Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Dermatology > Cross Staph Lecture > Flashcards

Cross Staph Lecture Flashcards

You may prefer our related Brainscape-certified flashcards:
Dermatology Board Prep flashcards
1
Q

differentiating lab properties of staphylococci?

A

nonmotile
no spores
catalase +

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what does catalase do

A

degrade hydrogen peroxide from neuts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

3 most important human staph pathogens

A

aureus
epidermidis
saprophyticus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how does staph aureus cause disease, generally?

A

producing toxins

inducing pyogenic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is predom organism of skin?

A

staph epi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

diseases by staph epi?

A

endocarditis, prosthetic joint/ hardware infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

staph sapro causes what disease

A

UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is colonization

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is colonization resistance

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

site of s aureus colonization

A

nose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

s sapro site of colonization

A

skin around GU

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what makes a s aureus plate yellow?

A

staphyloxanthin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Teichoic acids

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

peptidoglycan

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what strain of staph causes necrotizing PNA?

A

MRSA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

main types of staph virulence factors?

A

surface proteins, enzymes, toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

staphyloxanthin (carotenoid)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

coagulase

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

polysaccharide capsule

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

gamma-toxin/ leukotoxin

A

lyses phagocytes and RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

pyogenic s aureus infections

A

endocarditis, septic arthritis, osteomyelitis, postsurg wound inf, PNA–>empyema/abscess, sepsis, mastitis, abscess both from local inoculation and result of bloodstream inf

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

MRSA is common cause of infection and outbreak where?

A

childcare centers, IV drug users, wrestling teams, prisons, etc

28
Q

pathogenesis of SSS

A

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
Q

SSS symptoms

A

newborns 3-7 days; febrile, irritable, diffuse blanching erythema with blisters. No muc memb

30
Q

SSS lesions

A

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
Q

SSS recovery

A

no scarring
desquam
10 days

32
Q

what mediates S aureus food poison

A

Enterotoxin A

33
Q

What is enterotoxin A

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
Q

enterotoxin A symptoms

A

prominent vomiting, watery/non-bloody D+.

35
Q

why vomiting in s aureus food poisoning

A

cytokines from enterotoxin A –>macs, Th cells stimulate enteric nervous system to vomit center in brain

36
Q

cause of bullous impetigo

A

exfoliative toxin of s aureus.

37
Q

bullous impetigo present

A

young children. Vesicles enlarge to flaccid bullae w clear yellow fluid which becomes darker. Thin brown crust when ruptured. TRUNK freq.

38
Q

staph TSS pathogenesis

A

toxin-med/superAg. TSST at site enters blood–>toxemia. IL-1, 2, TNF. 5-25% s aureus carry TSST gene.

39
Q

when can staph TSS happen

A

when people don’t have Ab to TSST

40
Q

what clinical settings does staph TSS occur?

A

tampons, nasal packing in epistaxis, post-op inf

41
Q

blood cultures in staph TSS

A

NEGATIVE

42
Q

signs/symp of staph TSS

A

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
Q

Tx MSSA

A

b-lactamase, so naf/oxacillin, cephalosporins, vanc, augmentin if mild

44
Q

MRSA tx

A

vanco, dapto, linezolid, ceftaroline, bactim/clinda (mild)

45
Q

tx VISA/VRSA

A

dapto
linezolid
ceftaroline

46
Q

resistance mech of MRSA?

A

changes in PBP in cell memb. MecA genes on bact chrom encode them

47
Q

VRSA resistance mech?

A

genes encode enz that sub D-lactate for D-alanine

48
Q

VISA resistance mech?

A

synthe of unusually thick CW

49
Q

Tx staph TSS

A

supportive (10-20 L fluid/day, vasopressors like dopamine, NE); surgical; antibiotics (vanc/oxacillin + CLINDA)

50
Q

why give clindamycin w vanc/oxacillin in staph TSS?

A

suppresses protein synth and therefore toxin syth. Linezolid can have same effect

51
Q

prevent S aureus for surgeries

A

peri-op Cefazolin +/- vanc depending on rate of MRSA in that area

52
Q

role of mupirocin?

A

S aureus prevention to reduce colonization intranasally. combine w Hibiclens for bathing +/- doxy, bactrim. 1 week

53
Q

microbiologic props of S aureus

A

cat +
coag +
beta-hemolytic
ferments mannitol

54
Q

microbiologic props of S epi

A 
cat +
coag -
non-hemolytic
urease +
not mannitol ferm
novobiocin sens
55
Q

microbiologic props of s sapro

A 
cat +
coag -
non-hemolytic
urease +
not mannitol ferm
novobiocin RES
56
Q

differences in novobiocin sesitivity

A

S epi sens

S sapro R

57
Q

coagulase test for strep

A

+ for s aureus only

done with rabbit plasma

58
Q

settings of S epi inf

A

foreign devices. probably inoculated at time of implant

59
Q

pathogenesis of S epi

A
  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
Q

what staph makes biofilm

A

S epi, aureus

61
Q

S epi tx

A

VANCO. oxa/nafcillin if MSSE.
+ Rifampin, gent if prosth valve endocarditis
removedevice.

62
Q

MRSE mech of resist

A

changes in PBP in cell memb. MecA genes on bact chrom encode them. just like MRSA

63
Q

S sapro

A

2nd most common cause of comm-acq UTI in women

sex w/in 24 hrs

64
Q

tx S sapro UTI

A

Bactrim, Cipro

65
Q

Cipro

A

NOT for S aureus. Only S sapro

Dermatology (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions