOOD’S LAMP WITH FLUORESCENCE
B. Fungi with sexual and asexual stages
77.
C. Fungi that can be pigmented or non-
pigmented
D. None of the above
Dimorphic Fungi
• include a mold phase and a yeast or spherule phase
• Yeast or tissue state – seen in vivo or when the organism is
grown at 37°C with increased CO2
• Mold phase - seen when the organism is grown at room
temperature (22°C to 25°C) in ambient air conditions
• Thermally dimorphic fungal species associated with human
disease include Blastomyces dermatitidis, Coccidioides immitis,
Histoplasma capsulatum var. capsulatum, Paracoccidioides
brasiliensis, Sporothrix schenckii, and Penicillium marneffei.
Pigmentation
• Hyaline hyphae – are non-pigmented or lightly pigmented
• Phaeoid hyphae – are darkly pigmented because of the
presence of melanin in the cell wall
A.
Oval cells within macrophages
B.
Multipolar budding
C.
Large spherules containing endospores
D.
Thick walled oval yeast cells with broad based
budding
A 10/M came in with multiple nodules over the arm.
History started a few months ago when he
developed a nodule over the dorsum after
sustaining an injury while playing outdoors. These
nodules progressed to involve the upper arm.
Draining lymphatics became thickened and cord-
84. like. Microscopic examination revealed cigar
shaped yeast cells. Which of the following is another
finding consistent with your diagnosis above?
A. Sclerotic bodies
B. Asteroid bodies
C. Spherules
D. Tuberculate macroconidia
A 45yo/M came to your clinic presenting with a 10
year history of multiple firm nodules over the right
If this were to be Trichophyton mentagrophytes, foot. On history, you noted that he was often
which test would best differentiate it from barefoot when working in the garden. Close
Trichophyton rubrum? examination reveals the presence of draining
85.
80. A. Positive urease test sinuses. What is the most likely diagnosis?
B. Negative hair perforation test A. Chromoblastomycosis
C. Absence of spiral shaped hyphae B. Mycetoma
D. Presence of a deep red non-diffusible pigment C. Sporotrichosis
D. Phaeohyphomycosis
Mycetoma
• Chronic subcutaneous infection induced by traumatic
inoculation
• Local swelling with interconnecting draining sinuses that
contain granules (microcolonies of the organism)
• 2 Forms:
o Actinomycetoma
o Eumycetoma (Madura foot, Maduromycosis)
T. mentagrophytes T. rubrum
Eumycetoma
Microscopic Teardrop Clavate or peg
features microconidia shaped Causative agents include:
Hair Perforation • Pseudallescheria boydii
Test • Madurella mycetomatis
Urease • Acremonium falciforme
Actinomycetoma
A 35/M patient with leukemia presented with Causative agents include:
bloody nasal exudates and orbital cellulitis. Direct • Nocardia asteroides
examination of the nasal tissues revealed broad, • Streptomyces somaliensis
ribbon like hyphae with irregular branching and • Actinomadura madurae
absence of septations. The most likely organism
81. A 24/M, known case of HIV, presented with sudden
responsible for this patient’s condition is?
A. Aspergillus fumigatus onset headache, neck stiffness, and disorientation. A
B. Penicillium marneffei lumbar tap was done which revealed elevated
C. Candida pressure. CSF protein was 65mg/dL, glucose
D. Mucor 38mg/dL (serum glucose 100mg/dL), with elevated
Which of the following is true of Candida albicans? white count. On india ink preparation, clear halos
A. Pseudohyphae formation 86. were seen against a dark background. The causative
B. Production of large spherical chlamydospores agent was most likely acquired by which
82. mechanism.
C. Formation of true hyphae after incubation in
serum A. Traumatic implantation
D. All of the above B. Inhalation from bat guano
A 45/M from Ohio presented with prolonged cough C. Inhalation from pigeon droppings
and low grade fever. The patient recently went D. Endogenous yeast infection
spelunking before noticing these symptoms. Chest
X-ray revealed hilar lymphadenopathy and
83. pulmonary nodules. TB work up came back
negative. You are now entertaining the possibility of
systemic mycoses. If this were to be a case of
Histoplasmosis, which of the following would be the
expected findings?
Which serological profile of a patient with a history
hepatitis B infection is consistent with chronic
infection?
A. (-) HBsAg, (+) anti-HBs, (-) anti-HBc IgM, (-)
anti-HBc IgG, (-) HBeAg
89. B. (-) HBsAg, (-) anti-HBs, (+) anti-HBc IgM, (-)
C. (-) HBsAg, (+) anti-HBs, (-) anti-HBc IgM, (+)
D. (+) HBsAg, (-) anti-HBs, (-) anti-HBc IgM, (+)
anti-HBc IgG, (+) HBeAg
Key Fungal Structures Observed in Microscopic

