Cell-Associated Virulence:
o
1. capsule
o
2. PRO A: (bind Fc empnt lgG); stop phagocytosis &
complement activation
o
3. Clumping Factor: binds fibrinogen fibrin bacterial
aggregation
Extracellular Enzymes:
o
1. coagulase: prothrombin staphylothrombin fibrin
formation = clotting!
o 2. hyaluronidase/nucleases/lipases
o 3. catalase: stops MPO system; inhibit phagocytosis
o
4. staphylokinase: dissolves fibrin clots
o
5. PCNases: when inappropriate therapy
Toxins:
o Exfoliative/TSST-1 /Enterotoxins = release of cytokines
o
Cytotoxins lyse many cells
o
Panton-Valentine Leukocidin (PVL): leuko destruction/tissue
necrosis
Community acquired!
EPIDEMIOLOGY of STAPH AUREUS:
Asympomatic carriers
PATHOLOGY/DISEASE of STAPH AUREUS:
Inhalation Pneumonia
o
Community acquired after influenza (varied severity )
Aspiration Pneumonia:
o
Hospital-acquired after intubation
Hematogenous Pneumonia:
o From thrombus or vegetation
o Empyema, pulmonary infxn (common cause)
PREDISPOSING FACTORS:
Candidate Vaccines:
o
1. NABI Pharm (failed clinical trials)
o
2. Inhibitex (veronate. aurexis)
Non-immunc based:
5. pili: attachment
widespread in environment
carried on skin/feces
nml flora & opportunistic flora in hospital
Trans: sinks, fomites, plants, fruits, hands, etc
Primary
o
Inhalation therapy with nebulization
Secondary
o
Immunosuppression/ host compromise
o
Associated with bacteremia (IV drug use)
Clinically:
o
Nml Pts: toxicity, cyanosis, empyema
o
CF: chronic/recurrent. confined to respiratory tract, bilateral
w/residual damage
DX: