Micro 12/13 Flashcards
describe the stages on the sepsis continuum
infection or trauma, SIRS, sepsis, septic shock, multi organ failure
clinical signs of SIRS
“systemic inflammatory response syndrome”
high fever (or hypothermia), leukocytosis or leukopenia or bandemia, tachycardia, tachypnea
how does SIRS become sepsis?
requires an infection
progression of sepsis
w/ low BP it is severe sepsis, w/ persistent hypotension it is septic shock (need pressor drugs)
what is MODS
multi organ dysfn sydnrome- SIRS + persistent hypotension causes lots of problems: clotting, organ failure, cognitive impairment, metabolite accumulation
what are some microbial triggers of SIRS
lipid A component of LPS in G- outer membrane
lipoteichoic acid in G+ and peptidoglycan
bacterial toxins
what are some bacteria associated w/ hospital sepsis
G+ cocci- staph, strep, enterococcus
G- rods- E coli, pseudomonas, acinetobacter, klebsiella
describe pseudomonas aeruginosa
common in water and soil, forms blue green colonies, fruity smell w/ infected wounds
p aeruginosa and CF
chronic lung mucoid colonization w/ overproduction of polysaccharide
they have LPS defects making them more sensitve to complement
3 opportunistic G- rods that cause sepsis in hospitals
klebsiella pneumoniae, pseudomonas aeruginosa, acinetobacter baumannii
describe acinetobacter baumannii
common in soil and water, coccobacilli or cocci, similar risk factors to pseudomonas
aceinetobacter resistance
some are resistant to all known antibiotics
describe klebsiella pneumoniae
4 characteristics
enterobacteriacea family, colonizers of the GI tract, collector of drug resistant plasmids, large capsule
klebsiella resistance mechanism
have a klebsiella pneumoniae carbapenemase
catalase neg bacteria
strep and enterococcus
catalase pos bacteria
staph- either S. aureus or the coag neg S. epidermidis
give examples of beta, alpha, and gamma hemolytic bacteria
all catalase positive
beta: Group A- S. pyogenes, Group B- S. agalactiae
alpha: S. pneumoniae and S. viridans
gamma: entero
acute and sequelae effects of strep pyogenes
leading cause of pharyngitis and cellulitis, impetigo, strep toxic shock
sequelae: glomerulonephritis, rheumatic fever
fn of S. pyogenes M protein
binds Ab and complement, antiphagocytic
cause of rheumatic fever
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)
IE etiology
G+ cocci, G- HACEK, candida, blood culture neg
cases where staph aureus is even more likely to cause IE
in hospital, IV drug users, w/ diabetes
S. aureus is most common w/ native valves
location of IE causing colonies
Staph and strep on skin, viridans strep in mouth, enterococci in GI
compare strep viridans and staph aureus in IE
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
purpose of pili/fimbriae
adhesion organelles, found in G- and G+
staph aureus and complement
the microbes can bind C4BP regulatory protein and inactivate C4b
capsules in GAS and staph aureus
hyaluronic acid in GAS and S aureus have polysaccharide
fn of staph protein A
binds to Fc portion of Abs, inhibiting their interatction w/ complement and prevents phagocytosis
manifestations of staph and strep superantigens
can cause cytokine storm
toxic shock syndrome and food poisoning from staph and scarlet fever from strep
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
