Describe the virulence factors of Staphylococcus
aureus including slime layer, capsule, cell wall components, Protein A, cytolytic toxins, enterotoxins, exfoliative toxins, TSST, coagulase, catalase, hyaluronidase, staphylokinase, penicillinase.
- slime layer: helps bact stick to things; on very outer side of bact. Allows it to stick to catheters, heart valves, prosthetics, etc.
- capsule: underneath slime layer. Makes you more
- virulent. Made up of polysaccharides -> decreases phagocytosis.
- Cell wall: peptidoglycan -> activates complement, attracts monocytes and macrophages, brings in
- neutrophils (PMNs) -> pus (causes an abscess, generally internal). ALSO teichoic acid -> often how we ID strains.
- “Protein A”: built into cell wall -> binds to Fc region of IgG. Abs are binding backwards, so cant activate complement.
- Coagulase (in S. aureus only).
- Cytolytic toxins: alpha, beta, gamma, delta, PV (leukotoxic -> kills WBCs).
- Exotoxins: Cause cell damage and tissue destruction.
- Exfoliative toxins: breaks down desmosomes in epidermis. ETA and ETB
- Enterotoxins: GI tract -> some are superantigens
- (hooks up MHC to receptor without antigens present)
- TSST-1: toxic shock syndrome-1 (an exotoxin)-> a superantigen; binds to MHC II on macrophages, which in turn react w T-cell receptors -> massive release of cytokines by both macrophages and T-cells
- Superantigens: non-specifically activate T-cells. Ex: TSST: toxic shock syndrome toxin-> leads to multi-organ failure.
- Enzymes: coagulase (blood clotting), catalase (H2O2 breakdown), Hyaluronidase (hydrolyzes HA, present in acellular matrix of CT -> allows it to spread), Staphylokinase (breaks down blood/fibrin
- clots), penicillinase -> a Beta-lactam ring breaker-upper