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Portals of Entry:
• Skin:

Arthropod vectors:

Strep and staph bind to:

Primary barrier to infection but some pathogens can traverse it

Arthropod vectors inject pathogens into humans

Strep and staph bind to fibronectin in wounds and indwelling devices


Portals of Entry:
• Lungs:

How do pathogens overcome ciliary action? (2)

Up to 10,000 microorganisms are introduced into the lungs per day
o Adapt Strong Adhesins:

o Paralyze Ciliary Action:


Adapt Strong Adhesins:

Adapt Strong Adhesins:
• Rhinovirus uses capsid protein for attachment to ICAM-1-type molecule
• Mycoplasma pneumonia attaches to neuramic acid on host respiratory epithelium


Paralyze Ciliary Action:
Bordetella pertussis:
Influzena virus infection:

Paralyze Ciliary Action:
• Bordetella pertussis produces tracheal cytotoxin
• Influzena virus infection causes ciliated cell dysfunction


Gastrointestinal Tract:

Intestinal pathogens express:

Receptor specificity dictates:

Where are adhesins typically located? Why?

- Some microbes enter through what type of cells of Peyer’s patches?

Gastrointestinal Tract:

- Intestinal pathogens express receptor-specific adhesins

o Receptor specificity dictates colonization site and pathogenesis

o Adhesins typically located on the tip of bacterial pili to overcome cell-cell repulsion

- Some microbes enter through antigen sampling cells of Peyer’s patches


What are the best defense for the GI tract?
Disruption leads to:
What causes enterocolitis?

Resident microflora are the best defense for GI tract:
o Disruption can lead to opportunistic infections
o Antibiotic-associated enterocolitis is caused by overgrowth of resident opportunist


Urogenital Tract:

Vaginal pathogens:

Urethral Pathogens:
Primary defense (3):
Why are females more susceptible to UTIs?

Vaginal Pathogens: must colonize mucosa or take advantage of localized injuries

Urethral Pathogens: primary defense is flushing action of urine; mucus lining of the bladder and sIgA also provide defense against UTIs
o Female more susceptible to UTIs because of shorter urethra


Urogenital Tract:

What do UTI pathogens (E.coli) have that permits ascending infections?

UTI pathogens (E.coli) have adhesins that permit ascending infections

- Adhesins specialized for urinary epithelium
- Inflammatory response to UTI causes pathology


Different Mechanisms of Transmission (5):

- Respiratory
- Fecal-oral
- Sexual contact
- Vector-borne (malaria), person-person, or animal-person (rabies)
- Vertebrate reservoir (plague)


Routes of Infection:

Some pathogens transiently infect at a primary layer and rapidly shed (2):

Some pathogens invade deeper tissues and may be shed from secondary site (1):

Routes of Infection:

Some pathogens transiently infect at a primary layer and rapidly shed (influenza and Shigella)

Some pathogens invade deeper tissues and may be shed from secondary site (Varicella)


Vertical vs. Horizontal Transmission:

Vertical: from parent to offspring, via placenta, sperm, ovum, blood or milk

Horizontal: from person to person


Infectious Dose (ID50):

ID can vary: can range from very small (ie. only 10 cells) to very large (ie. 10,000,000 cells)

10: Shigella
10,000,000: Vibrio cholerae


Route of Infection Important:

What is the most effective means of person-to-person transmission?

Aerosol is the most effective means of person-to-person transmission
o Successful infections depend on receptors and localized defenses


Rhinovirus Route of Entry: Nasal vs. pharynx

A single rhinovirus particle in the nasal cavity causes successful infection

200 rhinovirus particles are required for infection if inoculation occurs in the pharynx


Stability of Organism in Environment: another factor involved in transmission.

