35. Staphylococci Flashcards

(45 cards)

1
Q

staphylococci, streptococci, & enterococci - catalase+/-?

A

catalase +: staphylococci

catalase -: streptococci & enterococci

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2
Q

staphylococci & O2?

A

facultative anaerobes

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3
Q

most virulent strains of staphylococci have a _____ which inhibits phagocytosis

A

polysaccharide capsule

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4
Q

many staphylococci have an outer _____ that facilitates the adherence of the bacteria to surfaces like catheters, shunts, and implants.

A

slime layer

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5
Q

staphylococcal orgs - coagulase + or -?

A

S. aureus = coagulase +

S. epidermidis, S. saphrophyticus, & S. lygdenensis = coagulase -

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6
Q

color of S. aureus and S. epidermidis on blood culture?

A

S. aureus = gold/yellow

S. epidermidis = white

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7
Q

the virulence of S. aureus depends on what abilities (4)?

A

evade host immune response

adhere to host tissues

destroy host tissue

evade abx tx

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8
Q

how does S. aureus evade the host immune response?

A
  1. capsule (helps inhibit phagocytosis by compromising neutrophil access)
  2. Protein A = cell wall protein w/multiple Fc IgG receptors - so binds IgG in an incorrect orientation so that the neutrophil doesn’t recognize it and thus inhibits phagocytosis
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9
Q

how does S. aureus adhere to host?

A

surface adhesions:

many adhesion proteins = MSCRAMM (includes protein A, also fibrinogen, fibronectin, elastin, and collagen) to facilitate adherence to host

Protein A binds to vWF (adhesion re: endothelial damage)

binds to host proteins

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10
Q

how does S. aureus destroy host tissues?

A

ENZYMATIC

promotes bacterial spread/invasion through tissues (coagulase & microthrombus formation to dist to other tissues, hyaluronidase & hydrol of hyaluronic acid to get through cartilage)

improves bacterial survival (catalase removes H2O2)

tissue destruction (fibrinolysin & dissolves fibrin clots; lipases & hydrol of lipids; nucleases & hydrol of DNA)

TOXIN:

cytotoxins (hemolysins and leukocidin like PV lyse cell membranes & destroy leukocytes, erythrocytes, and macrophages)

cytolytic peptides (recruit then lyse neutrophils, overproduced in CA-MRSA )

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11
Q

S. aureus and PCN resistance?`

A

95% resistance thanks to penicillinases

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12
Q

PV leukocidin?

A

cytotoxin that causes leukocyte destruction and tissue necrosis. It is present in many strains (marker for particularly virulent strains) of CA-S.aureus (esp S/ST and PNA)

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13
Q

which staphylococci toxins are always produced?

A

hemolysins and leukocidin

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14
Q

which staphylococci toxins are associated w/specific syndromes?

A

exfoliative toxins = scalded skin syndrome

enterotoxin = food poisoning

toxic shock syndrome toxin I = sepsis

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15
Q

S. aureus and methicillin resistance?

A

50% thanks to MecA gene making new PBP = PBP2A.

so resistant to all semi-synthetic pcns: nafcillin (IV) and dicloxacillin (oral)

confers resistance to other B-lactam agents

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16
Q

S.aureus and vancomycin resistance?

A

rare: 1%

encoded by vanA gene (VRE)

alteration of binding site (so no longer D-ala-D-ala but D-ala-D-lac)

all pts colonized w/BOTH VRSA and MRSA (so many vanA gene is shared)

VISA still common but still rare-> thickened cell wall resulting in inability of abx to penetrate (excess D-ala-D-ala soaks up all of the vancomycin)

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17
Q

what % of people are colonized w/ S. aureus?

A

30%

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18
Q

pyogenic infections caused by S. aureus?

A

cutaneous: impetigo, folliculitis, furuncles, carbuncles, wound infections
systemic: pna, empyema, osteomyelitis, septic arthritis, endocarditis, bacteremia

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19
Q

toxin-mediated clinical syndromes caused by S. aureus?

A

scalded skin syndrome, food poisoning, toxic shock syndrome

20
Q

impretigo re: S. aureus?

A

children

contagious

infection of superficial skin layer (small flattened red macule, into pus-filled vescicle/pustule w/erythrematous base, to ruptures w/ YELLOW CRUSTING)

21
Q

S. aureus & folliculitis?

A

pyogenic infection of hair follicles - raised painful lesion on indurated base

stye if at base of eyelid

22
Q

furuncles and carbuncles & S. aureus?

A

furuncle = boil

  • extension of folliculitis
  • large, painful, pus-filled nodules

carbuncle
- coalesce involving multiple hair follicles and spread into deeper subQ tissues

23
Q

S. aureus and wound infectoins?

A

after trauma/surgery (can be small)

possible foreign body: splinter, suture, implant

greater morbidity than other cutaneous pyogenic infections

24
Q

the likelihood that S.aureus bacteremia will progress to pna, osteomyelitis, septic arthritis, or endocarditis increases w/what?

A

duration of infection

25
HA-S.aureus occur as a result of what?
Rx (surgery, intervention, device, etc)
26
CA-S.aureus occurs in what type of people?
those without other medical conditions
27
clinical disease of CA-S.aureus?
furuncles, pna (rare)
28
clinical disease of HA-S.aureus?
device associated or surgical site infections
29
staphylococcal scalded skin syndrome?
toxinosis: infection usu in umbilical cord and the organism produces toxin which disseminates in the bloodstream young children w/no Abs epidermolytic toxins (exfoliative) - lysis of desmosomes in epidermal granular cell layer cutaenous blisters w/no organisms or inflammatory cell s(toxin only) no scarring self-limiting
30
bullous impetigo?
localized scalded skin syndrome local spread of toxin around a colonized/infected wound in ppl w/ some immunity against the toxin localized blistering occurs w/bacteria and inflammatory cell filled blisters (due to close proximity of infection/colonization)
31
staphylococcal food poisoning?
acute onset, w/in 2-6 hours N/V, diarrhea, and abd pain w/o fever ingestion of pre-formed toxin enterotoxins (SEA): heat and acid stable, superantigens (increase peristalsis, fluid loss, N/V/D), interacts w/vagal emetic receptors treatment is supportive (IV fluids)
32
staphylococcal toxic shock syndrome
acute onset fever, hypotension progression to sepsis/shock diffuse erythematous rash (often desquamates) ***TSST-1 is MOST COMMON tx of infection necessary - w/appropriate abx and CONTROL THE SOURCE
33
cagulase negative staphylococci - virulence factors?
slime layer many of the same enzymes as S.aureus (catalase, hyaluronidase, penicillinase) but no (few) toxins antimicrobial resistance common
34
S. epidermidis infection?
infections of prosthetic material (cental vascular catheters, prosthetic joint/heart valve, vascular or CNS shunts)...thnx to SLIME LAYER
35
S. saprophyticus infections?
young women UTIs leads to pyelonephritis sometimes
36
S. lygdenensis infections?
native valve endocarditis (virulent like S.aureus)
37
diagnosis of S. aureus infection?
clinical syndrome and culture evidence from sterile site or other site of inflammation (blood, skin site like abscess wound)
38
diagnosis of coagulase-negative Staphylococci infection?
clinical syndrome and culture evidence: from blood requires multiple positive cultures to rule out skin contamination from sterile site (like prosthetic material) - still need multiple positives
39
empiric therapy for a systemic staphylococcal infection?
vancomycin (or daptomycin if NOT PNEUMONIA)
40
empiric therapy for a localized staphylococcal infection?
clindamycin, TMP/SMX, doxycycline, linezolid
41
first line definitive therapy for serious staphylococcal infection?
anti-staphylococcal PCNs (nafcilin or cefazolin)
42
2nd line definitive therapy for serious staphylococcal infection?
vancomycin or daptomycin (if NOT PNA)
43
1st line definitive tx for outpatient staphylococcal infection?
anti-staphylococcal PCNs (dicloxacillin, cephalexin)
44
2nd line definitive tx for outpatient staphylococcal infection?
clindamycin, TMP/SMX, doxycycline (CA-MRSA), or linezolid but *** TMP/SMX and doxycycline may not cover streptococcus (the other common cause of S/ST infections)
45
S.aureus vs Strep skin infections?
S.aureus: abscess, cellulitis w/purulence, Rx as if MRSA Strep: raised, upper dermis; clear demarcations; intensely red