Enterobacteria Flashcards
enterobacteriaceae cell morphology
moderate-size gram-negative rods; non-spore-forming; motile
enterobacteriaceae physiology
all are facultative anaerobes
ferment glucose
reduce nitrates to nitrites
distinguishing metabolic characteristics
oxidase negative
lactose fermentation
resistance to bile salts
indole test
oxidase negative
do not have cytochrome C oxidase; distinguishes pseudomonas (+) from other gram-negative rods (-)
lactose fermentation
red colonies on MacConkey agar
dark colonies (with a green sheen) on EMB agar
distinguishes lactose-fermenting from lactose non-fermenting
resistance to bile salts
growth with bile salts
shigella is resistant
salmonella is sensitive
indole test
tryptophanase converts tryptopha to indole (red with Kovac’s reagent)
e.coli (+) vs enterobacter sp (-)
distinguishes between different species
enterobacteriaceae ecology
found worldwide in soil, water, vegetation and microbial flora of animals and humans; some are always associated with disease; some are normal flora that can become pathogens
clinical presentations of enteric infections
GI infections (watery diarrhea) dysentery (bloody diarrhea) skin and wound infections enteric fever/typhoid fever septicemia (blood infection) meningitis (inflammation, infection of fluid around brain and spine) UTIs
enteric diarrhea
2nd leading cause of death among children 5 or younger in developing countries
diseases caused by e. coli
neonatal meningitis causing E. coli (NMEC)
UTIs - UPEC; usually acquired from hospitals
gastroenteritis - category B pathogen; 300,000 deaths/yr
enterotoxigenic (ETEC)
traveler’s diarrhea
ETEC mechanism
mediated by heat-labile enterotoxin (like cholera) and heat-stable enterotoxin; activate guanylate cyclase and stimulate secretion of fluid
EHEC/ STEC
produces cytotoxin (verotoxin) - called shiga-like toxin; severe abdominal pain, bloody diarrhea, low fever (or no fever); low infectious dose (<100 viable bacteria can cause disease); treatment with antibiotics is contraindicated
hemolytic uremic syndrom
(EHEC/STEC) causes acute renal failure - toxin causes death of endothelial cells of glomeruli and afferent arterioles, reducing glomerular filtration, and causing kidney tissue necrosis
EPEC
childhood diarrhea; organism adheres to enterocyte plasma membrane and causes destruction of microvilli producing watery diarrhea; adhesiveness mediated by plasmid-encoded pilus; infants less than 1 year affected
EHEC
responds to quorum sensing signals
EAEC
causes inflammatory, water and often persisten diarrhea; persistent and acute diarrhea in children; commonly isolated from patients with traveller’s diarrhea; HIV-positive patients with diarrhea; asymptomatic infection; strain heterogeneity; host susceptibility
enteroinvasive (EIEC)
mechanism is more related to shigella than other pathovars of e. coli
invades and destroys colonic epithelium; fever/cramps/bloody diarrhea; uncommon; oftenn foodborne
Shigella
most common cause of dysentry and persistent diarrhea
shigella properties
aerobic, non-motile, glucose-fermenting, gram-negative rods; low infectious dose (as few as 10 cells, ~500,000 infectious doses fit on a pin head); spread by fecal-oral contact; invade colonic epithelium; produce enterotoxins that can be cytotoxic (shiga-toxin and serine protease autotransporters)
shigella species
shigella sonnei (most common in US) shigella flexneri (mostly in developing countries) shigella boydii (not see much in the US, mostly in developing countries) shigella dysenteriae (severe, episodic outbreaks in developing countries)
shigella incubation time
symptoms begin 1-2 days after exposure
shigella clinical symptoms
abdominal cramps, diarrhea, fever, bloody stools
shigella sonnei/shigella flexneri
pediatric disease (1-4 years old); associated with daycare centers, schools, and custodial institutions; spread by fecal-oral route (not washing hands); low infectious dose: <50 bacilli can establish disease
s. dysenteriae virulence
type 1 virulence factor: shiga toxin; irreversibly inactivates mammalian 60S ribosomal subunit; stops protein synthesis; targets sodium absorptive villus cell; produces decrease in sodium absorption; more fluid accumulates in lumen; cytotoxic: kills intestinal epithelial and endothelial cells yielding bloody diarrhea
shigella pathogenesis
colonizes small intestine and multipies during first 12 hours; initial sign of infection is profuse watery diarrhea without histological evidence of mucosal invasion; mediated by enterotoxin; invasion of colonic epithelium results in lower abdominal cramps, difficulty defecating, abundant pus, and blood in stool; bacteremia is uncommon
s. sonnei pathogenesis
has the same invasion process as other species, but with no dysentery only watery diarrhea
s. dysenteriae type 1
most sever possibly due to intensity of inflammatory response
s. flexneri
causes severe illness with dysentery and bloody diarrhea; has no genes for shiga toxin
salmonella characteristics
non-motile, gram-negative, non-spore-forming rod
solmonella enterica sources of infection
contact with animals; ingestion of contaminated water, food; by fecal-oral contact in children
enteric fever
typhoid fever
typhoid fever
average incubation period is 10-14 days, up to 60 days; gradually increasing high fever; rash, headach, abdominal pain, malaise, and decreased appetite; symptoms typically persist for a few days, fewer can continue for weeks to months without treatment; severe cases result in intestinal perforation; treated with antibioitcs (increasing antibiotic resitance)
carrier state can develop
gastroenteritis
more common disease of salmonella infections; more acid sensitive than shigella; septicemia in pediatric and geriatric patients
