35. Staphylococci Flashcards
staphylococci, streptococci, & enterococci - catalase+/-?
catalase +: staphylococci
catalase -: streptococci & enterococci
staphylococci & O2?
facultative anaerobes
most virulent strains of staphylococci have a _____ which inhibits phagocytosis
polysaccharide capsule
many staphylococci have an outer _____ that facilitates the adherence of the bacteria to surfaces like catheters, shunts, and implants.
slime layer
staphylococcal orgs - coagulase + or -?
S. aureus = coagulase +
S. epidermidis, S. saphrophyticus, & S. lygdenensis = coagulase -
color of S. aureus and S. epidermidis on blood culture?
S. aureus = gold/yellow
S. epidermidis = white
the virulence of S. aureus depends on what abilities (4)?
evade host immune response
adhere to host tissues
destroy host tissue
evade abx tx
how does S. aureus evade the host immune response?
- capsule (helps inhibit phagocytosis by compromising neutrophil access)
- 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
how does S. aureus adhere to host?
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
how does S. aureus destroy host tissues?
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 )
S. aureus and PCN resistance?`
95% resistance thanks to penicillinases
PV leukocidin?
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)
which staphylococci toxins are always produced?
hemolysins and leukocidin
which staphylococci toxins are associated w/specific syndromes?
exfoliative toxins = scalded skin syndrome
enterotoxin = food poisoning
toxic shock syndrome toxin I = sepsis
S. aureus and methicillin resistance?
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
S.aureus and vancomycin resistance?
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)
what % of people are colonized w/ S. aureus?
30%
pyogenic infections caused by S. aureus?
cutaneous: impetigo, folliculitis, furuncles, carbuncles, wound infections
systemic: pna, empyema, osteomyelitis, septic arthritis, endocarditis, bacteremia
toxin-mediated clinical syndromes caused by S. aureus?
scalded skin syndrome, food poisoning, toxic shock syndrome
impretigo re: S. aureus?
children
contagious
infection of superficial skin layer (small flattened red macule, into pus-filled vescicle/pustule w/erythrematous base, to ruptures w/ YELLOW CRUSTING)
S. aureus & folliculitis?
pyogenic infection of hair follicles - raised painful lesion on indurated base
stye if at base of eyelid
furuncles and carbuncles & S. aureus?
furuncle = boil
- extension of folliculitis
- large, painful, pus-filled nodules
carbuncle
- coalesce involving multiple hair follicles and spread into deeper subQ tissues
S. aureus and wound infectoins?
after trauma/surgery (can be small)
possible foreign body: splinter, suture, implant
greater morbidity than other cutaneous pyogenic infections
the likelihood that S.aureus bacteremia will progress to pna, osteomyelitis, septic arthritis, or endocarditis increases w/what?
duration of infection
HA-S.aureus occur as a result of what?
Rx (surgery, intervention, device, etc)
CA-S.aureus occurs in what type of people?
those without other medical conditions
clinical disease of CA-S.aureus?
furuncles, pna (rare)
clinical disease of HA-S.aureus?
device associated or surgical site infections
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
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)
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)
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
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
S. epidermidis infection?
infections of prosthetic material (cental vascular catheters, prosthetic joint/heart valve, vascular or CNS shunts)…thnx to SLIME LAYER
S. saprophyticus infections?
young women UTIs leads to pyelonephritis sometimes
S. lygdenensis infections?
native valve endocarditis (virulent like S.aureus)
diagnosis of S. aureus infection?
clinical syndrome and culture evidence from sterile site or other site of inflammation (blood, skin site like abscess wound)
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
empiric therapy for a systemic staphylococcal infection?
vancomycin (or daptomycin if NOT PNEUMONIA)
empiric therapy for a localized staphylococcal infection?
clindamycin, TMP/SMX, doxycycline, linezolid
first line definitive therapy for serious staphylococcal infection?
anti-staphylococcal PCNs (nafcilin or cefazolin)
2nd line definitive therapy for serious staphylococcal infection?
vancomycin or daptomycin (if NOT PNA)
1st line definitive tx for outpatient staphylococcal infection?
anti-staphylococcal PCNs (dicloxacillin, cephalexin)
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)
S.aureus vs Strep skin infections?
S.aureus: abscess, cellulitis w/purulence, Rx as if MRSA
Strep: raised, upper dermis; clear demarcations; intensely red
