Microbiology

⇨ Chest fungal infection due to neutropenic fever → asperigillous, candida don’t

make chest disease
⇨ Oxidase positive bacteria = possess cytochrome oxidase
⇨ Organisms that ferment lactose appear pink o MacConkey agar, black on EMB
agar
⇨ Cholera toxin is heat labile
⇨ Rash associated with Neisseria meningitides is due to small vessel vasculitis →
including palm & sole
⇨ Diagnosis of EBV:
- Monospot test → horse blood
- Paul Bunnell test → sheep blood
⇨ Anal masses are ulcerative in > 50% of cases
⇨ Wet mount in diagnosis T. vaginalis = saline microscopy
⇨ Gardnerella vaginalis is anaerobic gram variable rods
⇨ Foscarnet is administred IV route
⇨ S. Bovis endocarditis is unique that most of cases occur in patients without
preexisting valvular abnormality
⇨ Although there are many encapsulated bacteria, strept. pneumonie, Hemophilus
are by far the commonest cause of infection in SCD
⇨ Endocarditis after dental procedure in patient with MVP is very low and
antibiotics is not recommended, but cases can occur
⇨ The first stage of TB with unchecked intra-cellular growth take few weeks to
complete and macrophage begin to stimulate T-lymphocytes
⇨ Chloramphenicol cause dose dependent (reversible) & dose independent
(irreversible) aplastic anemia
⇨ Patients on mucor who respond initially to amphotrecin → switched to
posaconazole (monitor liver function tests on azole)
⇨ Genes encode for ESBL mostly on plasmid (transferred by conjugation) or
chromosomes, treatment is by carbapenems.
⇨ Gram negative is well known for the formation of sepsis, but gram positive
organisms also can form sepsis.
⇨ Miraviroc need tropism testing before usage
⇨ SSSS is caused by toxin against desmosome → damage into stratum spinosum
⇨ V. vulniferus typically occur in wound infection, may occur in oyster
consumptiosn
⇨ Aspergilloma can occur on top of any pre-exisiting lung cavity TB, Sarcoidosis,
emphysema
⇨ Neurosyphilis usually occur in tertiary syphilis but can occur at any stage
⇨ The only polyprotein (env, pol, gag) which is glycosylated is env protein to form
gp160 → cleaved to be gp 120, gp 41
⇨ Patients with HSV-2 are more contagious during recurrence
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 ⇨ HSV-1 can cause facial nerve palsy (not HSV-2)

⇨ The most common eye related complication of congenital CMV is chorioretinitis.
⇨ Tertiary neurosyphilis can cause tabes doraslis with locomotor ataxia
⇨ E.coli is the most common cause of UTI, and the commonest cause of UTI
bacteremia which can lead to septic shock, E.coli is B-hemolytic
bacteria
⇨ Some features of cat scratch disease: lymph nodes are tender usually affect tender
regional nodes, bacteria transmitted not only by scratch but also cat bites
❖ Describe Thayer-Martin medium? It is selective medium containing chocolate sheep
blood agar infused with vancomycin (to inhibit Gram positive bacteria), Colistin
& TMP (to inhibit gram negative bacteria), Nystatin (to inhibit yeast)
❖ Different clinical picture between EBV and CMV mono-nucleosis:
1) Sore throat & lymph nodes → pharyngitis & lymphadenopathy are typically
more common in EBV
2) Monospot test → usually the test is negative early in the disease, repeating after
one week either confirm EBV (positive) or CMV (negative)
❖ Sources of prevention from infection by influenza virus:
- The most important source of protection is antibodies directed against
hemagglutinin
- Antibodies to neuroaminidase are no the mainstream of rotection although have
some rotective effect
❖ Describe the immunological response against shistosomiasis:
- Th2 mediated granulomatous response against eggs → eosinophils, M2
macrophages → fibrosis & ulceration , scarring of the bowel / bladder → may
cause peri-portal / pipestem fibrosis
❖ What is the treatment of cryptococcal meningitis

❖ Clinical picture of disseminated gonococcal infection:

- Either frank urulent arthritis or triad of arthralgia, tenosynovitis & dermatitis
- Always there are overlap between the 2 syndromes \
- Although S. aureus is the commonest cause of septic arthritis, put Gonococci in
mind especially with seually active females, other DGI findings
❖ Causes of diarrhea with peripheral eosinophilia:
It denote parasitic infections → Strongyloides, Ancylostoma, Ascaris, Toocara,
Trichnella (not Goradia, Entameba)
❖ How to differentiate between fast lactose fermenter Gram negative rods:
- Indole test (ability to convert tryptophan to indole) is positive in E.coli but
negative in Enterobacter
❖ Non bullous impetigo:
• Blistering eruption usually perioral lead to formation of golden yellow crust,
usually seen in children and newborns

 • Mostly by Staph. aureus, less commonly by strept. pyogenes

• Following after 1-2 weeks → PSGN may occur due to immune complex deposition
and complement activation. (generally; PSGN > ARF)
❖ Hot tub folliculitis:
- Superficial pseudomonal infection of the hair follicle
- Pruritic, papuloustular rash, occur in outbreaks from public, hotel swimming or
hot tubs.
- Often begin with exposure to watersource or creation of a moist environment

❖ Intracytoplasmic & intranuclear inclusions in case of CMV,

owl eye appearance is due to perinuclear halox

❖ Clinical picture of dengue fever:

- There are two types of Dengue fever presentation; either classic Dengue fever or
hemorrhagic fever
- Primary infection is usually self limited or asymptomatic ➔ cause lifelong
immunity against the same serotype
- Secondary infection with another serptypes cause very severe serious illness due
to IC formation, accelerated T-cell response
- It also associated with ↑↑ liver function tests, leukopenia

 ❖ What is the classical clinical triad of meningitis important for diagnosis → high
fever, stiff neck, DCL
❖ Describe the process of detecting acid-fast bacteria:
- First, bacteria is treated with aniline dye (cabolfuchsin), taken up by the cell wall
(bind with mycolic acid in TB) → stain red
- Then the bacteria is treated with acid & alcohol which dissolve the outer
membrane of ordinary bacteria (cannot occur in TB due to mycolic acid)
- Counterstain dye is used (methylene blue) and taken up by non TB bacteira (non
color)
- So acid fast decolorisation → red, non-acid fast → blue
❖ Pathogenesis of cryptococcal meningitis: initially, the bacteria invade the
lung where it form initial asymptomatic lung disease, then
hematological spread to the blood → meningeal irritation
❖ What are the common causes of vaginal candidiasis:
• Antibiotic use *** (↓↓ lactobacilli)
• ↑↑ estrogen levels
• ↑↑ steroid therapy
• DM, HIV
❖ Difference between atropine like effect and botulinum toxicity:
- The main difference is effect on muscle action
- Botulism → ↓↓ release of Ach → ↓↓ nicotinic and muscarinic effect → ↓↓
compound muscle AP (CMAP; electrical response of the muscle) and improvemet
on repetitive AP stimulation ➔ diplopia, dysphagia, dysphonia occur
within 36 hr.
- While anticholinergic effect → block only muscarinic → no alteration in CMAP
with no effect on NMJ
❖ Therapeutic function of botulism, cons and pros:
- Injection of botulinum toxin type B → ↓↓ release of Ach in NMJ
- Regeneration of the nerve endings occur in 3 months so the therapeutic effect is
temporary

