Infection

Gould: Chpt. 4, Porth: Chpt. 17

• Infection: presence and multiplication of a microorganism on/in a host

(may or may not lead to disease)
• Host resistance to infection by microorganisms is provided by body defenses
Nonspecific Surface Defenses:
1) Structural Defenses
2) Mechanical Defenses
3) Biochemical Defenses
Nonspecific Interior Defenses:
1) Inflammation
2) Complement System
3) Phagocytosis
4) Interferon
Specific Immune Defenses:
1) Humoral Immunity
2) Cellular Immunity
The Normal Flora

• Ours bodies are inhabited by hundreds

of species of bacteria and fungi. The
microorganisms that coexist with
humans in a stable relationship are
called our Normal Flora
• Our normal flora helps to stimulate our
immune system and, most importantly,
relatively harmless microorganisms
successfully compete with many
dangerous pathogens. This is called
Microbial Antagonism
Sites of Normal Flora:
• Our normal flora include: skin,
conjunctivae, nasal cavity, mouth,
intestinal tract, vagina, and urethra

(7)
 Decreased Host Resistance
• Any defect in the host defenses will result in  host resistance:
– broken skin and mucous membranes
  secretions: mucous, tears, gastric
  motility through GI tract or urinary
tract
  inflammation and phagocytosis (e.g.
~ glucocorticoids)
– immunodificiency or immunosupression Figure 16.3 b, c Ingraham

– malnutrition, stress
– age (infants and elderly)
– presence of disease
• Opportunistic infections are those that occur when host resistance
is low, by microorganisms that would not normally cause infection
in a healthy individual
 Virulence
• Virulence: a microorganism’s ability to evade the host’s defenses
and cause disease
• Virulence is increased by the microorganism’s ability to:
1) Maintain a reservoir (a place to survive before and after
infection)
2) Invade the host’s tissues and cells (eg. Using enzymes)

3) Evade the body’s defenses (eg. resist phagocytosis, change

surface antigens
4) release toxins
 Pathogen Colonization factors

These are factors that determine the pathogens ability to

establish in the host tissues including;
-an effective portal of entry and exit (eg. In food, genital
mucosa etc.
- abiltity to reproduce rapidly (eg. Salmonella has a
doubling time of 20 minutes)
- adherence capability (eg. ability to fasten onto tissues
effectively
 Modes of Transmission
Transmission can be accomplished in five different ways:

A . Direct
i.) Contact – Person-to-person transmission such as
kissing , touching,or sexual intercourse. Also
includes prenatal (mother to unborn child) and
perinatal (birth).
ii.) droplet – a larger contaminated droplet emitted
when coughing, sneezing, talking, vomiting. The
fluids are not suspended so only travel a short
distance
 B. |Indirect Transmission

• i.)
i.) airborne.
airborne.When
Whena adroplet
dropletdries onon
dries a surface andand
a surface then thethe
then
droplet
droplet nuclei
nucleiincluding
includingthe
thepathogen
pathogen is is
swept upup
swept in air currents
in air currents
(( suspended)
suspended)and andspreads
spreadswidely
widely

• ii.) Vehicle – Transmission by inanimate objects, such as food,

• ii.) Vehicle
water, bedding,– utensils,
Transmission
sharedbydrinks,
inanimate objects,
cigarettes suchcalled
etc Also as
food, water, bedding, utensils, shared drinks, cigarettes etc Also
fomites.
called fomites.
 iii. Vector Transmission
The pathogen is transmitted by
living organisms. There are
two forms
. a. mechanical vectors. When
the pathogen is just
physically transferred with
not biological development or
multiplication. Eg. Flies
transmitting bacteria from
feces to food
b. Biological Vectors
The pathogen undergoes
reproduction or
development within the
vector.
eg. The malaria pathogen,
Plasmodium, is transmitted
between humans by
mosquitoes
 Course of Infectious Disease
• The course of an infectious disease can be divided into stages:
– Incubation period: pathogens replicate rapidly without causing
recognizable symptoms in the host
– Prodromal period: initial
appearance of symptoms – sense
of malaise, mild fever, muscle pain
(myalgia), headache, fatigue
– Acute period: maximum impact and
response to infection is seen ~
release of toxins, cell lysis, and
host’s immune response 
inflammation and tissue damage;
specific S/S Figure 17-6 Porth

– Convalescent period: containment and removal of pathogen and tissue

repair with decrease in symptoms; leads to resolution of the infection
• Some infectious diseases are subclinical in that they progress from
infection to resolution without the appearance of clinical symptoms
 Parasitic Infection
• In parasitic infections the prepatent
period is the time from infection until
the parasite becomes visible in the
body e.g. eggs in blood or stool
Plasmodium vivax in a RBC
• Parasites include the protozoa,
helmitnths (worms) and arthropods
(insects)
• Parasitic infections are prominent in
tropical countries
Pinworm ova in a fecal smear

Figure 4-8 B and D, Gould

 Signs and Symptoms of Infection
• Local Manifestations:
–signs of inflammation: redness, swelling, pain, heat
–exudate may be present (purulent ~ bacteria, serous ~ virus)