Examinations of Clinical Specimens
PREDOMINANT
MYCOSES
MORPHOLOGY
• Blastomycosis, Histoplasmosis,
Yeasts—single
Paracoccidioidomycosis, Penicilliosis,
or multiple buds
Sporotrichosis
Yeasts with
• Cryptococcosis Anti-
capsules Time Period HBsAg Anti-HBc HBeAg
HBs
Incubation
Hyphae—septate Aspergillus, Fusarium, Geotrichum, Positive Negative Negative Positive
Period
Trichosporon, et al.)
Acute Positive
Hyphae—septate Positive Negative Positive
Infection IgM
in skin or nail • Dermatophytosis
Window Positive
specimens Negative Negative Negative
Period IgM
Hyphae— • Mucormycosis—species of Rhizopus,
Complete Positive
nonseptate Lichtheimia, Cunninghamella, etc. Negative Positive Negative
Recovery IgG
Hyphae—
• Phaeohyphomycosis—species of Chronic Positive
septate; Positive Negative Negative
Bipolaris, Cladosporium, Curvularia, Carrier IgG
brownish cell
Exserohilum, etc. Chronic Positive
walls Positive Negative Positive
Active IgG
Yeasts and
• Candidiasis—species of Candida Vaccinated Negative Positive Negative Negative
pseudohyphae
Yeasts and
hyphae in skin • Pityriasis versicolor The 1918 Spanish Flu caused by an H1N1 virus was
scrapings estimated to have infected at least 500 million
people or one third of the world’s population. This
Spherules • Coccidiomycoses
has resulted to at least 50 million deaths worldwide.
Sclerotic cells—
Which of the following is responsible for facilitating
brownish cell • Chromoblastomycosis 90. the release of this virus from the infected cell
walls
surfaces during the budding process?
Sulfur granules • Mycetoma A. Hemagglutinin
Arthroconidia in B. Neuraminidase
• Dermatophytosis
hair C. Matrix protein
Conidia in D. Integral membrane protein
pulmonary All of the following correctly describes the
Aspergillus, Fusarium, etc.
cavity antigenicity of the virus above except?
Cysts (asci) in A. Capable of both antigenic shift and antigenic
pulmonary • Pneumocystis drift
specimens 91. B. Antigenic shifts result from genetic
reassortment
Which viral infection is most associated with C. Not capable of causing pandemics due to
aplastic anemia? Infections can also present as a limited capacity to alter its antigenicity
rash with slapped cheek appearance. D. Oseltamivir is effective against this virus
87. A. Rubella virus
B. Influenza A MEMORY AIDS
C. Parvovirus B19 SEGMENTED GENOME
D. Yellow fever virus B–O–A–R
A 25/M intern came to you for sores around the Bunyaviruses
mouth and lips. On inspection, you noted groups of Orthomyxoviruses (influenza)
vesicular lesions on an erythematous base. What is Arenaviruses
a cheap, rapid, but non-specific test used in the Reoviruses
88. presumptive diagnosis of this case?
A. Slit smear
B. Tzanck smear
C. Peripheral blood smear
D. Thick and thin smear
ANTIGENIC SHIFT ANTIGENIC DRIFT CD4 ETIOLOGY CLINICAL SYNDROME
(Pandemics) M. tuberculosis • disseminated tuberculosis
• Major changes based on the • Minor changes based on HSV • HSV esophagitis
genetic reassortment of point mutations in the < 500
C. albicans • esophageal candidiasis
segments of the genome genome RNA HHV-8 • Kaposi’s sarcoma
RNA • Leads to epidemics P. jiroveci • PCP pneumonia
• Leads to pandemics T. gondii • cerebral toxoplasmosis
< 200 C. neoformans • meningoencephalitis
A 5-year-old unvaccinated girl develops fever and
C. immitis • coccidioidomycosis
malaise followed by appearances of rashes on the
trunk, face, and limbs. (+) papules, vesicular lesions C. parvum • chronic diarrhea
described as dewdrop on rose petal, and crusted M. avium • invasive pulmonary disease
lesions. This asynchronous development of lesions < 50 H. capsulatum • histoplasmosis
92. CMV • CMV retinitis
is most typically seen in?
A. Measles
B. Rubella To design a vaccine against HIV infection, a logical
C. Varicella goal would be to alter some native molecule or
D. Coxsackie A16 product of the virion in order to make it highly
immunogenic. If you wish you prevent the
attachment of the virus to helper T lymphocytes,
97. which molecule or family of molecules might best be
targeted?
A. gp120
B. gp41
C. p17
D. Integrase
STRUCTURAL GENES
