Staphylococci Flashcards
Staph general apperance
- Gram positive cocci in pairs/clusters
- aerobic
- Catalase positive; coagulase +/-
- number 1 cause of bacteremia
- growth on blood/chocolate agar NOT MacConkey, ferments mannitol on mannitol salt agar
Staphylococcus aureus basic facts
- colonizes nares
- Coagulase +, catalase +, beta hemolytic
- golden color
- Clumping factor (protection from phagocytosis), protein A, DNAase, Mannitol salt – associated with coagulase
Staphylococcus epidermidi basic facts
- Catalase +, urease +, Coagulase neg
- infects prosthetic devices (hip implant, heart valve) and IV catheter by producing adherent biofilms
- component of nl skin flora; contaminates blood cultures
- novobiocin sensitive
Staphylococcus saprophytic basic facts
- Catalase +, Urease +, Coagulase neg
- 2nd most common cause of uncomplicated UTI in young women (first is e coli)
- Novobiocin resistant
Staph virulence factors
CELL WALL:
- Slime (coag -)
- Protein A )anti-phagocytic)
- Clumping factor
- PBP2a (resistance to methicillin by altering penicillin binding)
ENZYMES
- catalase (inhibit PMN killing), coagulase (abscess wall), leukocidin/PVL (anti-phag), Beta-lactamase (Penicillin resistance)
TOXINS
- Enterotoxin A-E (preformed; food poisoning)
- Exfoliatin A-B (Scalded skin syndrome-bind GM4 glycolipids)
- TSST-1 (toxic shock–enterotoxin B/C)
OTHER
- Lipoteichoic acid–attach fibronectin in human cells
- Hemolysins – all cause beta hemolysis
Protein A
major virulence factor in S. aureus
- attaches Fc of IgG to activate complement– prevents antibody-mediated phagocytosis
TSST-1
- TSST-1: superantigen stimulates cytokines, causing endothelial leakage and shock–eventual organ failure
where is staph most commonly found
- aureus: mostly nose, some skin, throat, vagina
- coag negative staph– most in skin; nose, throat
Mechanism of antibacterial resistance
- penicillinase– breaks down penicillin
- altered penicillin-binding proteins due to acquiring mecA gene(MRSA)-resistant to methicillin
- VRSA–vanA gene from enterococcus; minimal inhibitory concentration has been increasing over time
- Erythromycin-induced Clindamycin resistance–test with D test (erythromycin induces erm gene to make resistant to clindamycin)
is staph more local or spreading disease
- more local
- tends to wall off into abscesses
- rarely causes necrotizing fasciitis
Diseases from S. aureus
Inflammatory Diseases: skin infections (cellulitis), organ abscesses, pneumonia (often after flu virus infection), endocarditis, septic arthritis, osteomyelitis (most common cause)
- Toxin-mediated: toxic shock, scalded skin syndrome, rapid-onset food poisoning (enterotoxins–more vomiting)
- MRSA– important cause of nosocomial and community-acquired infections; resistant to methicillin and nafcillin due to altered penicillin binding proteins
most common cause of osteomyelitis
S. aureus
Disseminated Staph septicemia
- tends to occur in adolescent males
- often associated with endocarditis and thrombophlebitis
- protease + strains
Major host defense against staph and staph’s resistance
- phagocytosis
- this is impeded by protein A, Panton-Valentine Leukocidin, Localizing factors (clumping factor/coagulase)
chronic granulomatous disease
- sex linked neutrophil defect
- most common neutrophil defect
- imparied H2O2 in white cells so harder to kill pathogens
Jobs syndrome
-Hyper IgE cold abscess -poor neutrophil chemotaxis--less WBC response - Increased IgE - get chronic infection
Scalded skin syndrome
- only certain strains of Staph aureus produce this toxin (exfoliatins)
- painful, erythroderma, + Nikolsky sign (skin sloughs when you touch it), bullous impetigo
- if you have pre-existing Ab, only get disease if have local toxin (bullous impetigo, bullous chicken pox)
- no preexisting Ab, get systemic toxin–severity of dz depends on age and amount of receptors you have on skin (fewer receptors in older kids vs infants-Ritter’s disease in newborns vs SSS in infants vs Staph Scarlet fever in older child)
Staph Scarlet fever
- older children–milder form of scalded skin syndrome
Toxic shock syndrome
- acute fever, erythroderma (desquamation, usually late), hypotension, multi-organ system involvement (mucous membranes–conjunctiva/oral, renal, hepatic, GI, heme, CNS, muscular)
MAJOR criteria (all required) - acute fever, hypotension, Rash (late desqamation)
Minor Criteria (any 3)
- Mucous membrane inflammation (conjunctiva, “strawberry tongue”)
- Liver abnormalities
- Renal abnormalities,
- Muscle abnormalities
- CNS abnormalities
- Low platelets
TSS Pathogeneisis
risk factors
- exposures to TSST-1
- right environment for toxin production – abscess, vagina (anaerobic)
- no pre-existing antibody
- host having large cytokine production
Enterotoxin Food poisoning
- preformed toxin in contaminated food
causing vomiting/diarrhea–mediated by cytokine release (mast cells) - classic cause of food poisoning
virulence factor of coag - staph
“slime”
- Staph epidermidis (skin), saprophyticus (UTI)
Treatment for coag neg staph
vancomycin & Rifampin, remove foreign body
Staph aureus localizing factors
Coagulase, clumping factor, protein A
Can you treat any staph with penicillin
NO
Methicillin susceptibility
- MSSA, Coag (-) staph
- NOT MRSA
What is MRSA resistant to
- penicillin
- methicillin
- 1st/2nd gen cephalosporins
- quinolones
what can you treat MRSA with
- Vancomycin
- Aminoglycosides
- Rifampin
- Trimethoprim-sulfa
- Erythromycin
- Clindamycin
What can you treat Coag (-) staph with
- methicillin, 1st/2nd gen cephalosporins, vancomycin, rifampin
