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
purpose of pili/fimbriae
adhesion organelles, found in G- and G+
26
staph aureus and complement
the microbes can bind C4BP regulatory protein and inactivate C4b
27
capsules in GAS and staph aureus
hyaluronic acid in GAS and S aureus have polysaccharide
28
fn of staph protein A
binds to Fc portion of Abs, inhibiting their interatction w/ complement and prevents phagocytosis
29
manifestations of staph and strep superantigens
can cause cytokine storm toxic shock syndrome and food poisoning from staph and scarlet fever from strep
30
enterococci drug resistance
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