–lymphadenopathy (swollen and tender lymph nodes)

–system-specific signs e.g. vomiting or diarrhea ~ GI tract,
sneezing, coughing and difficulty breathing ~ respiratory
tract
• General Systemic Manifestations:
–fever (or subnormal temperatures with some viral infections)
–fatigue and headache
–anorexia, nausea
–malaise
–muscle pain (myalgia) and joint pain
 Bacterial Infections

• Bacteria cause disease by Medically Important Bacteria

several mechanisms: Classification Genus Diseases
1. Gram-positive
1. Disruption of normal a. Cocci Streptococcus
Staphylococcus
Pneumonia, pharyngitis, tooth decay, endocarditis
Surgical infections, food poisoning, pneumonia
physiological b. Rods Bacillus Anthrax
Clostridium Gas gangrene, tetanus, botulism
processes Cornebacterium Diphtheria
2. Gram-negative
2. Invasion and a. Cocci Neisseria Meningitis, gonorrhea
b. Rods Haemophilus Meningitis, pneumonia
destruction of host Bordetella Whooping cough
Legionella Pneumonia
tissue Escherichia Enterocolitis, UTI
Klebsiella Pneumonia
3. Stimulation of Salmonella Enterocolitis, typoid fever
Shigella Enterocolitis
inflammation Proteus UTI
Helicobacter Gastritis, peptic ulcer, gastric cancer
4. Releasing toxins Vibrio
Pseudomonas
Cholera
Pneumonia
3. Acid-fast Mycobacterium Tuberculosis, leprosy
5. Post-infection or 4. Intracellular Rickettsia Rocky mountain fever
Chlamydia Urethritis
autoimmune 5. Spirochetes Treponema Syphilis
Borrelia Lyme disease
6. Wall-less Mycoplasma Pneumonia

Compiled by Joe Gordon, MSc

 Endotoxin
• In addition to directly
damaging infected tissues, LPS
bacteria can cause disease by
releasing endotoxins and Activates Activates Activates
exotoxins. Macrophages Complement Coagulation

• Endotoxins: IL-1 TNF Inflammation Disseminated

Lipopolysaccharide released , vasodiation, intravascular
hypotension coagulation
from outer membrane of
Gram-negative bacteria when
Fever Inflammation Thrombosis,
they die. , vasodiation, petechial
hypotension bleeding
• Endotoxins produce extreme
toxic effects on the body, such
as fever, inflammation,
edema, and bleeding.
• These symptoms could be
accompanied by a life-
threatening drop in blood
pressure called septic shock.
 Exotoxins
• Exotoxins: highly destructive proteins exported by both Gram-negative and
Gram-positive bacteria
• Exotoxins have very specific effects that increase the bacteria’s virulence,
but are generally cleared from the body quicker than endotoxin. They can
bind to cell receptors or be enzymes. Examples include:
1. Streptolysin O: A hemolytic enzyme that breaks down red blood cells,
which is produce by streptococcal bacteria
2. Streptokinase: Breaks down fibrin within a blood clot preventing
streptococcus from being ‘walled-off’ at the site of inflammation
3. Botulinum toxin: Blocks neural impulses and produces paralysis,
produced by clostridium botulinum
4. Cholera toxin and E. coli enterotoxin: Increases gut secretions and
causes diarrhea and dehydration
5. Toxic shock syndrome toxin: Produced by streptococcus and
staphylococcus, causing massive release of IL-1, IL-2, and TNF resulting
in hypotension and shock
 Sepsis
• A systemic effect of infection can be sepsis (ie. Septicemia). This can
occur if bacteria or their toxins enter the blood and are circulated
throughout the body. Sepsis can be defined in the following stages:
1. Bacteriaemia: Occurs when detectable amounts of bacteria enter the
blood stream. Usually asymptomatic, but can cause secondary
infections particularly in the presence of cardiac valve disease or a
prosthetic joint. Examples include the skin bacteria staphylococcus
aureus and epidermidis, and the dental bacteria streptococcus
mutans.
2. Sepsis: Occurs when circulating bacteria cause systemic
inflammation. Signs include fever, tachycardia, tachypnea, and
leukocytosis.
3. Severe Sepsis: Includes all signs of sepsis and organ failure.

