Staphylococcus spp. Flashcards
Staphylococcus spp.
Morphology
Gr+ cocci, grape clusters
Staphylococcus spp. (CoNS)
Diagnostic criteria
catalase + & coagulase -
gamma hemolysis (blood agar)
Grow on mannitol-salt agar (no color change)
Grow on egg-yolk salt agar (no surrounding zone)
S. aureus
Diagnostic criteria
Catalase +
coagulase +
Beta hemolysis (blood agar)
Grows on mannitol-salt agar –> pink to yellow
grows on egg-yolk salt agar –> cloudy surrounding zone
Staphylococcus spp.
Defense/immunity structure
K (evasion) - capsule
Biofilm (adhesion & evasion)
Peptidoglycan (endotoxins, PBPs –> MRSA)
Teichoic & lipoteichoic acids (antigenic & adhesion)
Surface adhesion proteins
- SPA: inhibit AB-clearance, binds IgGs Fc –> immobilization & no immune complex formation –> decreased C’ system capacity.
- Fibronectin-binding protein A: bind fibronectin
- coagulase: bind fibrinogen –> fibrin formation around abcsess, shield from macrophages (for only S. aureus)
- others: binding elastin & collagen
Staphylococcus spp.
Enzymes
-
catalase
H2O2–>H2O + O2, evasion (H2O2 is a weapon used by phagocytes) -
hyaluronidase
hyaluronic acid breakdown of CT - invasion -
fibrinolysin
dissolve fibrin clots –> spreading -
lipases
hydrolyze lipids in skin –> colonialization -
Beta-lactamase
degrade beta-lactam rings in antibiotics
S. aureus
Enzymes
- coagulase
fibrinogen –>fibrin, cause clumpming of S. aureus & protective fibrin layer around S. abscess - nuclease
hydrolyze neutrophil extracellular traps (NETs) consisting of extracellular DNA.
S. aureus
Cytotoxins: alpha toxin
disrupt smooth muscle of blood vessels & toxic to RBCs, leukocytes, hepatocytes & platelets.
Bind target –> pore formation –> rapid electrolyte eflux –> osmotic swelling & cell lysis
S. aureus
Cytotoxins: beta toxin
toxic to RBCs, fibroblasts, leukocytes & macrophages.
catalyst of hydrolysis of membrane phospholipids
Straphylococcus spp.
Cytotoxins: delta toxin
Toxic to RBCs & other mammalian cells and their intracellular structures.
S. aureus
Cytotoxins: gamma toxin
lyses neutrophils and macrophages
Great hemolytic activity
pore formation –> osmotic instability
Panton-Valentine leucocidin
not hemolytic, act on neutrophils & macrophages –> supressing phagocytosis
pore formation –> osmotic instability
S. aureus
Exfoliative toxins (mechanism & clinical picture)
Mechanism: split desmosomes –> cell bridges in skin are dissolved (no inflammation or cytolysis)
Clinical picture: Staphylococcal scalded skin syndrome, SSSS, perioral redness & inflammation –> (2days) spread to body –> large liquid-filled subcutaneous blisters –>epithelium heals (7-10days) with production of ABs. No scarring.
S. aureus
Enterotoxin (mechanism & clinical picture)
Heat-stable & resistant to hydrolysis by GI-juices –> staphylococcal food poisioinng
Mechanism: superantigens (non-specific activation of T cells + cytokine storm), stimulate mast cell release of inflammatory mediators (–> vomiting). Bind MHC-II & TCR –> cytokine storm –> severe inflammatory reaction. Intoxication
Clinical: contaminated food (not detectable) –> rapid & acute onset (4h) –> severe vomiting, watery non-bloody diarrhea, abdominal pain, nausea and sweating & headache. NO FEVER.
S. aureus
Toxic shock syndrome toxin-1 (TSST1), mechanism, clinical picture
Mechanism: superantigen produced in vagina or wound –> toxin released to blood –> cytokine storm –> endothelial cell leakage or cytotoxic (dose dependent) –> systemic effect –> hypovolemic shock & multiorgan failure.
Clinical: abrupt fever, hypotension, diffuse macular erythematous rash, mutliorgan failure and death.
S. aureus
Mediated diseases
Suppurative
- impetigo
- folliculitis
- furuncles/boils
- carbuncles
Others
- bacteremia
- pneumonia & empyema
- osteomyelitis
- septic arthitis