 ❖ Gingiva-stomatitis:
- The disease occur in infant (primary herpetic lesion), when recur in adult it cause
cold sores
- Peak age = 6 months – 5 years
- Begin by viral prodroe with latent perio 1 week
- Vesicular lesions seen on lips, hard palate
- Accompanied with fever and cervical lymph nodes
- Vesicles occur due to cell lysis, necrosis, fluid accumulation between dermis &
epidermis → due to pain, it lead to dehydration → commonest cause of
hospitalisation
❖ What is the main Virulence factor of salmonella in SCD OM: it has special
capsule called “Vi (virulence) antigen” which protect the bacteria from opsonisation,
phagocytosis. In SCD, vasco-occlusive crisis cause focal areas of bone necrosis →
can be nidus for infection
❖ Toxins responsible for ecthyma gangrensum and role of each:
- exotoxin A: protein synthesis inhibiton
- elastase: degrade elastin (important for BV detruction)
- phospholipase C: destroy cellular membrane
- pyocyanin: release ROs
❖ Clinical picture & pathogenesis of Ecthyma gangernosum:
- Strongly associated with pseudomonas bacteremia (common in febrie
neutropenia where absolute neutophilic count is < 500)
- It is due to perivascular bacterial invasion of arteries an veins in the dermis and
SC tissue → release of exotoxins
- Appear as skin patches with necrosis and ulceration due to ↓↓ blood flow
❖ Causes of non EBV mononucleosis: CMV, HIV, Toxoplasmosis
❖ Pathogenesis of IMN:
- EBV infect and replicate in the pharyngeal mucosa & tonsillar crypts, then the
bacteria gain its access to blood
- Once enter the blood, the EBV gp350 bind to CD21 (CR2) which is the cellular
receptor for C3d complement
- When infect the B-cells → meake the B-cells enter the cell cycle and proliferate
continuously (immortalization); This action occur when EBV-encoded oncogenes
→ inhibit apoptosis
- Immunocompetent people; immune response hold B-celproliferation but
maintain the ability to form Igs with no complete virions release (so no EBV
antigens circulate in the blood)
-
- Tc cells (CD8) cloncally expand in response to destroy virally infected cells →
these CD8 cells cause the atypical lymphocytosis
❖ Pathogenesis of the Neisseria meningitides:
the bacteria colonize the nasopharynx then the bacteria penetrate the epithelium and
enter the bloodstream, when the bacteria penetrate the capillary endothelium or the
choroid plexus

 ❖ Specific microbiological character so EHEC: Don’t ferment sorbitol, don’t produce

glucurinidase
❖ Clinical picture suggestive of legionnaire disease: it is no specific, but anyptient
with radiographic evidence of pneumonia & very high fever with GIT
symptoms (e.g. diarrhea) should suggest the diagnosis
❖ Role of vitamin A supplementation in measles:
- Acute measles deplete vitamin A stores → ↑↑ risk of keratitis, corneal ulceration
- Vitamin A here prevent & treat these ocular complications
- ↓↓ risk of other comorbidities, recovery time, length of hospital stay
❖ Cause of hyponatremia in legionnaire disease:
- Related to inappropriate ADH secretion, renal tubuloieterstitial disease impairing
Na reabsorption due to either effect of Leigonella, cytokines
- May be associated with ↑↑ ALT, AST
❖ Mention the characters of post herpetc neuralgia: occur mainly in old patients >
70%, with persistent of local dermatomal pain for several months following zoster
eruption
❖ Mention the effect of ether and organic solvent on microbes:
Ether and other solvent lead to inactivation of the enveloped viruses (which have
outer lipid bilayer coat acquired from the host cell plasma membtane) indering
them non-infective
❖ Mention the (role not mechanism) of the virulence of pertussis in disease process
- Pertactin → basis of the vaccine, adherence to the URT
- Tracheal cytotoxin → destruction of tracheal tissue, cause cough
- Pertussis toxin → prevent effective phagocytosis → prolonged disease course,
lymphocytosis
❖ What is the mechanism of edema factor in B.anthracis:
- Protective antigen is needed to induce the toxin inside the cell (obligatory)
- EF → act as calmodulin dependent adenylate cyclase that ↑↑ cAMP →
accumulation of fluid between cells, ↓↓ neutrophil and macrophage function.
❖ Mode of transmission & clinical presentation of Campylobacter jujeni:
- It is the commonest cause of acute GE in children & adults in industrilised
countries
- Cuase inflammatory diarrhea (initially watery then bloody), cramoing and EBCs
in stool. May mimic appendicitis
- Caused by transmission form domestic animals as cattle, sheeps, dogs, also
transmitted by milk and poultry
❖ Pathogenesis of sporotrichosis:
- The fungus enter the skin through breaks (thorn prick) causing intial reddish
nodules that ulcerate later
- The fungus ascend through lymphatic’s forming SC nodules and ulcers
- The L/M of the lesion show typical granuloma formation

❖ Mechanism of action of alcohol as disinfectant :

• It include ethanol, isopropanol

 • It cause denaturation of protein (while chlorhexidine cause coagulation of

cytoplasm) → when mixing with chlorohexidine it is best used in surgical and
percutaneous procedures
• Require water for maximal activity, mostly at concentration of 60 – 90%
concentration
• They are effective against bacteria, TB, fungicidal, virus
• Formaldehyde and glutaraldhyde function by alkylating and cross link DNA and
protein
❖ Prophylactic measures against rabies:
-
- Prophylactic vaccines is recommended for individulas at high exposure risk
- After bite, postexposure prophylaxis with Ig, vaccine. If Rabies virus reach to the
brain and cause encephalitis, post-exposure prophylaxis is useless and all
patients die
- The rabies vaccine is inactivated by β-propiolactone
- Important clue for diagnosis is parasthesia radiating proximally from a wound
site
❖ Clinical picture of arisch Herxiemer reation:
Development of acute febrile illness few hours after penicillin / antibiotic for
spirochetal infection due to rapid lysis of spirochaetes and spillage of its
components into the blood
❖ How Corynobacterium gain its pathogenicity:
- Through process of lysogenization, which is specialized transduction
- Corynophage beta infect the cell and contain Tox gene, incorporated into the
bacterial genome
❖ Mentions infections that predispose to GBS other than C. juejuni.
URT viral infections, EBV, CMV, HIV, Zika virus, influenza
❖ What is the compositon of pseudomembran ein diphtheria: diphtheria bacteria,
WBCs, fibrin, necrotic epithelium with tight binding with the underlying mucosa
❖ Treatment of PID: 3rd generation cephalosporins (for gonorrhea) +
azithromycin / doxycycline (for chlamydia)
❖ Which drugs added to gancyclovir lead to severe BM suppression. Zidovudine
SMX-TMP

❖ Mention the lifecycle of strongyloides stercoralis :

 - Infection is made by penetrating the skin by filariform (infectious) larave from

soil. Feces, most commonly in wet reas in southern Asia
- The diagnoss is made by localization of rhabditiform (non infectious) larvae in
stool
- Associated with Larva currens: as the larva migrates SC to the thigh and
buttocks away from the perianal region.
- Diagnosis is made by finding the non infectious larvae in the stool, as egs not
found except in the intestinal biopsies

 - Hyperinfection may occur as the eggs hatch I the intestine to non

infectious larvae may transform into infectious ones and autoinfect
the intestine → more common occur in immunosuppressants ,
HTLV-1
❖ Casues of eosophigitis in HIV patients:
- Commonestis candida√√, CMV (large linear shallow ulcerations at distal
esophagus), HSV -1
❖ Causes of resistance to HAART :
⇨ The main cause of HAART resistance is continuous mutation sin the HIV genome
make it escape from death
⇨ Pol gene mutation → responsible for the emergence of HIV protease variants, also
responsile for changes in reverse transcriptase (remember that pol gene
responsible for reverse transcriptase, protease, integrase)
⇨ Env gene Mutation → responsible for formation of escape mutants that that no
longer susceptible to host antibody neutralization
❖ Cause of genetic instability of HCV genome:
1) Hypervariable genomic regions that found in envelope glycoproteins
2) No proofreading 3’ → 5’ exonuclease activity in RNA dependent RNA polymerase
→ multiple genetic error during action of RNA polymerase
⇨ Most patients are infected b single genotype → high mutation rate after infection
(especially in envelope glycoprotein) → continuous variations halt any effective
immune response
❖ Commonest causes of bacterial meningitis:
- Strept. pneumonie is the commonest cause of bacterial meningitis at
all age groups
- Menningiococci is the 2nd most common cause in patients < 60 years
- Gram negative rods are the 2nd most common cause in patients > 60
years negative
❖ Clinical progression of Woolsorters disease:
After inhalation, bacteria ingested by mediastinal lymph nodes → toxin act to
destroy the lymph nodes causing hemorrhaging mediastinitis → septic shock & death
❖ Appearance of B.anthracis on colonies: long adherent chains that descrbed as
“serpentine” or “medusa head” on appearance
❖ Mechanism of biofilm production instaph. epidermidis:
- Any FB enter the bood, surrounded by many proteins including fibrinogen,
fibronectin
- These proteins act as binding sites for the bacteria which attach to these proteins
- Then the bacteria multiply and communicate with each others to induce synthesis
of extracellular polysaccharide matrix which encase the bacteria → hiding it from
antiiotics, killing
- These biofilms can disperse and seed into blood stream, only definitive treatment
is FB removal
❖ Mechanism of action of oseltamivir.

 - Shorten the corse and complications of influenza A, B infections if taken within

48 hr. of the onset of symptoms
- Slow viral penetration of the mucuous secretion that protect respiratoy
epithelium. (prevent influenza)
❖ Medium used for cholera: TCBS (thiosulfate citrate bile salts sucrose) agar
❖ Adverse effects of NNRTIs:
1) Hepatic failure → Abrupt onset flu like symptoms, pain, fever, jaundice (mostly
during first month of therapy)
2) Rash → may lead to SJS, TEN
❖ Treatment of diphtheria infection:
1) Antitoxin → which inactivate blood toxin, ineffective against toxins enter the
nerves
2) Antibiotics (penicillin & erythromycin) →kill the bacteria, no new toxins appear
3) Active immunization
❖ In case of HBV infection, which serological marker appear before the symptoms,
which after:
• HBsAg (1st), HBeAg, HBV DNA → appear before the symptoms
• ALT, anti-HBc IgM → shortly before the symptoms
❖ Mechanism of HCC in case of HBV infection.
1) Integration of viral DNA with host genome
⇨ Protein HBx activate IGF-II, IGF-IR → ↑↑ cell proliferation
2) Suppression of P53
3) Chronic inflammation lead to accumulation of mutations in hepatocytes.
❖ Describe the process of transformation, examples:
- Hemophilus, streptococcus, Neisseria, Bacillus

❖ Mention Extra-pulmonary manifestations of mycoplasma∷ SJS, joint pain,

encephalitis, cardiac arrhythmia, bullous myringitis, AIHA
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 ❖ What is the receptor of mycoplasma: bind to oligosaccharide (I-antigen) that

present on oth respiratory epithelium and erythrocyte
❖ Mechanism of action of protein A of staph. aureus
Protein A bind to the Fc portion of the IgG antibodies at the site of the complenment
binding site → ↓↓ complement activation
❖ Microbiological features of bacteroides & treatment :
- They are gram negative anaerobic rods that produce β lactamase enzymes
- Can be effectively treated with penicillins + lactamase inhibitors
❖ Side effects of dapsone treatment :
- fever, rash
- hemolytic anemia with G6PD deficiency
- methemoglobinemia
❖ risk of sexal transmission between HBV, HCV
- HBV → most common mode of transmission in developed countries > 70%
- HCV → can occur but inefficient, with risk very low with incidence of 0.07% per
year
❖ Difference in action between vancomycin and penicillin:
- Penicillin → it has the same structure as D-Ala D-Ala → bind to PBP
(transpeptidases one of them )→ cross link the peptidoglycan in cell wall)
- Vancomycin → glycopeptide antibiotic → bind to the cell wall glycol-protein (D-
ala itself) which revent transpeptidase from forming the cross links
❖ Mechanism of resistance to ceftriaxone : alteration of thepenicillin binding globulin
composition which prevent ceftriaxone binding, production of β lactamase is not a
mechanism of resistance here
❖ Foods associated with HUS:
- More in children < 10 years, EHEC + antibiotics
- Undercooked ground beef, person to person contact in families and childcare
- Drinking unpasteurized milk
- Swimming / drinking from sewage contaminated ater
❖ Commonest cause of traveler’s diarrhea:
• Mostly due to ETEC presented by watery diarrhea + abdominal cramping, N & V
+/- ow ggrade fever
• Occur in travelers to developing countries, poor sanitation
❖ Difference between dissiminated TB & MAC intracellular :
- MAC → more marked anemia, HSM, ↑↑ ALP & LDH due to widespread
involvement of the RES
- More higher temperature than TB
- The best temperature for growth in vitro is 41C
- Treated by WEEKLY Azithromycin
❖ mention the different chemotherapeutic prophylaxis in contact s with meningitis:
1) Oral rifampin √√
2) IM ceftriaxone (not preferred due to IM route)
3) Ciprofloxacin (not in children)
⇨ Best if taken within 24 hours of diagnosis

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 ❖ Clinical picture of pharygo-conjunctival fever:

- Caused by adenovirus in outbreaks
- Acute onset of fever, cough, congestion, pharyngitis, conjunctivitis
❖ Clinical picture of aseptic meningitis:
- Caused by enteroviruses in >90%
- Similar presentation like meningitis but less severe, with ususally absent focal
neurological signs, seizures, DCL
- CSF is a must → negative gam stain, sterile culture
❖ Mention the virulence factors of shigella:
(The most common in US is S. Sonnei, mainly in pediatrics)
• Mucosal invasion ***: is the most essential factor in pathogenicity, it invade
the GI mucosa (M cells of Peyer’s patches) → lyse the phagosome and spread to
the adjacent cells by actin poymerisation
• Shiga toxin → this toxin play minor, no essential role in pathogenecity, as non
toxogenic strains also do the sam disease
❖ Mention organsims cause diarrhea with very low infectious inoculum:
1) C. jeujeni
2) Shigella

3) Entameba histolytica
4) Giardia lamblia
❖ Clinical picture of bacterial vaginosis :
• No vaginal inflammation yet there is mild pruritis
• Grayish white vaginal discharge with fishy odor
• Treatment of the partner is not recommended
❖ Mechanism of achalasia in T.cruzi:
- Transmitted by Reduviid bug
Parasite related inflammation and immune mediated cross reactivity between the
parasite and eneteric ganglia → destruction of plexuses of nerves
❖ L/M of Trypanosoma cruzi:
Slender of C / U shaped flagellated parasite with darkly staining nucleus and
kinetoplast

❖ What is meant by ribosylation of EF-2: exotoxin transfer ribose form NAD to

histidine on EF-2 → inactivation
❖ Clinical picture of acute & chronic Q fever:
• Acute Q fever:
- Lobar pneumonia

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 - Fatigue, myalgia and other non specific febrile illness with Fever > 10 days
- Severe retro-orbital headache
- Normal TLC, ↓↓ platelets, ↑↑ LFT
• Chronic Q fever: fatal, gram negative infective endocarditis
❖ Clinical picture of vaginitis:

❖ Mention the special characters of children rash caused by chickenpox → pruritic,

vesicular rash with different ages
❖ Mention the special characters of children rash caused by parvo virus → slapped
chee appearance
❖ Mention the special characters of children rash caused by rubella → occipital & post
auricular lymph nodes
❖ Mention the special characters of children rash caused by measles → Koplik spot,
conjunctivitis
❖ Mention the special characters of children rash caused by Roseola → rash appear
after fever subside
❖ Mention the special characters of children rash caused by Scarlet fever:
- Associated always with strept pharyngitis
- Inflamed tongue giving the strawberry appearance
- Rash: begin at flexures → boiled bloster appearance → then become sandpaper
like rash
- Flushed cheeks with circumoral pallor, at the end desquamation occur at the groin
❖ How to prevent HIV transplacental transmission:
- All pregnant women are advised to take HAART (risk of transmission reduced
from > 35% to only 1 – 2%)
- ART should be continued during breastfeeding period
- Infants are advised fro several weeks of prophylaxis by AZT (ziduvudine)
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 - Any teratogenic ART is avoided

❖ Characters of HSV encephalitis:

• HSV-1 priamry infection or reactivation →travels through olfactory nerve →
temporal lobe edema / hemorrhage
• Unilateral involvement is most common (+/- bilateral)
• CSF show hemorrhagic lymphocytic pleocytosis with ↑↑ Opening pressures &
protein
❖ Microscopic characters of diphtheria: nonmotile, found in clumps (chinese
characters) or joined in V or Y shaped, contain metachromatic granules that stain
with aniline dye (methylene blue), they are non motile
❖ Mechanism of CCL4 hepatic toxicity :
Metabolized in liver by Cytochrome P450 enzymes → form free radicles → lipid
peroxidation → form new free radicals ➔ rapidly liver toxicity
❖ Microbiological characteristic of Klebseilla pnumonie:
- Occur mainly in alcoholics, colonization of oropharynx followed by
microaspiration of upperway secretions
- The hallmark is mucoid capsule which appear as halo around bacteria

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 ❖ Granuloma inguinale (donovanosis):

• What is donovanosis∷ granuloma inguinale (donovanosis)
• Causative organism of donovanosis∷ klebseilla granulomatis
• Clinical picture of donovanosis: extensive painless progressive serpingious
ulcerative lesions without lymph nodes
• Diagnosis of donovanosis: either by gram stain (difficult, will show Gram negative
bacteria), deeply stained intra-cytoplasmic cysts can appear (Donovan bodies)

15

 ❖ Methenamine silver stain

❖ Chancroid:
• Clinical picture of Chancroid: painful deep ulcers with ragged borders & grey
exudate, painful inguinal lymph nodes, not present in US
• Causative organisms for Chancroid: hemophilus ducreyi, gram negative curved
rodes with clumping pattern
❖ Clinical picture of allergic broncho-pulmonary asperigillosis (ABPA):
- Occur mainly in asthma, cystic fibrosis patients → allergic hypersensitivity
reaction to the fungus.
- Very serum IgE, eosinophilia, IgE + IgG aspergillus.
- Repeated exacerbations may produce transient pulmonary infiltrates, proximal
bronchiectasis.
❖ Microbiolgical features of bites (cat, dog, human)
- Pasteurella multicoides → mouse like odor due to indole positivity
- Treatment of dog bites → Augmentin®
- Other bacteria in dog bite: capnocytophaga canimorsus

16

 ❖ What affect the tropism of the enveloped virus:

- The extent to which the viral surface proteins can bind to complementary host
cell plasma membrane receptors
- The ability to attach to the host cell generally depend on if the viral envelope
glycol-protein can bind to host cells with high affinity.
- Mutation of capsid protein, RNA polymerase, endonuclease non specifically
affect viral replication
❖ Clinical presentations of nocardia:
Common in immunecompromised patients with TB like lung disease, brain abscess
and cutaneous involvement, differentiated by sputum analysis which show Gram
positive branching / beaded organism
❖ Prevention and treatment of neonatal tetaus:
• Prevention by giving the mother the tetanus toxoid vaccine which provide the
fetus with Igs → ↓↓ risk by 95%
• Treatment include antibiotics & immunoglobulins
• N.B. tetanus vaccine is not given to neonates, usually the first dose is given at
age of 2 month
❖ Parvovirus B19:
• Describe the rash progression of Parvovirus B19: after 1 – 2 weeks IP,
nonspecific prodrome is followed by Slapped cheek rash (spare the nasolabial
folds, after the initial symptoms have resolved), then followed by lacy reticular
rash spreading over the trunk & extremities.
• Cycle of replication in parvovirus B19: replicate in the erythrocyte
precursors in the BM (which express blood group P (globoside) → cellular
receptor for parvo B19) → IC deposition & IgM, IgG and ↑↑ levels.
❖ Describe the immune response against histoplasmosis:
• Alveolar macrophage engulf the yeast, but the pathogen elude macrophage
mediated destruction of phagolysosome and replicate in unchecked fashion.
Drainage to the mediastinal lymph nodes → cellular immune response
❖ Why mucormycosis is common in DKA, describe its route of infection:
■ Infection always acquired by spore inhalation → ascend from nasal passages to
the sinuses → pass through the cribriform plate to reach the brain →
rhinocereberal mucromycosis
■ In DKA → ketone reductase activity of the rhizopus → allow it survive in acidic
medium, also due to ↑↑ iron release from binding protein during ketoacidosis
which facilitate its growth
■ It must be differentiated from aspergillosis by biopsy
❖ Tzank smear → multinucleated giant cells:

17

 ❖ L/M of mucormycosis: they contain many species as Mucor, Rhizous, Absidia

❖ L/M of blastomycosis : large yeast (> RBCs) with a single broad based bud
Immunocomptent → lung disease, flu
like symtoms
Immunocomprimised → dissiminated
disease with lytic bone involvement

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 ❖ L/M of coccidioides: spherule packed with endospores, the spherues may be

ruptured or empty, the main difference between it and histoplasma is the
size compared to RBCs, spherules are larger than RBCs, while in
histoplasma they are much smaller than RBCs

❖ L/M of histoplasmosis: macrophages with intracellular ovoid / round yeasts

❖ Clinical picture of cryptococcal infection

• The infection occur only in immunocomprimised (any cause), no man – to – man
transmission.
• First infection is lung (route of infection) → mainly asymptomatic
• The main burden is meningioencephalitis
❖ Clinical picture of scabies infection.
• Highly pruritic (more at night) rash with excoriations, small crusted papules →
due to type IV hypersensitivity against mites, eggs
19

 • Mostly affect flexors of wrist, finger webs, lateralsurface of the finger

• The most important findings is linear burros → confirm by L/M
❖ Gross and L/M of actinomycosis:
• Gross: sulfur granules appear yellow which are formed by calcified bacterial
filaments
• L/M: H&E sulfur granules appear as amorphous basophilic appearance, while the
bacteria appear as branching gram positive bacteria
• They normally colonize the mouth, colon, vagina

❖ Mention the renal toxicities associated with amphotrecin B:

1) Renal vasoconstriction, ↓↓ GFR
2) Direct toxicity on renal epithelial cells → ATN, RTA
3) Severe hypokalemia, hypomagnesaemia → due to damage in DCT
4) ↓↓ EPO production
❖ Clinical picture of West Nile fever virus:
- Occur in warm climate, more common in the summer by Culex bite
- Mostly: flu like illness + rash on back & chest
- Neuroinvasive: more in older, organ transplant → encephalitis,
meningitis, asymmetrical flaccid paralysis + parkinsonian features
- Diagnosis is made by clinical picture + CSF with viral pattern with PCR is not
often needed
❖ Microscopic appearance of the giardiasis:
Ellipsoidal cysts with smooth, well defined walls, +2 nuclei, may be appeared as pear
shaped, flagellated trophozites.
❖ Mention cephalosporin resistant bacteria causing meningitis. Listeria,
MRSA, enterococci, atypicals
❖ Causes and clinical picture of septic abortion:
- Due to infection of retained products of conception → fever, abdominal pain,
uterine tenderness, foul smelling vaginal discharge
20

