Cross Staph Lecture Flashcards

(65 cards)

1
Q

differentiating lab properties of staphylococci?

A

nonmotile
no spores
catalase +

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2
Q

what does catalase do

A

degrade hydrogen peroxide from neuts

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3
Q

3 most important human staph pathogens

A

aureus
epidermidis
saprophyticus

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4
Q

how does staph aureus cause disease, generally?

A

producing toxins

inducing pyogenic inflammation

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5
Q

diseases caused by s aureus

A

abscess, septic arthritis, endocard, food poison, SSS, TSS; hosp-acq PNA ,septicemia, surgical wound infections; folliculitis, impetigo, bact conjunctivitis

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6
Q

what is predom organism of skin?

A

staph epi

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7
Q

diseases by staph epi?

A

endocarditis, prosthetic joint/ hardware infections

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8
Q

staph sapro causes what disease

A

UTI

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9
Q

what is carrier state

A

individual harbors pot’l pathogen and can infect others. Usually those who have recently recovered from a dis and still carry, OR those with asymp inf

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10
Q

What is colonization

A

acquisition of a NEW organism and may cause infection or may be elim by host defenses

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11
Q

what is colonization resistance

A

nonpathogenic resistant bacteria ocupy attachment sites on skin and mucosa, interfering with colonization by pathogenic bacteria

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12
Q

site of s aureus colonization

A

nose

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13
Q

s sapro site of colonization

A

skin around GU

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14
Q

what makes a s aureus plate yellow?

A

staphyloxanthin

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15
Q

Protein A

A

S. aureus. Binds Fc portion of IgG at complement binding site and prevents complement act; major comp of CW; **no C3b prod so phagocytosis of organisms is greatly reduced

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16
Q

P-V leukocidin

A

S. aureus. Pore-forming toxin kills cells, esp WBC, by damaging cell membranes; severe skin/soft tissue inf, also severe necrotizing PNA. Prod by MRSA, usually community-acq

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17
Q

Teichoic acids

A

S aureus. Mediates adherence to mucosal cells. Induces rel of IL-1, TNF from macs

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18
Q

peptidoglycan

A

S. aureus. Endotoxin-like prop. can act compelment, coag cascade, cytok

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19
Q

what strain of staph causes necrotizing PNA?

A

MRSA

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20
Q

main types of staph virulence factors?

A

surface proteins, enzymes, toxins

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21
Q

staphyloxanthin (carotenoid)

A

S. aureus. causes golden color. Inactivates microbicidal effect of superoxides and ROS in neuts

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22
Q

coagulase

A

S. aureus. Prothrombin –> thrombin, so fibrin clot forms. Walls off inf, delays migration of neuts to the site

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23
Q

hemolysins/alpha toxins

A

S aureus. hemolyze RBC and use the iron req for bact to grow. causes necrosis of skin and hemolysis

