Epidemiology and Pathogenesis of Infectious Diseases Flashcards
- Found in Gram-negative bacteria.
- The lipid A component of LPS triggers fever, inflammation, and septic shock when released
during bacterial lysis.
Endotoxin in Lipopolysaccharide (LPS) Layer:
Prevents the bacterium from being engulfed and destroyed by phagocytic immune cells like
macrophages and neutrophils.
Anti-Phagocytic Proteins Induced by oxyR:
- A component of the LPS that inhibits killing by phagocytes.
- Plays a role in immune evasion by altering antigenic properties.
O Antigen:
- Provides motility, allowing the bacterium to move toward favorable environments.
- Aids in immune evasion by inhibiting phagocytic killing.
Flagellum (H Antigen):
- Helps the bacterium adhere to host tissues, a critical first step in colonization and
infection.
Type 1 Fimbriae (Adherence):
- Facilitates bacterial adhesion to and invasion of host cells
inv Encoded Surface Appendage (Adherence):
Molecules secreted by the bacteria to scavenge iron from the host, which is essential for
bacterial growth and survival
Siderophores:
A circular DNA element carrying genes for virulence factors, such as toxins and enzymes
that contribute to pathogenicity.
Virulence Plasmid:
inhibits complement binding, protecting the bacterium from complement
mediated lysis and promoting survival in the host
*Vi Capsule Antigen:
Two types of Exotoxins
Cytotoxin
Enterotoxin (Diarrhea):
Disrupts host cell protein synthesis and induces calcium influx into the host cells, facilitating bacterial adherence
and causing host cell death.
Cytotoxin
Causes the host’s intestinal cells to secrete water and electrolytes, leading to diarrhea. This helps the pathogen
spread to new hosts.
Enterotoxin (Diarrhea):
Corynebacterium diphtheriae
* Causes cell death, leading to the formation of a
pseudomembrane in the throat and systemic
complications.
Diphtheria Toxin
Shigella dysenteriae and some Escherichia coli
strains (e.g., E. coli O157:H7)
* Causes bloody diarrhea (dysentery) and hemolytic
uremic syndrome (HUS)
Shiga Toxin
Bordetella pertussis
* Weakens the immune response and damages
respiratory epithelial cells, leading to whooping
cough.
Pertussis Toxin
- Bacillus anthracis
- Causes tissue necrosis and systemic effects in
inhalational anthrax.
Anthrax Toxin (Lethal Factor)
- Streptococcus pyogenes
- Contributes to diseases like necrotizing
fasciitis and strep throat.
Streptolysin S and Streptolysin O
- Clostridium perfringens
- Causes gas gangrene and massive tissue
destruction.
Alpha-Toxin
- Pseudomonas aeruginosa
- Contributes to tissue damage in infections,
particularly in burn patients.
Pseudomonas Exotoxin A
- Helicobacter pylori
- Contributes to peptic ulcers and gastric
cancer.
VacA (Vacuolating Cytotoxin A
Neutralizes stomach acid, enabling survival in the gastric
environment.
Urease
Lyse red blood cells, releasing iron for bacterial growth.
Hemolysins
Degrades DNA to reduce pus viscosity and enhance
bacterial motility.
DNase
Breaks down lipids for nutrient acquisition in sebaceous
glands.
Lipase
Dissolves clots, allowing bacteria to spread from trapped
sites.
Streptokinase
Promotes clot formation to shield bacteria from immune
cells.
Coagulase
Breaks down collagen to allow deeper penetration into
tissues.
Collagenase
Degrades hyaluronic acid to facilitate tissue invasion.
Hyaluronidase