 - Staph. aureu (the commonest pathogen), less common is E.coli, GBS → all
these are normal vaginal flora
❖ Clinical features, causes of necrotizing fasciitis:

❖ Clinical picture of babesiosis:

• Babesiosis / malaria are suspected in any patient with febrile illness with intra-
erythrocytic ring inclusions
• Babesiosis → more in northeastern USA (as Lyme) both which transmitted by
Ixodes (alos anaplasmosis)
• May be associated with anemia, LFT → intravascular hemolytic anemia
• More common in asplenic patients → severe infections mauy form ARDS
• Blood film may show maltese cross rather than ring inclusions

❖ Commonest pathogens causing nosocomial bloodstream infections: staph.

aureus, Staph. epidermidis, enterococci, candida

21

 ❖ L/M of Cryptococci
Budding yeast with thick polysaccharide capsule, stained by either india ink or
mucuramine stain

❖ Charcters and sites of candida albicans.

• They are normal flore in skin, mouth, vagina, intestine
• They are yeast (one cell) → appear as budding yeasts with pseudohyphae
• For candida albicans, germ tubes are diagnostic → inoculation of the organism
at 37 for 3 hr. → true hyphae form the yeast

22

 ❖ Type of meningococcal vaccines available in US & their use.

• Quadrivalent conjugate vaccine: capsular polysaccharide antigen (A,C,Y,W)
conjugated to diphtheroid toxin carrier → presented on MHC of APCs
⇨ Part of routine immunization
• Sero-group B vaccine: because capsular polysaccharide against serogroup B is
very similar to human protein. The vaccine is available in recombinant form
⇨ Specific high risk population e.g. asplenia, complement deficiency
❖ Infantile HBV infection:
• In maternal HBV, what are the risk factors for transmission to infant?
Maternal viral load & HBeAg are the strongest risk factors for infant infection,
with chance >95% of acquiring infection when HBeAg are Positive, (when
negative → 20%). Most transmission occur transvaginally during birth, btmay
occur transplacental
• Clinical picture of infantile HBV due too placental transmission.
- The damage in HBV is due to immune response of the body rather than the
virus itself.
- In infants due to immature T-cell system, the infants enter immune tolerant
phase of chronic HBV infection with normal liver functions
- Over time (without treatment or vaccine) very high risk for progression to
cirrhosis & HCC (90%) so ASAP give the infant vaccine and immunoglobulin.
❖ Optimum temperature of autoclaving.
The optimum temperature is ~ 134 C (spores can resist temperature up to 120)
❖ Describe the chemical composition of peptidoglycan
- Major component of cell wall in both G+ve, G-ve bacteria.
- Composed of linear glycan of 2 alternating sugars (N-acetylglucosamine, N-
acetylmuramic acid) which cross linked by short peptides.
- The enzyme glycosyltransferase add glycan molecules to the growing
peptidoglycan chain
- Responsible for the bacterial shape and cell lysis
❖ Composition and function of M-protein in GAS.
M-protein (alpha helical coil, coil protein) share the structure of tropomyosin &
myosin → major virulence factor of GAS, its major function is prevent phagocytosis,
↓ complement bindings, epithelial attachment

23

 ❖ Viral composition of HEV: it is single stranded non enveloped RNA virus

❖ Mechanism of resistance of INH:
- Mutation & → ↓↓ expression of the catalase – peroxidase enzyme
- Modification of protein target binding site for INH
- What is the role of capsule in Hemophylus ib in infection.
Polysaccharide capsule composed of polymer polyribosylribitol phosphate (PRP) →
protect the bacterium against phagocytosis & complement mediated lysis by binding
factor H (which is circulating protein normally ↓↓ C3b deposition on host cells)
❖ Most common bacteria cause intra-abdominal abscess.
They are usually polymicrobial, most common is Bacteroides fragilis √√ (tend to
cause abscess), E.coli, enterococci, streptococci
❖ Mention the virulence factors of E.coli and role of each of them in disease

❖ Mechanism of action of zidovudine (AZT)

AZT bind to the reverse transcriptase enzyme incorporated at viral genome as
thymidine analog with modified 3’ end (replacement of –OH group with azido
group) → chain termination and prevent chain elongation.
❖ What is the composition & role of cord factor in vivo & vitro:
- Composed of mycolic acid + trehalose (dimycolte trehalose)
- Vitro: the cord factor form hydrophobic urface glycolipid → cells arranged in
serpentine cords
- Vivo:
o It form cylindrical micelles surrpund the organism and prevent macrophage
mediated destruction in phagosome
o Form toxic crystalline monolayer → caseation
❖ Infections caused by Listeria:
• Immunocomprimised (↓↓ cell mediated immunity) → sepsis, meningio-
encephalitis

24

 • Pregnancy → greatest risk at 3rd trimester, flu like symtoms, preterm infant
with neonatal sepsis
• Food borne infection → as it can multiply in refrigerator in both anaerobic &
microaerophilic conditions, it cause febrile gastroenteritis
❖ Importance of cat in pathogenesis of toxoplasmosis. Cat feces contain oocytes
while meat contain pseudocysts
❖ Treatment of toxoplasmosis
⇨ Pyrimethamine + (sulfadizine / clindamycin )
⇨ Folinic acid
❖ Type of EMB agar.
It is selective and differential medium used to osolate & identify enteric pathogens
with multiple bacteria, lactose fermenters bind to the dye → green metallic sheen
❖ Cellular components of primary CNS lymphoma
- PCNSL is diffuse large non Hodgkin lymphoma composed of B-cells
- While T-cells accumulated is AIDS associated T-cell lymphoma
❖ Type of immunity activated by tetanus vaccine.
Tetanus is toxoid vaccine (formaldhyde inactivated) so it activated only humoral
immunity → antibodies against toxin (antitoxin)
❖ Difference between T.solium infection and neurocytisrcosis:
• Ingestion of eggs from stool of tapeworm carriers lead to cystisercosis, while
ingestion of infected undercooked pork which contain larval cysts lead to teniasis
❖ Difference in rash between rubella & rubeola
• Rubella: post auricular lymph nodes, faster rash spread
• Measles: coalescent & darken, slower spread, Koplik spots , conjunctivitis &
Coryza
❖ Enumerate the intra-cellular organisms (obligate & facultative)

25

 ❖ What are the measures sould be taken to ↓↓ GBS infections.

• Universal prenatal screening for GBS by vaginal & rectal culture at 35 – 37 weeks
• If Positive or previous baby with GBS → intrapartum antibiotics (penicillin √/
ampicillin
❖ Mechanism of action of C. difficile toxins:
- They are toxin A (enterotoxin), toxin B (cytotoxin) , both actions are overlap bbut
toxin B is more virulent
- Both; inactivate Rho-regulatory proteins (involved in signal transduction),
actin cytoskeletal structure maintenance → disruption of intra-cellular
tight junctions→ cellular retraction → paracellular intestinal fluid secretion
- Some additional actions; neutrophil recruitment (inflammation), induce
apoptosis
❖ Describe the life cycle of HBV.
• It is partially dsDNA molecule, replicate through reverse transcription.
• Once entered, the repaired dsDNA act as template for single stranded mRNA
• RNA act as template for translation of viral proteins and reverse transcription into
ssDNA intermediate → partially ds DNA

26

 ❖ C. difficile is a normal flora, when they become symptomatic.