p24 – capsid protein
gag
p17 – matrix protein
Reverse transcriptase
pol Integrase
Protease
gp120 – attachment to host CD4 T cell
env
gp41 – fusion and entry
Coreceptor
Macrophages
T cells
Which of the following is not a member of the
picornaviridae? A 5 year old boy presented with a 3 day history of
A. Poliovirus fever, headache, joint pains, and retroorbital pain.
93.
B. Coxsackie virus A The general physician is highly considering dengue.
C. Hepatitis A Which of the following tests provides the most
D. Smallpox 98. reliable evidence of an active dengue infection?
Ebola and Marburg virus belong to which family? A. Isolation of dengue virus
A. Filoviridae B. Detection of dengue NS1 antigen
94. B. Flaviviridae C. Analysis of paired acute and convalescent sera
C. Arenaviridae D. Single high titer of dengue IgM
D. Bunyaviridae In a patient with HIV-1 infection, which of the
A 26-year-old young actor was recently diagnosed following is most predictive of the patient’s
with HIV. He refused anti-retroviral therapy telling prognosis
you that this is all part of Big Pharma’s scheme. 99. A. CD4+ cell count
Several months later, patient was admitted for B. CD4:CD8 cell ratio
difficulty of breathing. He was hypoxic on C. Rate of decline in anti-HIV antibody
admission. Chest X-ray revealed bilateral D. Level of HIV-1 in the plasma
interstitial fluffy infiltrates. Examination of BAL
revealed presence of cysts. Which of the following ORGANISM INCLUSION
95.
can be inferred from this patient’s clinical Herpes simplex / VZV
presentation?
Yellow fever
A. Patient probably has a CD4 count of <200
cells/uL HPV
B. Increased CD4:CD8 ratio Molluscum contagiosum
C. Absolute indication for prophylaxis against Smallpox
MAI Rabies
D. Disease is self-limited, no medication required Measles
The above infection could have been prevented by Cytomegalovirus
taking which drug?
A. Sulfamethoxazole- trimethoprim
96.
B. Ciprofloxacin
C. Doxycycline
D. Dapsone
A 50/M complains of fever, fatigue, and vague right
upper quadrant discomfort. A hepatic abscess was
seen on ultrasonography. An “anchovy paste” paste
like material was obtained on subsequent
aspiration. Which of the following is true of the
above infection?
A. The patient was able to acquire the infection
through ingestion of trophozoites with
100.
characteristic RBCs in the cytoplasm
B. The brain is the most common extra-intestinal
site
C. A granulomatous tumor like mas may form on
the intestinal wall which may cause
obstruction
D. The most common type of infection is amoebic
colitis
A 10/M presented with sudden onset seizures. MRI
revealed numerous cysts in the subarachnoid space
as well as parenchymal cysts in the gray white
matter junction consistent with neurocysticercosis.
101. The most appropriate treatment for this patient is? Babesiosis may present with high fever, hemolytic
A. Praziquantel anemia, hemoglobinuria, and jaundice that may be
B. Mebendazole mistaken for Plasmodium falciparum. The two
C. Albendazole infections are different in terms of?
D. Metronidazole A. Fever in babesiosis never recurs
A 12 boy develops abdominal cramping and B. Splenectomized patients are rendered
104.
diarrhea with rotten egg odor. A direct fecal smear relatively immune to babesia
was done which showed trophozoites with floating C. Absence of pigment in the red cells and
leaf like motility. Where is the site of excystation of gametocytes favors diagnosis of Babesia over
102. this organism? falciparum
A. Stomach D. Plasmodium falciparum typically presents
B. Duodenum with maltese cross formation
C. Jejunum A 35/M, farmer from Leyte, non-alcoholic beverage
D. Colon drinker, presented at the emergency room with
The above organism will encyst in which site? hematemesis. Initial assessment was bleeding
A. Stomach esophageal varices with portal hypertension. If the
103. B. Duodenum patient tested positive for Schistosoma mansoni, the
105.
C. Jejunum organism will most likely be found in which site?
D. Colon A. Superior mesenteric veins
B. Inferior mesenteric veins
C. Splenic vein
D. Portal vein
Eosinophils may accumulate in the lungs in