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24
Q

polysaccharide capsule

A

S. aureus. Stim macs to produce cytok, activates comp/coag

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25
gamma-toxin/ leukotoxin
lyses phagocytes and RBC
26
pyogenic s aureus infections
endocarditis, septic arthritis, osteomyelitis, postsurg wound inf, PNA-->empyema/abscess, sepsis, mastitis, abscess both from local inoculation and result of bloodstream inf
27
MRSA is common cause of infection and outbreak where?
childcare centers, IV drug users, wrestling teams, prisons, etc
28
pathogenesis of SSS
S. aureus. Exfoliatin, Exfoliative toxins A and B. Acts as a protease that cleaves desmoglein in desmosomes, leading to sep'n of epidermis at granular cell level
29
SSS symptoms
newborns 3-7 days; febrile, irritable, diffuse blanching erythema with blisters. No muc memb
30
SSS lesions
serous fluid exudates, deH, elyte imbalance. Flaky desquam and sloughing as healing occurs. diffuse blanching erythema with blisters/bullae 1-2 days later in flexural areas, butt, hands, feet.
31
SSS recovery
no scarring desquam 10 days
32
what mediates S aureus food poison
Enterotoxin A
33
What is enterotoxin A
S aureus food poisoning. superAg in GI tract, stim IL-1 and IL-2 from macs, Th cells. Heat resistent, acid resistant. Incubation period 1-8 hours
34
enterotoxin A symptoms
prominent vomiting, watery/non-bloody D+.
35
why vomiting in s aureus food poisoning
cytokines from enterotoxin A -->macs, Th cells stimulate enteric nervous system to vomit center in brain
36
cause of bullous impetigo
exfoliative toxin of s aureus.
37
bullous impetigo present
young children. Vesicles enlarge to flaccid bullae w clear yellow fluid which becomes darker. Thin brown crust when ruptured. TRUNK freq.
38
staph TSS pathogenesis
toxin-med/superAg. TSST at site enters blood-->toxemia. IL-1, 2, TNF. 5-25% s aureus carry TSST gene.
39
when can staph TSS happen
when people don't have Ab to TSST
40
what clinical settings does staph TSS occur?
tampons, nasal packing in epistaxis, post-op inf
41
blood cultures in staph TSS
NEGATIVE
42
signs/symp of staph TSS
fever, hypoTN, dizzy, syncope, diffuse macular erythroderma that desquamates 1-2 wks post onset; V/D, severe myalgia w CPK ^, renal fail, hyperbilirubin, thrombocytopenia, AMS
43
Tx MSSA
b-lactamase, so naf/oxacillin, cephalosporins, vanc, augmentin if mild
44
MRSA tx
vanco, dapto, linezolid, ceftaroline, bactim/clinda (mild)
45
tx VISA/VRSA
dapto linezolid ceftaroline
46
resistance mech of MRSA?
changes in PBP in cell memb. MecA genes on bact chrom encode them
47
VRSA resistance mech?
genes encode enz that sub D-lactate for D-alanine
48
VISA resistance mech?
synthe of unusually thick CW
49
Tx staph TSS
supportive (10-20 L fluid/day, vasopressors like dopamine, NE); surgical; antibiotics (vanc/oxacillin + CLINDA)
50
why give clindamycin w vanc/oxacillin in staph TSS?
suppresses protein synth and therefore toxin syth. Linezolid can have same effect
51
prevent S aureus for surgeries
peri-op Cefazolin +/- vanc depending on rate of MRSA in that area
52
role of mupirocin?
S aureus prevention to reduce colonization intranasally. combine w Hibiclens for bathing +/- doxy, bactrim. 1 week
53
microbiologic props of S aureus
cat + coag + beta-hemolytic ferments mannitol
54
microbiologic props of S epi
``` cat + coag - non-hemolytic urease + not mannitol ferm novobiocin sens ```
55
microbiologic props of s sapro
``` cat + coag - non-hemolytic urease + not mannitol ferm novobiocin RES ```
56
differences in novobiocin sesitivity
S epi sens | S sapro R
57
coagulase test for strep
+ for s aureus only | done with rabbit plasma
58
settings of S epi inf
foreign devices. probably inoculated at time of implant
59
pathogenesis of S epi
1. bact adhere. Surf prots bind to fibrinogen, fibronectin, etc on foreign matl. Many have adhesins critical 2. ECM, slime made to encase bact. barrier to antibiotic, interfere w defenses
60
what staph makes biofilm
S epi, aureus
61
S epi tx
VANCO. oxa/nafcillin if MSSE. + Rifampin, gent if prosth valve endocarditis removedevice.
62
MRSE mech of resist
changes in PBP in cell memb. MecA genes on bact chrom encode them. just like MRSA
63
S sapro
2nd most common cause of comm-acq UTI in women | sex w/in 24 hrs
64
tx S sapro UTI
Bactrim, Cipro
65
Cipro
NOT for S aureus. Only S sapro