The intestinal microbiome (mostly anaerobic) suppresses overgrowth of C.difficile by
competing for nutrients and adhesion sites within the gut., common antibiotics →
clindamycin, penicillin, cipro, cephalosporins.
❖ Why listeria is common at extremities of age.
Patients with impaired cell mediated immunity are greatest risk for invasive listeria
infections particularly at extremities of age & immunocomprimised
❖ Describe the rash of measles:
• Rash occur after the viral prodrome of symptoms
• Maculopapular rash (exanthema) start on face and spread downwards sparing
palm & sole, differentiated from rubella that here the rash is usually
coalescent & darken

27

 ❖ Clinical picture and diagnosis of giardiasis :

• May be asymptomatic or watery diarrhea, malabsorption.
• Diagnosis by microscopic analysis of stool or fecal immunoassay
• Biopsy will show villous atrophy & crypt hyperplasia (similar to celiac disease)
❖ Describe the lining of hydatid cyst.
• Inner wall consinsts of inflammatory reaction involve monocyte & esoinophils +/-
egg shell calcification
• Outer wall is composed of gelatinous sheets surrounded by thick fibrous capsule
• Unilocular → E. granulosus, multilocular → E. multilocularis
❖ Mention the mechanism of emergence of swine flu epidemic:
- Influenza virus is RNA segmented virus with two main virulence (HA, NA) each
of them occur in different segment of RNA which allow for genetic reassortment
- So the emergence of different strain with different tropism (human
instead of swine or vice versa) is best explained by reassortment
- Influenza A virus can infect birds, if avian coinfection with human influenza A,
animal influenza A → human type HA and animal type NA → bot are on same
virion → emergence of novel strain or human with no immunological resistance
❖ Mention the very specific adverse effect associated with abacavir:
- Abacavir hypersensitivity reaction (AHR) is an allergic reaction in 2 – 8 % of
patients and strongly associated with HLA-B 57:01 allels
- The drug binds directly to this allele → production of self antigens → type IV
hypersensitivity reaction.
- Clinical picture is fever, GI symptoms and delayed rash
- Absence of the HLA-B 57:01 allele has 100% NPV for AHR
❖
❖ Characters of HSV genital infection and diagnosis
• Multiple superfifical painful ulcers with erythematous base & dysuria (vesicles are
usually absent )
• Diagnosis is made by PCR, direct fluorescence antibody, viral culture XX, Tzank
smear

28

 ❖ What are regulatory genes involve in HIV infection

❖ What is the mechanism of action of miraviroc, enfuvirtide?

- The gp120 on HIV bind to CD4 molecules (as primary receptor), and also bind to
CCR5 / CXCR4 (as coreceptors)
- Binding of BOTH → conformational changes of gp120 → express underlying gp41
→ fusion of the virus to host cells
- Miraviroc → it antagonize CCR5/CXCR4 → which are the chemokine receptos
→ prevent expression of gp41
- Enfuviratide → block gp41 itself
❖ Describe the mechanism of actions of caspofungin:
- It inhibit the synthesis of fungal cell wall by inhibit formation of 1,3 β-glucan
- Most active against → candida, aspergillus
- Limited against → Mucor, Rhizopus
- Not active against → Cryptococci
N.B: terbinafine → inhibit squalene epoxidase → ↓↓ ergosterol synthesis

29

 ❖ Describe the different stages of giardiasis:

• Trophozoite (pathogenic stage): bilaterally symmetrical pear shaped organism
with multiple flagella & 2 nuclei giving the owl’s eye appearance
• Cyst (infective stage): oval shaped with up to 4 nuclei

30

31

 ❖ Cryptococcus neoformis appears as budding yeast under India ink stain

❖ Cyto-Megalo virus (CMV) infection: Enlarged cells with basophilic intra-nuclear
inclusion bodies
❖ Lyme disease :
• Early disseminated phase: facial palsy, AV block
• Late disease: unilateral knee arthritis, subacute encephalopathy

⇨ Treatment is by Doxycycline, early infection can be haltered by giving ceftriaxone

❖ Syphilitic aneurysms are uncommon in USA, mostly from immigrant cases.
❖ Teratogenic effect of Tetracycline :
o Deposits in the dentin & enema of the developing teeth→yellow/ gray/ brown
staining.
o If exposure near term → affect permanent teeth
o Children < 8 years are avoided to take tetracycline.
o Amoxicillin is the 1st drug used in Lyme disease in pregnancy
❖ Diagnosis of Malaria Falciparum →
peripheral blood smear with Giemsa stain,
multiple trophozites, and banana shaped
gametocytes
❖ Treatment of Malaria:
o Chloroquine sensitive area → chloroquine
“long term use of chloroquine cause
retinopathy”
o Chloroquine resistant area → mefloquine
o For P.ovale, P.vivax → add primaquine (for
hypnozites)
“these 2 species can form latent infection (exo-eryhtrocytic cycle) → relapse
o Other treatment : atovoquine-proguanil, artemisinins
❖ Pseudomonas aeroginosa produce many toxins, exotoxin A has the same
mechanism like the diphtheria toxin.
❖ Foscarnet → chelate calcium ➔ hypocalcemia; Foscarnet induced magnesium wasting ➔
hypomagnesemia → ↓↓ PTH release → more hypocalcemia ➔➔➔ both cause seizures
32

 ❖ N. gonorrhea infection produce IgA, IgG but due to antigenic variability no

memory cells or protection for future infections.
❖ Meningitis :
o Strept. pneumonia maeningitis (Gram positive) cause release of much
inflammatory cytokines due to bacterial sub-capsular antigens as
peptidoglycan , teichoic acid ➔So pneumococcal meningitis is benefits
from the administration of dexamethasone.
o Other forms of meningitis as H.influenzae, N.meningitidis not benefitis from
steorids as they have less peptidoglycan and low teichoic acid

❖ Kaposi Sarcoma (KS):

o Reddish / violet flat maculopapular
lesions to raised hemorrhagic
nodules or polypoidal masses
o L/M: spindle cells with cellular
atypia, BV proliferation,
extravasated RBCs

❖ Coccidioides:
• Present in patients recently travel to southwestern US e.g. California, Arizona,
New Mexico, Texas , Northern Mexico
• Most common presentation is acute pneumonia
❖ Congenital toxoplasmosis :
o Classic triad of hydrocephalus, intra-cranial calcifications, chorioretinits +/-
HSM
o Hydrocephalus → due to CNS inflammation
o Chorioretinitis → yellow / white cotton like exudates seen on the retina
o Occur only if the mother get Toxo infection in the first 6 months
o So, pregnant women must be advised to avoid contacts with cats during
pregnancy
❖ IgE dependent mast cell degranulation ➔ due to environmental antigens, stings,
sulfa drugs
33

 ❖ IgE independent mast cell degranulation ➔

o Caused by medications as vancomycin, opioids, radiocontrast agets
o Mechanism of degranulation by activation of rotein kinase A, PI3 kinase
❖ Isoniazid induced liver toxicity:
• 10 – 20%: mild hepatic dysfunction → transient ↑↑ AST & ALT, continue
INH → resolution of symptoms & lab changes in 4 – 6 months.
• < 1 % : Frank hepatitis → severe hepatic dysfunction & death
❖ Entrobius vermicularis :
• Commonest helminthic infection in US
• Occur in children 5 – 10 years
• Inhabit caecum & appendix
• Adult worm deposit eggs more at night
• Treatment: aldendazole √, pyrantal pamoate (pregnant)
❖ Human papilloma virus (HPV) :
• Serotype 6, 11 cause condyloma acuminate, respiratory papllomatosis
• It affect squamous stratified epithelium present in True vocal cords → weak cry,
hoarseness & stridor
• True vocal cords, only area in respiratory tract covered by stratified
squamous epithelium to withstand continuous friction & abrasion to produce
sound
• False folds (ventricular folds) lined by respiratory epithelium → help to
lubricate the true vocal cords by mucus , protect airway from foreign bodies.

