Brainscape's Knowledge GenomeTM

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


See full index

Microbiology Exam 1 > Staphylococcus aureus > Flashcards

Staphylococcus aureus Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

How do you differentiate staph and strep?

A
  1. gram stain - both + and cocci
  2. catalase- staph will bubble and + (strep will not)
  3. latex agglutination for coagulase - staph will be + (confirmatory)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

staph aureus characteristics

A

grape like, fac anaerobe, non-motile, skin and mucous membranes, carriers in nares

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

staph aureus epidemiology

A

opportunistic skin infection (unless coag negative); can survive on dry surfaces for a long time

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

staph aur. spreading

A

URI sneezing

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

protein A

A

a surface protein. coats surface of most SA, linked covalently to peptidoglycan; binds Fc receptor if IgG - prevents from recog. FAB region - masks staph from host

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

adherins

A

surface protein - collagen elastic and fibronectin binding protein

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

cytolytic enzymes

A

alpha and beta toxin gamma toxin and some have PVL

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

exfoliate enzymes

A

ETA AND ETB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

enterotoxins

A

food poisoning. stable at 100 degrees for 30 min so sometimes cooking won’t even kill it. resistant to hydrolysis in GI and jejunum. some are super antigen. emesis is common and thought to be due to inflam mediators from mast cells

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

TSS-1

A

cause TSS. superantigen. heat and proteolysis resistant.

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

ETB

A

plasmid - proteases cleave a skin protein - cause SSS or bulleous impetigo

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

ETA

A

phage - proteases cleave a skin protein – SSSS and buleous impetigo

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

biofilms

A

an ECM (polysacc) - microorg hides inside. serves as a barrier to enviro. helps with resistance to abx. place to exchange genetic material. - common with OM CF UTI chronic lung infection and CVL infection

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

impetigo

A

localized pyogenic cutaneous infection. impetigo- young ppl - face and limbs - v. contagious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

folliculitis

A

stye or hair follicle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

faruncle

A

extension of folliculitis. may spont drain

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

carbuncle

A

coalesced faruncle, deeper, multiple sinuses

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

wound infections

A

s/p sx or foreign body, deeper than others and inc risk of cellulitis, after trauma possibly

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

consequences of deep tissue invasion

A

bacteremia, endocarditis (flu —-> rapid deterioration), pneu (aspiration, spread through blood), osteomylitis or trauma induced osteochondrosis, septic arthritis and joints (s/p injection or prosthesis)

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

SSSS staph scalded skin syndrome

A

happens in young. happens far away from initial infection. often on eyes. clear liquid. no exudate

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

staph food poisoning

A

enterotoxins. common if human carrier makes something and it sits out a while. creates toxin but organism need not be present. rapid onset and course – S+S GI (NO FEVER!!!!!!!) you C/S organism

22
Q

TSS toxic shock syndrome

A

superantigen TSS1, tampons, abrupt onset of fever and then rapid deterioration (MODS and HYPOTENSION) - fatality 5%

23
Q

peptidoglycan

A

cross linked gives rigidity. this also keeps it from drying out. endotoxin like activity - has techoic acids

24
Q

pyrogens

A

peptidoglycans endotoxin like activity. endogenous - activate complement and release of IL-1 - activates aggregation of PMNs to make an abcess.

25
Q

techoic acids

A

peptidoglycan - helps to attach to mucous membrane

26
Q

importance of cytoplasmic membrane

A

important to maintain an osmotic barrier. anchors cellular enzymes

27
Q

capsule

A

polysacc slime layer, 11 capsular serotypes, protective against chemotaxis and phagocytosis by PMNs, faceplates attachment to artificial surfaces.

28
Q

coagulase

A

converts fibrinogen to fibrin - (only in + staph) - gives a protective layer to localise infection - via abcess

29
Q

catalase

A

h2o2 to o2 and h2o

30
Q

haluronidase

A

hydrolizes h. acid - helps spread into tissues

31
Q

staphilokinase or fibrinolysin

A

dissolves clot to break abcess and help spread

32
Q

lipases

A

hydrolyze fat - so once past dermis and epidermis it can spread into fatty areas and sebaceous glands etc. superficial skin infection in form of caruncle and feruncle

33
Q

nuclease

A

when cells die they release nucleic acids - it helps chew it up and spread it

34
Q

pcn-ase

A

facilitates resistance by cleaving beta lactam ring or mob in genetic elements

35
Q

pcn binding protein PBP2a

A

makes resistance to oxicillian (MRSA)

36
Q

communitiy aq. Staph A

A

scc mec gene, with increased virulence - remains susceptible to beta lactams, usually deem-necrotic and the most freq skin infection to present to the er

37
Q

scc cassette chromosomes

A

mobile genetic component r/t abx resistance

38
Q

resistance to oxicillian

A

pcn binding protein PBP2a

39
Q

hospital aq Staph A

A

scc mec gene and abx resistence

40
Q

MRSA resistance

A

pcn binding protein PBP2a

41
Q

alpha toxin and beta toxin

A

cytolytic toxins, alpha can make a pore in RBCS, leuko, plots (alpha hemolysin)

(beta - sphyngomylinase C) - hydrolysis of lipids to get inside - RBCS, leuk, macrophages and fibroblasts)

42
Q

beta and alpha toxin- what happens when they work together?

A

damage tissue and form abcess

43
Q

gamma toxin

A

lyse macrophages and neutrophils via a pore

44
Q

PVL

A

in some staph aureus - if high conc- NECROSIS and if low conc - APOPTOSIS

45
Q

differentiate bulleous impetigo and SSSS and caused by _____?

A

caused by ETA AND ETB (exfoliative enzymes)

SSSS - systemic and clear fluid

BImpetigo - yellow and local

46
Q

what do super antigens do? (ie. TSS1 in TSS)

A
  1. nonspecific cytokine release from macrophages and t cells
  2. inc hypersensitivy to endotoxin
  3. at low conc increase leakage of endothelial cells
  4. at inc conc - inc cytotoxic effects
  5. hypovolemic shock and mods cause death
47
Q

quorem sensing

A

has to do with gene exp. up reg release of secreted toxins and down reg of surface proteins (which regulates super antigen) - this is because the organism uses up all nutrients as it continues to grow.

48
Q

coag negative staph

A

staph epi

49
Q

staph epi

A

normal flora in ALL ppl. ltd virulence but very abx resistance. good with biofilms.

50
Q

staph epi - who is at risk?

A

immuno comp and preemies

51
Q

what does staph epi cause?

A

endocarditis (not naive valves but if so its congenital)

CVL and shunt inf.

prosthetic joints

UTI from catheter

likes foreign bodies etc artificial things

52
Q

how do you dx staph?

A

you scrape bottom/base of abcess and gram stain it.

use specific agar and C+S

biotype to differentiate type of staph

test for abx suscpetibily

NOOOOO SEROLOGY!!!!

Microbiology Exam 1 (6 decks)

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