response to Ascaris infection. Which form of the
parasite may be found in the lungs?
106. A. Adult worm
B. Larva
C. Embryonated Egg
D. Unembryonated Egg
The habitat of adult Schistosoma haematobium is
the?
A. Urinary Bladder
107.
B. Superior mesenteric vein
C. Inferior mesenteric vein
D. Vesical plexus
A six-year-old boy developed unilateral swelling of A 28/F visited her OB GYN because of vaginal
the left eyelids accompanied by fever and fatigue. No pruritus. On speculum examination, cervix was
consult was done. Years later, the patient started erythematous with punctate hemorrhage
having difficulty swallowing and abdominal pain accompanied by a greenish frothy discharge. On wet
which prompted consult. Examination revealed mount, numerous parasites with jerky tumbling
108. enlargement of the heart, esophagus, and colon. 109. motility were observed. Trichomonas vaginalis. The
This patient was most likely bitten by? infective stage of this organism is?
A. Glossina fly A. Quadrinucleated cyst
B. Phlebotomus sandfly B. Embryonated Ova
C. Triatoma C. Trophozoite
D. Simulium fly D. Decorticated ova
FEATURE NORMAL CANDIDIASIS TRICHOMONIASIS BACTERIAL VAGINOSIS
Vulvar itching and/or Profuse discharge; Malodorous;
Symptoms none
irritation Vulvar itching Slightly inc. discharge
Scanty
Clear / Often profuse Moderate
Scanty, white
Discharge translucent White/yellow White or gray
Clumped adherent plaques
Non- Homogenous Homogenous
homogenous
Erythema of vagina Erythema of vagina and
Inflammation of
None Vulvar dermatitis vulva None
vulva/vagina
Fissures common Colpitis macularis
pH of the vaginal
Usually < = 4.5 Usually < = 4.5 Usually > = 5 Usually > 4.5
fluid
Amine fishy odor None None May be present Present
Normal Few leukocytes, clue cells
epithelial cells Leukocytes, epithelial cells Leukocytes, motile No/ few lactobacilli
Microscopy
Lactobacilli Pseudohyphae trichomonads outnumbered by profuse mixed
predominant microbiota
• Miconazole 100mg
vaginal suppository • Metronidazole or
• Clotrimazole 100mg tinidazole 2gm oral single
• Metronidazole 500mg BID x 7
Treatment None vaginal tablet daily for 7 dose
days
days • Metronidazole 500mg BID
• Fluconazole 150mg oral x 7 days
single dose
• None
Management of • Treat with metronidazole
None • Topical treatment if with None
partner 2gm single dose
candida of penis
A 30/M patient sought consult due to fatigue. On ORGANISM ASSOCIATION
examination, patient was had pale palpebral • Biliary tract disease,
conjunctiva and nail beds. CBC showed Hgb Clonorchis sinensis
cholangiocarcinoma
9.5mg/dL, Hct 30%, WBC count 9.8, Plt 200,000, Neurocysticercosis
MCV 120fL, MCH 30, MCHC 330, and RDW 16. Stool • Brain cysts, seizures
(T. solium)
110. examination revealed operculated eggs. The most Schistosoma • Hematuria, Squamous cell
like cause of this patient’s condition is? haematobium bladder cancer
A. Necator americanus Echinococcus granulosus • Liver (hydatid cyst)
B. Fasciolopsis buski Ancylostoma, Necator • Microcytic anemia
C. Schistosoma japonicum
Trichinella spiralis • Mylagias, Periorbital edema
D. Diphyllobothrium latum
Enterobius • Perianal pruritus
Schistosoma mansoni,
• Portal hypertension
Schistosoma japonicum
• Vitamin B12 deficiency
Diphyllobothrium latum
(Megaloblastic anemia)
Trichuris trichiura • Rectal prolapse
• Cardiomyopathy, Megacolon,
Trypanosoma cruzi
Megaesophagus
• Primary amoebic
Naegleria fowleri
meningoencephalitis
• Keratitis, Granulomatous
Acanthamoeba
Amoebic Encephalitis
A 38/M came in with a 1 week history of fever and
cough. He initially noted lost of taste and smell
A 25-year-old male physician went swimming in a
following a drinking spree. 3 of his friends
lake during a camping trip. He complained of