34

 o A → rabies virus (Q ID : 1402)

o B → tetanospasmin
o C → Diptheria toxin
o D → Listeria (food bourne infection causing meningitis)
o E → Botulism
❖ Flucytosine → treatment of cryptococcal meningitis
Fluconazole → prophylaxis of cryptococcal meningitis
❖ mRNA purified from virus → cause infection ➔ must be single stranded &
positive sense viruses (dsRNA, SS-ve ) need additional enzymes
❖ Normal CD4 count = 400 – 1400, opportunistic infection only if CD4 < 200
❖ Drugs metabolized by Cytochrome P450 ➔ oral hypoglycemic, tacrolimus,
cyclosporine
❖ SMX – TMP :
o SMX → compete with PABA to prevent di-hydropteroate synthetase
o TMP (bacteria), MTX (human), pyrimethamine (parasite) → inhibit DHFR

o
o SMX – TMP cause sequential blockage
o Pyrimethamine → active against malaria, toxoplasma
❖ Azoles :
o Inhibit demethylation of lanosterol → ergosterol (fungal membrane)

❖ Bacillus anthracis :
o If no history of animal contacts → suspect bio-terrorsim, contact health
authorities (100% mortality of pulmonary form)
o Common in places where livestock vaccines is not possible (rare in US)
o Spread through lymphatics to blood
❖ Baitracin → inhibit cell wall synthesis
❖ Gonorrhea infection:
o Diagnosed by nucleic acid amplification test
o Treatment : Dual antibiotics → 3rd cephalosporin (ceftriaxone) +
macrolide (azithromycin)
o Addition of azithromycin → avoid
resistance & chlamydia co-infection
❖ Candidemia always affects patients with
central venous catheter, TPN nutrition
Usually susceptible to fluconazole,
echinocandins (e.g cuspofungin)

35

 ❖ Aspergillosis → narrow V-shped septated

hyphae
o Monomorphic
o Invasive aspergillosis : occur in
neutropenia, with diagnosis made by L/
M. treatment is amphotrecin B
o ABPA : treatment is corticosteroirds

❖ Amphotrecin B ➔ the most toxic antifungal

drug
o Most dangerous is
nephrotoxicity →
1) Hypokalemia → flat T wave, ST depression, prominent U wave, PVCs
2) +/- hypomagnesemia ➔ due to its toxic effect on DCT
3) Anemia ➔ due to ↓ GFR, toxic effects on tubules
❖ Acyclovir nephrotoxicity : occur due to crystalisation of acyclovir → can be ↓↓ by use
excess hydration & ↓ infusion rate.
❖ Outcome of HBV infection
1) Acute hepatitis & complete resolution → >95%
2) Fulminant hepatitis → < 1%
3) Chronic hepatitis → 4 – 5%
⇨ 10% arise HCC
⇨ 20 – 50% develop cirrhosis
❖ Rhizopus → right angled, non septated branched fungus

36

 ❖ Staph. Epidermidis endocarditis :

o Normally, s. epidermidis is component of normal flora → distinguish
contamination vs. infection by same results in repeated blood cultures
o Initial treatment is vancomycin, after results of C & S appears → if it is
MSSA (not MRSA) → switch to naficillin
o MRSA due to alteration in PBP due to altered mecA gene
❖ Congenital rubella syndrome: classic triad of SNHL, PDA, congenital cataracts.
➢ Head: microcephaly, MR
➢ PDA, pulmonic artery stenosis
➢ Rubella Vaccination :
o Live attenuated
o Children : 12 - 15 months, 4 – 6 years
o Female at child bearing period whose serum test is –ve ➔ avoid pregnancy
for 4 weeks
❖ Granuloma inguinale :

❖ Syphilis diagnosis :
o VDRL ➔ antibody to cardiolipin – cholesterol – lecithin antigen, antibodies
against lipids released from damaged cells.
o Treponemal tests : florescent treponemal antibody absorption, treponima
pallidum enzyme immunoassay
o Secondary syphilis ➔ hepatitis, oral lesions, epitrochlear LNs
o Primary syphilis ➔ ddirect visulaisation is not widely used, treponemal tests as
FTA-Ab, TP-EI is more sensitive and commonly used
❖ Shigellosis:
o Most commonly due to S. Sonnei in industrial countries
o It specifically invade M (Microfold) cells in Peyer’s patches → pass the cells by
endocytosis & lyse endosomes → invade other cells laterally → infectious
diarrhea.

37

 o M –cells in Peyer’s patches: M-cells sample gut content → transfer the antigens to basal
lamina within endosomes → at the base of cells inside specialized pocket (microfolds) immune
response occur

❖ Infantile botulism :
o Due to ingested if honey (12%), 1st clinical picture is constipation then paralysis &
Floppy baby.
o Diagnosed rapidly by ELISA & PCR testings
❖ Staph. Aureus:
o Food poisoning :
▪ Due to Pre-formed heat stable exotoxin so no person to person
transmission.

▪ Caused by mayonnaise containing food, pultry & egg products,

meat, egg, tuna, chicken, potato, macaroni salad, cream filled
pastries, milk & dairy products.
▪ Exotoxins cause : toxic shock syndrome , Gastor-enteritis, SSSS
❖ Important updates of flowchart in gram
positive bacteria :
o Bacitracin test : DD between
S.pyogenes & GBS ➔ replaced by PYR
test
▪ PYR positive : S.pyogenes,
enterococci
▪ PYR negative : S. agalacticae
(GBS)
o Non group E enterococci → grow on bile but
not in the presence of hypertonic ( 6.5%) saline
o Bile soluble = addition of bile salts with bacteria
(turbid) → loss of turbidity of cells due to cell lysis
o Optoschin sensitive → see pic.

❖ Not all 3rd & 4th generation

cephalosporins are anti-pseudomonal !
Cefipime & ceftazidine

38

 ❖ Fidaxomicin:
o Macrocyclic antibiotic (related to macrolides)
o Inhibit sigma subunit of RNA polymerase→ ↓↓protein synthesis
o Oral, bactericidal against C. difficile, low systemic absorption → high fecal
concentration
o Narrow spectrum of activity against normal flora than vancomycin.
o Usually used for recurrent infections with C.difficile colitis
❖ Candida infection :
o Host defense against candida either :
▪ Th cell response → prevent superficial candidiasis
▪ Neutrophil response → prevent hematological spread of candida
▪ In HIV alone, superficial candia may occur but not fungemia except
the patient is neutropenic
❖ Daptomycin :
o Lipopeptide antibiotic against MRSA
o Creat transmembrane channels → intra-cellular ion leakage → depolarization
and cell death
o Usually inactivated by lung surfactant … not in pneumonia
o ↑↑ CK levels → due to muscle membrane disruption
❖ Bordet-Gengou medium → Bordetella pertussis
❖ Macckonkey agar → contain bile salt as PH indicator
❖ Vancomycin is glycopeptide antibiotic
❖ Antibiotic resistance
o Aminoglycosides : methylation of Aminoglycosides binding portion of the
ribosom, efflux pumps, altering chemical structure of enzymes\