Spore producing vs respiratory and STDs

Respiratory and sexually transmitted pathogens are unstable: need person-to-person contact

Spore producing organisms: spores can persist in the environment for years


Microbe Replication Rates:

E. coli vs Mycobacteria

- Can take minutes (E.coli) or days (Mycobacteria spp.) to double


Susceptibility to Infection is Influenced by Genetic Determinants in the Host:

Host Specificity (measles, Shigella vs rabies):

Some pathogens only infect humans or closely related primates (measles, Shigella)

Others are capable of infecting a wide range of hosts (rabies)


Intraspecies Genetic Determinants Dictate Susceptibility:

Sickle cell: heterozygous vs aa:

Effect to Plasmodium falciparum parasite:

Individuals heterozygous for sickle cell trait are less susceptible to malaria

Sickle cell trait due to aa substitution in Hb (HbS)

Result is Plasmodium falciparum parasite (causes malaria) is unable to utilize the altered Hb


Why are individuals homozygous for sickle cell trait susceptible to other infections?

What are they susceptible to?

Individuals homozygous for sickle cell trait are susceptible to other infections (due to functional asplenia)

Susceptible to infection with encapsulated bacteria, which are usually filtered by the spleen
- Positive selection for sickle cell trait occurs amongst populations in endemic areas


Regulon definition:

A regulon is a collection of genes or operons under regulation by the same regulatory protein. This term is generally used for prokaryotic systems.


Virulence Factor Genes for Various Bacteria:

Uropathogenic E.coli

Shigella spp.


Cholera toxin production


o Adhesins (uropathogenic E.coli)
o Invasion attributes (Shigella spp.)
o Antigenic drift of M protein (S.pyogenes)
o Environmentally responsive regulon (cholera toxin production)
o Antigenic variation of pili (Neisseria)


Streptococcus pyogenes

Gene or gene product

Effect on virulence

Gene or gene product: M protein, a cell wall component

Effect on virulence: Antiphagocytic, autoimmune complications


Yersinia enterocolitica

Gene or gene product

Effect on virulence

Gene or gene product: Invasion surface protein

Effect on virulence: Uptake into epithelial cells and phagocytes


Shigella spp

Gene or gene product

Effect on virulence

Gene or gene product: Invasion plasmid antigens

Effect on virulence: Escape from vacuole and cell-cell spread


Neisseria gonorrhoeae

Gene or gene product

Effect on virulence

Gene or gene product: Pili and outer membrane proteins

Effect on virulence: Attachment and antigenic variation


Herpes simplex virus

Gene or gene product

Effect on virulence

Gene or gene product: Envelope glycoprotein C

Effect on virulence: C3b binding, blockage of classical complement pathway


Mechanisms Bacteria and Protozoa Use to Resist Complement Mediated Killing:


Salmonella typhi:

S.aureus and S.pyogenes:

What can degrade complement?

Capsule (S.pneumoniae)

Long LPS O antigen (Salmonella typhi)

Coating with immunoglobulins (S.aureus and S.pyogenes)

Membrane-bound enzymes can degrade complement


Mechanisms Bacteria and Protozoa Use to Resist Phagocytosis (5)

1. Release toxins that kill phagocytes

2. Catalase to resist oxidative killing

3. Prevent phagosome fusion with lysosome; still taken up by phagocyte

4. Escape from phagolysosome and live in cytoplasm; still taken up by phagocyte

5. Defenses against cytokines:
- Secretion of IL-2 receptors that prevent T cell activation during malaria
- Secretion of enzymes that cleave IL-2 and IFN-gamma


Mechanisms Bacteria and Protozoa Use to Resist Phagocytosis:

A. S.aureus and S.pyogenes

B. S.aureus

C. Mycobacterium tuberculosis

D. Trypanosoma cruzi

E.1 Plasmodia spp.

E.2 Pseudomonas aeruginosa

A. Staph. aureus and Strep. pyogenes release toxins that kill phagocytes
B. Staph. aureus produces catalase to resist oxidative killing
C. Mycobacterium tuberculosis prevents phagosome and lysosome fusion
D. Trypanosoma cruzi escapes from phagolysosome and lives in the cytoplasm of macrophage
E. Pathogenic microbes have evolved defenses against cytokines
1. Plasmodia spp. secrete IL-2 receptors that prevent T-cell activation during malaria
2. Pseudomonas aeruginosa secretes enzymes that cleave IL-2 and IFNγ


Highly adapted parasites can live in host for long periods (years). Shed of persistent microbes into the environment may be (2):

Continuous (ie. shed of Hepatitis B virus into the blood)

Intermittent (ie. tubercle bacillus)