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Flashcards in Staphylococci Deck (29)
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1

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

2

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

3

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

4

Staphylococcus saprophytic basic facts

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

5

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



6

Protein A

major virulence factor in S. aureus
- attaches Fc of IgG to activate complement-- prevents antibody-mediated phagocytosis

7

TSST-1

- TSST-1: superantigen stimulates cytokines, causing endothelial leakage and shock--eventual organ failure

8

where is staph most commonly found

-aureus: mostly nose, some skin, throat, vagina
- coag negative staph-- most in skin; nose, throat

9

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)

10

is staph more local or spreading disease

- more local
- tends to wall off into abscesses
- rarely causes necrotizing fasciitis

11

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

12

most common cause of osteomyelitis

S. aureus

13

Disseminated Staph septicemia

- tends to occur in adolescent males
- often associated with endocarditis and thrombophlebitis
- protease + strains

14

Major host defense against staph and staph's resistance

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

15

chronic granulomatous disease

- sex linked neutrophil defect
- most common neutrophil defect
- imparied H2O2 in white cells so harder to kill pathogens

16

Jobs syndrome

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

17

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)

18

Staph Scarlet fever

- older children--milder form of scalded skin syndrome

19

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

20

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

21

Enterotoxin Food poisoning

- preformed toxin in contaminated food
causing vomiting/diarrhea--mediated by cytokine release (mast cells)
- classic cause of food poisoning

22

virulence factor of coag - staph

"slime"
- Staph epidermidis (skin), saprophyticus (UTI)

23

Treatment for coag neg staph

vancomycin & Rifampin, remove foreign body

24

Staph aureus localizing factors

Coagulase, clumping factor, protein A

25

Can you treat any staph with penicillin

NO

26

Methicillin susceptibility

- MSSA, Coag (-) staph
- NOT MRSA

27

What is MRSA resistant to

- penicillin
- methicillin
- 1st/2nd gen cephalosporins
- quinolones

28

what can you treat MRSA with

- Vancomycin
- Aminoglycosides
- Rifampin
- Trimethoprim-sulfa
- Erythromycin
- Clindamycin

29

What can you treat Coag (-) staph with

- methicillin, 1st/2nd gen cephalosporins, vancomycin, rifampin