39

 ❖ α (partial )hemolysis
❖ Streptokinase → released by strept.
pyogenes
❖ Clostridium perferingins :
o Uses carbohydrates for
energy
o Toxin : lecithinase
(Phospholipase C, α toxin)
❖ Aspergillosis :
o Q ID : 273
o Galactomannan & β D glucan assays are high
❖ Pneumococci:
o Outer polysaccharide capsule → appear sweels & halo around the blu stained
bacteria when specific anti-capsular antibiotics & methylene blue dye are added
“Quellung reaction”

❖ HIV drugs:

40

 o Integrase inhibitors (Raltegravir) : inhibit integration of the viral cDNA

into host DNA → inhibit formation of viral mRNA
❖ Corynobacterium:
o Catalase positive, aerobic / facultative anaerobic
o Diphtheria and non-diphtheria
o Grow on cysteine-tellurite → dark black, slightly iridescent colonies

❖ Herpes simplex virus :

• Treatment to ↓↓ recurrence: daily oral valacyclovir √, acyclovir, famcyclovir,
typically the drug continued for years
• Acute treatment : short course of oral acyclovir to ↓↓ viral shedding
❖ Hemophilus influenza
• Capsulated (serotype a – f) → type B is the most invasive strain as it contain PRP
capsule → inhibit complement activated phagocytosis → invasion & meningitis…
• Un-capsulated (un-typeable)
❖ Meningococcemia :
• IgA protease → responsible for nasopharyngeal colonization as it destroys the
mucosal antibodies
• Pilli → attachement and colonisation on nasopharyngeal epithelium

“antigenic variations due to on-off gene switching & horizontal gene

transfer”
• Opa protein → aid in endothelial attachment and invasion
• capsular oligosaccharide → resist phagocytosis & complement activation
• LPS & outer membrane → TLR 4 bind to Endotoxin ➔ release of IL1, IL6, TNF-α
→ septic shock LPS is the responsible of septic
shock in case of any gram negative bacteria
❖ Satellite phenomena of H. influenza: Colonies of
Hemophilus will grow around β hemolysis of staph. aureus
due to release of NAD from staph & ↑↑ release of hematin
from lysed RBCs
❖ Mycoplasma :

41

 • CXR usually more worse than the clinical picture

• Need cholesterol medium to grow
❖ Norovirus (Calicivirus) :
• ssRNA, most common cause of viral watery GE in developed countries
• resitant ot enzyems→ easily transmitted feco-orally
• IP = 1 – 2 days, diagnosis by clinical picture only bt PCR need to confirm
outbreaks
• Rotavirus outbreak is ↓↓ to due to immunization.
❖ Bronchiolitis(LRT infection):
• Most commonly by RSV, less
commonly by Para-influenza
virus
• < 2years ➔ classic findings which
are severe
• > 2 years ➔ mild, self-limited illness
• < 2 months ➔ may lead to apnea, respiratory failure
❖ Cause of greenish sputum & pus in bacterial infection:
⇨ Due to neutrophil myeloperoxidase ; which is blue green heme based
pigmented molecule contained within the azurophilic granules of neutrophils
and catalyze the production of hypochlorus acid .
❖ Lympho-granuloma venereum (LGV) :
• Initially painless genital ulcer, followed by painful inguinal lymph nodes (buboes,
due to lymphatic affection) may lead to abscess and rupture
• It may cause fibrosis, lymphatic obstruction, anogenital stricture & fistula
• L/M: mixed granulomatous & neutrophilic inflammationwith inclusion bodies.
• DD: klebseilla granulomatis which lead to granuloma inguinale →
also appear as painless genital papule that ulcerate without
lymphadenopathy→ diagnosed by intra-cytoplasmic Donovan bodies →
if not treated ➔ scarring and lymphedema
❖ Botulism: highly potent toxin, but is highly heat labile → can be destroyed by
heating the food. Manifestations of toxicity os 3D→ Dysphonia, Dysphagia,
Diplopia later on GIT manifestations may occur

42

 ❖ Mechanisms of resistance against aminoglycosides:

1) Aminoglycoside modifying enzymes √√√ → they add chemical groups to
the drug → ↓↓ ability to bind to 16S rRNA (within 30S subunit) → ↑↑ minimum
inhibitory conc. → ↓↓ bactericidal effects
⇨ These enzymes usually arises via transfer of plamid / transposons rather than
chromosomal mutations
2) Mutated porin protein.
3) Alteration of subunits of rRNA
❖ Pathogenesis of post-viral pneumonia :
1) Influenza destroy cells in URT → loss of cilia
2) Neuroaminidase cleave sialic acid → glycoprotein ➔ colonization of bacteria
• Diagnosed by sudden deterioration of patient condition after partial
improvement
• Commonest pathogens; staph. aureus (young previously healthy), strept.,
H.inflluanzae
❖ Intra-nuclear inclusion bodies: acidophilic → HSV, basophilic → CMV
❖ Pick’s bodies ➔ round intra-cytoplasmic inclusion body seen on silver stain
❖ Examples of prion disease e.g. CJD, Bovine spongiform
encephalopathy (mad cow disease)
❖ HBV infection:
• Proliferative phase: the entire virion is present, viral
HBsAg & HBcAg are expressed with MHC-I →
activate Tc cells to destroy the hepatocyte (the virion
itself is not cytotoxic)
• Integrative phase: the HBV DNA is incorporated
inside the genome, so cannot be destroyed by the
immune system, antibodies appear to ↓↓ infectivity,
but risk of HCC is high due to the incorporated
genome.
• Host HBsAb neutralize HBV infection by
preventing the HBsAg from binding to the
hepatocyte receptors (before entering the cell)
❖ Chronic HBV pathology ➔ show ground glass
appearance: due to accumulation HBSAg inside the
hepatocyte → homogenous pale eosinophilic cytoplasm. This is the most specific
findings
⇨ Mallory bodies: clumped amorphous eosinophilic intra-cytoplasmic inclusion
made of tanged intermediate filaments. ➔➔➔➔
43

 ❖ Herpetic encephalitis:
• Commonest cause of sporadic encephalitis
• CSF show viral pattern but RBCs may exist in the CSF, protein must be ↑↑
• HSV-1 enter the brain through the olfactory tract → olfactory cortex (medial
temporal lobe) → edema of the temporal lobe
❖ Diagnosis of tetanus :
• It depends solely on History & clinical picture :
- History of penetrating trauma
- History of immunization, last dose
• N.B. C. tetani is locally found in wound, where the toxin is the responsible for
clinical picture as it travels through the nerves
❖ Hand hygiene is the single most important measure to reduce the risk of transmission
of bacteria. It should be done before & after touching the patients, before aseptic
conditions, after contact with body fluids
❖ Isoniazid:
• Similar to vitamin B6, compete with its
action.
• Vitamin B6 helps transformation of
glutamate to GABA
• Isoniazid → a) ↑↑ excretion of vitamin b)
compete with action → neurotoxicity
• So vitamin B6 is co-administered
❖ Mechanism of action of anti-virals:
• nucleoSIDE analogues antivirals →
phosphoryalted to its trinucleotide form (to
be active)
⇨ they are transforme d to their mono-
phopshate form by viral phosphorylating
enzymes
⇨ the host cell kinases tansofro mono-
phosphate to tri-phosphate for → active
⇨ resistance casued to acyclovir by lacking of viral phosphorylating
enzymes (thymidine kinase deificency in varicella zoster virus occur mainly
in AIDS)
• nucleoTIDE analogue (contain 1 phosphate group) only need to be
phosphorylated by Host cell kinases (e.g. Foscarnet, cidofovir)
o

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