4. Septic Shock: Severe sepsis plus refractory hypotension. Occurs

mainly with Gram-negative bacteria with release of endotoxin. Can
also occur with staphylococcus aureus and streptococcus pyogenes
that can produce toxic shock syndrome toxin.
 Antimicrobial Drugs
• Medicinal treatment of infectious diseases involves the use of
antimicrobial drugs which attempt to kill the invading microbe, but not
the host i.e. are selectively toxic
• A microorganism has drug resistance when it can grow and reproduce
in the presence of a particular drug (c.f. drug-sensitive)
• Resistance can be natural, or acquired through genetic alteration of
the micro ~ mutation or exchange of genetic material with a naturally
resistant strain
• In acquired resistance, the genetic modification ~ resistance is passed on
to subsequent generations
• Occasionally, an antibiotic is not tolerated well by the host. This can be
due to an immune reaction to the drug (ie. Allergy), the drug becomes
toxic to the host in high doses or with prolonged use, and metabolites of
the drug may be toxic to the liver or kidney.
• Note: exposure to antibiotics does not make a strain resistant!
However, antibiotic use selects for and promotes the survival of resistant
strains…
Antibiotic Resistance
Resistance occurs when bacteria continue to grow in the presence of the drug.
Resistance can innate or acquired. For example, penicillin innately does
not work very well on Gram-negative bacteria since these bacteria have
very little cell wall. However, when penicillin can no longer kill Gram-
positive cocci, this resistance is said to be acquired. This resistance is
passed on to the cell’s progeny and creates a resistant strain.
Acquired resistance occurs by two mechanisms:
1) A genetic mutation.
2) A genetic acquisition. This occurs when a bacteria obtains a plasmid
from another bacteria.
These genetic alterations can create resistance by:
1) Modifying the drug’s target protein.
2) Allowing the bacteria to produce an enzyme that destroys the drug
(eg. -Lactamase).
Most importantly, overuse of antibiotics causes selection of resistant strains,
since all sensitive strains are destroyed. Therefore, antibiotics do not
create resistant strains, but they promote their survival.
 Selection
S S S
S
S
S
• Bacterial selection implies that antibiotics S R
S S
promote the survival of resistant strains by S
S
S
destroying all sensitive strains. Therefore, S

antibiotics select for resistance strains

Apply
• For example, if an antibiotic was applied to a antibiotic
colony of bacterial that contain both sensitive
and resistant strains, the sensitive strains will R
be destroyed, while the resistant strains will
not
• This reduces the competition for space and
resources, and the surviving bacteria will
flourish. The colony now contains only
R R
resistant strains
R
R
R
• Antibiotics (unfortunately ) select for resistant R
R
strains R
R R
Viral Infections
• Viruses cause infections by injecting their genetic material into the hosts
cells. Viral genes are then expressed using the host cell machinery. In
general, there are four different types of viral infections: (7)

Lytic: Virus multiplies Persistent: Long Latent: Virus is Cancer-causing: Virus

and kills host cell term, continuous dormant until causing uncontrolled
(eg. Rhinovirus). release of virus (eg. activated (eg. HIV, cell replication (eg.
Hepatitis B/C, HIV). herpes, varicella). Human papilloma,
hepatitis B).
 Red Measles (Rubeola)
• Etiology and Pathophysiology:
– caused by measles virus (morbillivirus); multiplies in resp. tract
and lymphoid tissue
– virus destroys and agglutinates RBCs and fuses human cells together
– highly communicable disease: contact transmission (resp. droplets)
– serious ~ complications: ear infections and pneumonia, encephalitis
• Signs and Symptoms:
– specific: Koplik spots inside mouth
(first few days); red macular rash
begins on face and spreads
inferiorly: spots eventually merge
 red, puffy skin
– general: general malaise, noticeable
Figure 61-33 Porth
fever, cough, runny nose (coryza)
conjunctivitis, myalgia Figure 26-10 b Ingraham
 German Measles (Rubella)
• Etiology and Pathophysiology:
– caused by rubella virus which is contracted by inhalation of
respiratory droplets
– infection is usually mild, lasting ~ 3 days
– the rubella virus is a strong teratogen:
infection during 1st trimester  abortion
and defects of the eyes, heart, brain
• Signs and Symptoms:
– local: diffuse macular Figure 61-32 Porrth
rash begins on trunk, spreads
to extremities; cough,
congestion, runny nose
– systemic: mild fever; lymphadenopathy
(tender, swollen lymph nodes)

Figure 26-11 Ingraham

 Mumps (Parotitis)
• Etiology and Pathophysiology:
– epidemic parotitis or mumps is infectious inflammation of the
parotid glands
– caused by mumps virus which is carried in the saliva or resp.
secretions of infected persons
– replicates in upper resp. epithelium and spreads to salivary glands,
then to bloodstream and occasionally body tissues
− Can cause orchitis in post-puberty boys, as well as aseptic
meningitis.
• Signs and Symptoms:
– parotitis and perhaps inflammation
of other salivary glands with
swelling below the ear
– mild pain and fever
– headaches, loss of balance
– can cause brain damage if spreads to CNS
Figure 23-4 Ingraham
 Chickenpox (Varicella)
• Etiology and Pathophysiology:
– caused by varicella zoster virus (a herpesvirus), which also causes
shingles (herpes zoster) in adults (~latent infection)
– generally affects skin: may lead to 2° bacterial infections

• Signs and Symptoms:

– skin lesions: red macules 
vesicles (containing live viruses) 
granular scabs
– lesions first appear on trunk,
spread to limbs, scalp, lining of
mouth, upper resp. tract
– mild fever (before lesions appear)
– pruritus
– cough and runny nose
Figure 26 a Ingraham