Micro 12/13 Flashcards

1
Q

describe the stages on the sepsis continuum

A

infection or trauma, SIRS, sepsis, septic shock, multi organ failure

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2
Q

clinical signs of SIRS

A

“systemic inflammatory response syndrome”

high fever (or hypothermia), leukocytosis or leukopenia or bandemia, tachycardia, tachypnea

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3
Q

how does SIRS become sepsis?

A

requires an infection

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4
Q

progression of sepsis

A

w/ low BP it is severe sepsis, w/ persistent hypotension it is septic shock (need pressor drugs)

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5
Q

what is MODS

A

multi organ dysfn sydnrome- SIRS + persistent hypotension causes lots of problems: clotting, organ failure, cognitive impairment, metabolite accumulation

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6
Q

what are some microbial triggers of SIRS

A

lipid A component of LPS in G- outer membrane

lipoteichoic acid in G+ and peptidoglycan

bacterial toxins

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7
Q

what are some bacteria associated w/ hospital sepsis

A

G+ cocci- staph, strep, enterococcus

G- rods- E coli, pseudomonas, acinetobacter, klebsiella

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8
Q

describe pseudomonas aeruginosa

A

common in water and soil, forms blue green colonies, fruity smell w/ infected wounds

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9
Q

p aeruginosa and CF

A

chronic lung mucoid colonization w/ overproduction of polysaccharide

they have LPS defects making them more sensitve to complement

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10
Q

3 opportunistic G- rods that cause sepsis in hospitals

A

klebsiella pneumoniae, pseudomonas aeruginosa, acinetobacter baumannii

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11
Q

describe acinetobacter baumannii

A

common in soil and water, coccobacilli or cocci, similar risk factors to pseudomonas

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12
Q

aceinetobacter resistance

A

some are resistant to all known antibiotics

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13
Q

describe klebsiella pneumoniae

4 characteristics

A

enterobacteriacea family, colonizers of the GI tract, collector of drug resistant plasmids, large capsule

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14
Q

klebsiella resistance mechanism

A

have a klebsiella pneumoniae carbapenemase

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15
Q

catalase neg bacteria

A

strep and enterococcus

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16
Q

catalase pos bacteria

A

staph- either S. aureus or the coag neg S. epidermidis

17
Q

give examples of beta, alpha, and gamma hemolytic bacteria

A

all catalase positive
beta: Group A- S. pyogenes, Group B- S. agalactiae

alpha: S. pneumoniae and S. viridans
gamma: entero

18
Q

acute and sequelae effects of strep pyogenes

A

leading cause of pharyngitis and cellulitis, impetigo, strep toxic shock

sequelae: glomerulonephritis, rheumatic fever

19
Q

fn of S. pyogenes M protein

A

binds Ab and complement, antiphagocytic

20
Q

cause of rheumatic fever

A

molecular mimicry of M proteins- Abs attack host antigens that are similar and cause inflammation/ tissue damage to heart valves, joints, and basal ganglia (st vitus dance)

21
Q

IE etiology

A

G+ cocci, G- HACEK, candida, blood culture neg

22
Q

cases where staph aureus is even more likely to cause IE

A

in hospital, IV drug users, w/ diabetes

S. aureus is most common w/ native valves

23
Q

location of IE causing colonies

A

Staph and strep on skin, viridans strep in mouth, enterococci in GI

24
Q

compare strep viridans and staph aureus in IE

A

viridans are lower virulence, cause slow progression IE to previously damaged valves

aureus is higher virulence, affects normal valves, and has rapid onset of fever/sepsis

25
Q

purpose of pili/fimbriae

A

adhesion organelles, found in G- and G+

26
Q

staph aureus and complement

A

the microbes can bind C4BP regulatory protein and inactivate C4b

27
Q

capsules in GAS and staph aureus

A

hyaluronic acid in GAS and S aureus have polysaccharide

28
Q

fn of staph protein A

A

binds to Fc portion of Abs, inhibiting their interatction w/ complement and prevents phagocytosis

29
Q

manifestations of staph and strep superantigens

A

can cause cytokine storm

toxic shock syndrome and food poisoning from staph and scarlet fever from strep

30
Q

enterococci drug resistance

A

low affinity for beta lactams, resistant to clindamycin, can absorb folate from host (no Tmp-Smx), resistant to aminoglycosides at relevant doses, resistance to vanc is growing