Virulence Factors

1. Alpha toxin - pore forming
2. Coagulase - protect from phagocytosis

S. aureus
Exfolatin - cleaves desmoglein

S. Aureus
Exfloatin - cleaves demoglein

Alpha toxin. Activates NLRP3 . Secretes IL-1 and IL-18

Toxic Shock Syndrome toxin (TSST) → SuperAg that spreads systematically

Staph enterotoxin A & B (SEA & SEB) → SuperAg in GI tract stimulates cytokine

1. Streptokinase: Activates plasminogen
2. Pyrogenic Exotoxin: SuperAg
3. Exotosin B: Protease
4. M Proteins

VF: Pyrogenic Exotoxin → SuperAg

Exotoxin B - protease, destroys tissue

VF: erythrogenic toxin (SuperAg) → host has no Abs against toxin

VF: M proteins → cross-reactivity cause Ig against M proteins to bind to proteins in the heart valves
→ complement activation!

VF: Cross-reactivity of Ig against Strep Ag forming immune complexes that are deposited into
kidney → complement activation

VF: Capsule → binds to factor H to degrade C3b (prevents complement activation)

Pneumolysin: cytotoxic to endothelial
cells, impairs ciliary action, suppresses
phagocytosis

Anthrax toxin
- Protective Antigen (PA): binds anthrax toxin receptor (ATR) on host cell surface
- Edema Factor (EF): increases cAMP
- Lethal Factor (LF): cleaves MAPK proteins → TNF-a secretion → death of macrophages +
endothelial cells

Emetic toxin (Cereulide) - heat, pH and proteolysis resistant; induces 5-HT that bind to
receptors on vagal afferent neurons

VF: Enterotoxin - ADP-ribosylating toxin (adds ADP ribose to G protein → increases cAMP

Virulence Factor: Diphtheria Toxin (DTX)
- B subunit: heparin-binding epidermal growth factor receptor (EGFR)
- A subunit: ADP ribosylation of EF-2 → prevents protein synthesis

-Internalan: actin reorganization for further infection to ADJACENT cell
- Listeriolysin O: bacterial escape into host cytoplasm by degrading endosome/phagosome
- Phospholipases: destroy cell mb to release bacteria and spread to tissues

Neuraminidase: attach + penetrate

VF = Virulence associated protein A (Vap A): plasmid encoding resistance to phagolysosome formation to increase survival in macrophages