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Infectious Disease Unit 1 > Staphylococci > Flashcards

Staphylococci Flashcards

1
Q

Staph general apperance

A
  • 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
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2
Q

Staphylococcus aureus basic facts

A
  • colonizes nares
  • Coagulase +, catalase +, beta hemolytic
  • golden color
  • Clumping factor (protection from phagocytosis), protein A, DNAase, Mannitol salt – associated with coagulase
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3
Q

Staphylococcus epidermidi basic facts

A
  • 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
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4
Q

Staphylococcus saprophytic basic facts

A
  • Catalase +, Urease +, Coagulase neg
  • 2nd most common cause of uncomplicated UTI in young women (first is e coli)
  • Novobiocin resistant
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5
Q

Staph virulence factors

A

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
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6
Q

Protein A

A

major virulence factor in S. aureus

- attaches Fc of IgG to activate complement– prevents antibody-mediated phagocytosis

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7
Q

TSST-1

A
  • TSST-1: superantigen stimulates cytokines, causing endothelial leakage and shock–eventual organ failure
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8
Q

where is staph most commonly found

A
  • aureus: mostly nose, some skin, throat, vagina

- coag negative staph– most in skin; nose, throat

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9
Q

Mechanism of antibacterial resistance

A
  • 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)
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10
Q

is staph more local or spreading disease

A
  • more local
  • tends to wall off into abscesses
  • rarely causes necrotizing fasciitis
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11
Q

Diseases from S. aureus

A

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
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12
Q

most common cause of osteomyelitis

A

S. aureus

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13
Q

Disseminated Staph septicemia

A
  • tends to occur in adolescent males
  • often associated with endocarditis and thrombophlebitis
  • protease + strains
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14
Q

Major host defense against staph and staph’s resistance

A
  • phagocytosis

- this is impeded by protein A, Panton-Valentine Leukocidin, Localizing factors (clumping factor/coagulase)

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15
Q

chronic granulomatous disease

A
  • sex linked neutrophil defect
  • most common neutrophil defect
  • imparied H2O2 in white cells so harder to kill pathogens
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16
Q

Jobs syndrome

A 
-Hyper IgE
cold abscess
-poor neutrophil chemotaxis--less WBC response
- Increased IgE
- get chronic infection
17
Q

Scalded skin syndrome

A
  • 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)
18
Q

Staph Scarlet fever

A
  • older children–milder form of scalded skin syndrome
19
Q

Toxic shock syndrome

A
  • 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
20
Q

TSS Pathogeneisis

A

risk factors

    • exposures to TSST-1
  • right environment for toxin production – abscess, vagina (anaerobic)
  • no pre-existing antibody
  • host having large cytokine production
21
Q

Enterotoxin Food poisoning

A
  • preformed toxin in contaminated food
    causing vomiting/diarrhea–mediated by cytokine release (mast cells)
  • classic cause of food poisoning
22
Q

virulence factor of coag - staph

A

“slime”

- Staph epidermidis (skin), saprophyticus (UTI)

23
Q

Treatment for coag neg staph

A

vancomycin & Rifampin, remove foreign body

24
Q

Staph aureus localizing factors

A

Coagulase, clumping factor, protein A

25
Q

Can you treat any staph with penicillin

A

NO

26
Q

Methicillin susceptibility

A
  • MSSA, Coag (-) staph

- NOT MRSA

27
Q

What is MRSA resistant to

A
  • penicillin
  • methicillin
  • 1st/2nd gen cephalosporins
  • quinolones
28
Q

what can you treat MRSA with

A
  • Vancomycin
  • Aminoglycosides
  • Rifampin
  • Trimethoprim-sulfa
  • Erythromycin
  • Clindamycin
29
Q

What can you treat Coag (-) staph with

A
  • methicillin, 1st/2nd gen cephalosporins, vancomycin, rifampin

Infectious Disease Unit 1 (19 decks)

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