Staphylococci Flashcards

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1
Q

staphylococci characteristics

A

gram +, clusters

single cell membrane, thick cell wall

non-motile, non-sporeforming, facultative anaerobe

polysac capsule differs among strains

catalase positive

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2
Q

Staph aureus

A

catalase +

coagulase + (prothrombin to thrombin–>fibrinogen to fibrin–>clot)

beta-hemo, golden colonies

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3
Q

normal flora of staph aureus

A

anterior nares; also vaginal, perirectal, inguinal areas

enter by beaks in skin, trauma, insect bites, catheters, etc

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4
Q

What does this picture show?

A

pyrogenic disease–> cellulitis of skin with our without absecess (point to area of least resistance)

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5
Q

What are other pyrogenic skin manifistation?

A

impetigo, folliculitis, furuncle, carbuncle

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6
Q

Enterotoxin

A

pre-formed by bacteria in food before ingestion–>food poisoning

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7
Q

TSST-1 produced locally (eg. cellulitis or vaginal tampon)–>blood systemic effects

A
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8
Q

If staph aureus becomes bacteremic what can it cause?

A

endocarditis, osteomyelitis

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9
Q

What is the mechanism of suprantigens?

A

cross link T cells R and class II MHC molecules–> stimulate T cells non specifically–> release of pro-inflammatory cytokines (TNFa)–>shock

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10
Q

What caused this?

A

toxic shcok syndrome- may occurs with localized infection such as cellulities or with vaginal tampon or post surgical packing

manifistations- fever, erythema of the skin, followed by desquamation, conjuctivitis, strawberry, delirium, and shock

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11
Q

What bacteria causes this?

A

staph aureus–>scalded-skin syndrome

infants/young children

fever and generalize desquamation with large bullae

exfoliant, a protease, caues separation of layers in the spidermins

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12
Q

virulance factors: adhesion to host cells and substances:

A

teichoic acids- polymers of ribitol phosphate and lalow bacterial to stick to mucosal cells

lipoteochoic acid- pro-inflammatory

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13
Q

virulance factors: enzymes

A

coagulase- clots that walls off abscss from leukocytes

staphylokinase- plasminogen activator, lyses fibrin, allow spread of infection

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14
Q

virulance factor: PV-leucocidin-

A

post forming tocin that damages WBC, associated w/ severe skin/soft tissue infect and MRSA

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15
Q

virulance factor: avoidance of host responses

A

proteins A binds to Fc fragment of IgG at site that complement binds, thereby preventing activation of complement

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16
Q

virulance factors: carb capsule

A

poorly immunogenic

17
Q

Treatment for suppurative infections?

A

incision and surgical drainage may be enough, AB alone not enough

18
Q

tx for TSS- remove foreign body or drain the suppuration. support BP and cardiac fxn

A
19
Q

Diagnosis for s. aureus

A

gram stain smears show gram + cocci in clusters, but absence does not rule out!

in TSS- profound systemic effects, but blood cultures are often negative

no antigen, toxin, or ab test

20
Q

What does a positive blood culture for S. epidermidis tell us?

A

may be from contamination at phlebotomy site

21
Q

s. epidermidis characteristics

A

coagulase -

novobiocin sensitive

infect acquire through hospital or invasive med procedure, catheters, artificial heat valves, foreign body, etc.

lack toxins and invasion enzymes, no TSS

22
Q

Biofilms

A

bacteria attached to foregn body express exopolysaccharide

will help bacteria avoid immune defenses (eg. phagocytosis)

Biofilms also occur w/ S. aureus

23
Q

antibiotic resistance

A

penicillin–>methicillin/nafcillin/cephalosporins–>vancomysin–>daptomycin/quinupristin-daldopristin

24
Q

MRSA

A

90% strains have plasmid that encode a beta-actamase enzyme–>thus penicillin resistant

>50% of hospital strains and increased number of community acquired strains carry transferable mecA genes that encode altered penicillin-binding proteins–>met resistant (also to nafcillin, oxacillin, and cephalosporins

  • may be resistance to fluroqinolones, and topical muprocin
  • vanco resistant too, but less frequent.