developed similar symptoms while the rest were
headache and fever accompanied by nasal
apparently well. Upon arriving at the ER, his
discharge. Patient was admitted and managed as a
temperature was 38.9°C, BP 120/80, HR 98, RR 26,
case of bacterial meningitis. Despite timely
with an O2 sat of 82% on room air. He denies
administration of empiric antibiotics, patient 112.
111. dyspnea, chest pain, and other symptoms. All of the
succumbed 3 days later. Which parasite should have
following markers are expected to be elevated
been considered in the diagnosis?
except?
A. Plasmodium falciparum
A. Ferritin
B. HsCRP
C. Acanthamoeba castellani
C. LDH
D. Taenia solium
D. Procalcitonin
He developed respiratory failure over the course of COVID 19 ( SARS-CoV-2)
the hospitalization and had to be intubated. This • Formerly novel coronavirus 2019 (2019-nCoV)
patient will most likely benefit from treatment with • Positive sense, single-stranded enveloped RNA
which of the following drugs? • Family Coronaviridae
113.
A. Tocilizumab • Area of emergence- Wuhan, China
B. Remdesivir • Key hosts- Bats
C. Dexamethasone • Entry receptor- ACE2 receptor
D. Hydroxychloroquine
The etiologic agent is known to enter to host cell
using which receptor?
A. Sialic acid
114.
B. CCR5
C. M2 Receptor
D. ACE2 Receptor
Transmission
END OF MICROBIOLOGY PHASE 3
QUESTION ANSWERS
BUZZ WORDS Profuse diarrhea,
QUESTION ANSWERS vomiting, rice-water
Most common stool à rapid Vibrio cholerae
complication of Infertility / sterility dehydration, electrolyte
gonococcal PID imbalance
Major target cell of EBV B lymphocytes • Childhood disease
• Anti-Streptolysin O – antecedent • High-grade fever
pharyngitis; more often found in • Patchy areas of flaccid paralysis
Streptococcal evidences
rheumatic individuals and muscle atrophy
of infection Poliovirus
• Anti-DNase B – antecedent skin • Destruction of lower motor
infections neurons
Disease process of Involvement of heart, kidney, • Global campaign to eradicate
diphtheria adrenals disease (WHO)
Other technique in • Dry coughs, low grade afternoon
diagnosis of whipworm fever
Saturated brine flotation technique
infection other than • Emaciated
Tuberculosis in adults
fecal smear • Harsh breath sounds
Has direct cytotoxic • Increased upper lung fields
activity and can kill CD8 T helper cells densities on xray
infected cells • Infection in the past
Primary target cell of Positive tuberculin test
T lymphocytes (CD4) • Latent infection
HIV Layer of tubercle (TB
• Antisense granuloma) where TB
• RNA-dependent RNA Central zone
bacilli is isolated and
Negative-sense RNA polymerase cultured
• Cannot encode proteins, must be • EBV
converted to mRNA first • Malaise, headache, fatigue, sore
Predominant organism throat
Pasteurella multocida
in cat bites • Lymphadenopathy,
AIDS-defining illness, splenomegaly
fungi causing brain Infectious
Cryptococcus neoformans • Elevated SGOT, SGPT, ALP,
abscess (soap bubble mononucleosis
Bilirubins
lesions) • Elevated WBC, lymphocytic
Ingestion of dog meat Echinococcus granulosus predominance – large atypical T
Mobile and transferable segments lymphocytes
Transposons of bacterial DNA • Recovery after 4-5 weeks
“Jumping genes” • Malignant transformation
Mosquito breeds in this water and EBV
• Burkitt lymphoma
may travel to homes • Fever, muscle, bone pain, then
bleeding shock and eventual
Cross-over Preventive Medicine death
Reason for call to clean
• Enhanced 4S Strategy “Aksyon • Probably due to second dengue
up water-holding Hemorrhagic dengue
Barangay Kontra Dengue in infection with a different
receptacles and plant
communities (4S)” serotype as previous
containers close to
o Search and Destroy
homes • Key feature is increased vascular
o Seek Early Consultation
permeability
o Self-Protection Measures
• Multiple painful lesions of
o Say yes to fogging only during
grouped vesicles on suprapubic
outbreaks
Herpes progenitalis area
Major virulence factor of
M protein • Sexually transmitted
Streptococcus pyogenes
• Tzanck smear
Progressive general
weakness (symmetric • Alaise, fever, sore throat, non-
on bilateral upper and productive cough à productive
lower ex), sudden cough with blood-tinged sputum.
diplopia, dysphagia, • Mild leukocytosis
Botulism Mycoplasma pneumoniae • CXR: pulmonary consolidation
slurred speech. Afebrile.
Respiratory distress, • Treated with Tetracycline and
cardiac arrest, death. Erythromycin
Ingestion of leftover • Cell wall defective
canned sardines • Diagnosed through serology
Distinguishing factor of Known regulatory
adaptive vs. innate Antigen-specific antibodies mechanisms for • Staph cassette chromosome (SCC
immunity antibiotic resistance mec)
Ig for mucosal development
immunity, protects • Trypanosoma cruzi
mucous membranes IgA • Amastigote in heart muscle
from bacterial and viral Chagas disease • Most common serious
attacks complication is interstitial
• Necator myocarditis
Transmission: larval • Ancylostoma • Clawing deformity of both hands
penetration of skin • Strongyloides • Reduced sensation at small
• Schistosoma Hansen’s disease patches of skin
MCC viral infection in • Macular rashes without
HPV sensation
reproductive system
Ghon lesion Primary tuberculosis
QUESTION ANSWERS QUESTION ANSWERS
More malignant and • Foul smelling vaginal discharge –
progressive type of Negative lepromin test due to overgrowth of anaerobes,
leprosy decreased lactobacilli, increased
Laboratory procedure to vaginal pH
establish leprosy Skin biopsy • Whitish gray in color adherent to
Bacterial vaginosis
diagnosis the vaginal wall but none on
• Cough, malaise, fever cervical os
• Inhalation of airborne candida • Clue cells adherent bacilli, no
• CXR: collection of hyphae, mucus, PMN seen
Aspergillosis
and cellular debris • Tx: Metronidazole BID x 7 days
• Mgt: lobectomy to remove mass • Increased mucosal discharge
and surrounding tissues Trichomonas vaginalis • Yellow green, frothy adherent to
• Creeping eruption (cutaneous vaginal wall
larva migrans) • Horticulturist / gardener
• Walking barefooted on beach or • Multiple subcutaneous nodules
soil and abscesses occurring along
Serpiginous pruritic
• Animal hookworms – Sporotrichosis lymphatics of right upper
eruption on leg
Ancylostoma braziliense (cat extremity
extending upwards
hookworm); Ancylostoma • Biopsy and culture
caninum (dog hookworm) • Tx: oral Itraconazole
• Mgt: Albendazole, cold ice or • Vesicle at anorectal area, u
cryosurgery ulcerated
Round smooth • Painful lymphadenopathies in
fluorescent greenish- inguinal and rectal areas
colored colonies, Pseudomonas • papule or vesicular which
hemolytic and oxidase Lymphogranuloma
ulcerates and leads to
positive venereum
suppurative inguinal
Pseudomonas infection lymphadenitis (buboes)
with necrosis of skin Ecthyma gangrenosum • treatment success when there’s
involved in burn complete healing of suppurative
• Profuse diarrhea, nausea, adenitis
vomiting Diabetic usually exposed
• Stool exam: gram-negative bacilli to hot stove develops • monilial intertrigo
• Non-lactose fermenter erythematous pruritic • candida albicans
Typhoid fever • Culture negative patches beneath breast • KOH: oval budding spores and
• Antimicrobial therapy is essential and armpit areas with pseudohyphal elements
• Important carriers are humans satellite lesions • Grows on sweaty areas, warm,
working as food handlers scattered around the moist and unaerated
• Multiplies in lymphoid tissue area
• TSST 1 super antigen
Toxic Shock Syndrome • Staphylococcus aureus
• Cytokine release

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TOPNOTCH MEDICAL BOARD PREP MICROBIOLOGY MAIN HANDOUT BY PACIFICO ERIC E.

CALDERON, MD, MBEth

Important Legal Information

5. Virology 72 • Animal parasites

Welcome to Microbiology review! Here are some pointers for a

Mastering Biology Pearson

As a mnemonic in remembering the size of the ribosomes

Mayo Foundation of Medical Education and Research

SPONGIFORM ENCEPHALOPATHIES Curious about kuru? Check out this video:

ANIMAL PRION DISEASES

• Primary - Amino acid sequence in a polypeptide chain

III. BACTERIAL STRUCTURE

Peptidoglycan structure GUIDE QUESTION 3

• Porin proteins – Facilitate passage of small, hydrophilic

GRAM-NEGATIVE CELL WALLS

It is extremely difficult to stain mycobacteria by ordinary

Cell Wall As described previously

©Topnotch Medical Board Prep

✔GUIDE QUESTION IV. BACTERIAL GROWTH

Handwashing with soap and water: PHASE REMARKS

AEROBIC METABOLISM • Nocardia, Bacillus cereus, Neisseria,

VIII. INFECTION BIOLOGY

ENDOTOXINS IX. DIAGNOSTIC MICROBIOLOGY

GENERALITIES ON BACTERIAL STRUCTURE

SITES OF ACTION OF ANTIMICROBIALS

✔GUIDE QUESTION Which antibacterial agent (or combination of antibacterial agents) is

TYPES OF PARASITES What is the most likely etiology?

PARASITES OF MEDICAL IMPORTANCE

© Topnotch Medical Board Prep

PROTOZOA I. ENTAMOEBA HISTOLYTICA

• Stool culture – Robinson’s and Inoki medium, Diamond medium

SPECTRUM OF DISEASE: Amebiasis COMMENSAL AMOEBAE OF MINOR IMPORTANCE

II. FREE LIVING AMEBA

IV. TRICHOMONAS VAGINALIS TREATMENT

LEISHMANIASIS CUTANEOUS MUCO-CUTANEOUS VISCERAL

• Nasal stuffiness, discharge,

VI. TRYPANOSOMA CRUZI • Xenodiagnosis

VII. TRYPANOSOMA BRUCEI

Transmitted by tsetse fly bite. Trypanosoma brucei trypomastigotes.

LIFE CYCLE OF PLASMODIUM

• Late Phase (Meninoencephalitic stage)

Parasitemia Can be high Highest Low Low Lowest

Cerebral malaria No Yes No No No

Recrudescence Yes Yes No No Yes

Relapse No No Yes Yes No

Drug resistance Few Many Few Few Few

IX. BABESIA MICROTI

AREAS OF HIGH AREAS OF CHLOROQUINE

PHARMACOLOGY AND LIFE CYCLE -

XI. CRYPTOSPORIDIUM PARVUM

SPECTRUM OF DISEASE: Toxoplasmosis

• Presence of Salmonella in the intestines aggravate balantidiases

SPECTRUM OF DISEASE: Cryptosporidiosis

SHELLFISH POISONING SYNDROMES

Location Species Disease Transmission Treatment

SPECTRUM OF DISEASE: Ascariasis

• Acute intestinal obstruction

II. NECATOR AND ANCYLOSTOMA

SPECTRUM OF DISEASE: Hookworm Infection

Hookworm egg Buccal spears of filariform III. TRICHURIS TRICHIURA