Enterobacteria

Question 1

enterobacteriaceae cell morphology

Answer 1

moderate-size gram-negative rods; non-spore-forming; motile

Question 2

enterobacteriaceae physiology

Answer 2

all are facultative anaerobes

ferment glucose
reduce nitrates to nitrites

Question 3

distinguishing metabolic characteristics

Answer 3

oxidase negative
lactose fermentation
resistance to bile salts
indole test

Question 4

oxidase negative

Answer 4

do not have cytochrome C oxidase; distinguishes pseudomonas (+) from other gram-negative rods (-)

Question 5

lactose fermentation

Answer 5

red colonies on MacConkey agar
dark colonies (with a green sheen) on EMB agar
distinguishes lactose-fermenting from lactose non-fermenting

Question 6

resistance to bile salts

Answer 6

growth with bile salts
shigella is resistant
salmonella is sensitive

Question 7

indole test

Answer 7

tryptophanase converts tryptopha to indole (red with Kovac’s reagent)

e.coli (+) vs enterobacter sp (-)

distinguishes between different species

Question 8

enterobacteriaceae ecology

Answer 8

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

Question 9

clinical presentations of enteric infections

Answer 9

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

Question 10

enteric diarrhea

Answer 10

2nd leading cause of death among children 5 or younger in developing countries

Question 11

diseases caused by e. coli

Answer 11

neonatal meningitis causing E. coli (NMEC)

UTIs - UPEC; usually acquired from hospitals

gastroenteritis - category B pathogen; 300,000 deaths/yr

Question 12

enterotoxigenic (ETEC)

Answer 12

traveler’s diarrhea

Question 13

ETEC mechanism

Answer 13

mediated by heat-labile enterotoxin (like cholera) and heat-stable enterotoxin; activate guanylate cyclase and stimulate secretion of fluid

Question 14

EHEC/ STEC

Answer 14

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

Question 15

hemolytic uremic syndrom

Answer 15

(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

Question 16

EPEC

Answer 16

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

Question 17

EHEC

Answer 17

responds to quorum sensing signals

Question 18

EAEC

Answer 18

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

Question 19

enteroinvasive (EIEC)

Answer 19

mechanism is more related to shigella than other pathovars of e. coli

invades and destroys colonic epithelium; fever/cramps/bloody diarrhea; uncommon; oftenn foodborne

Question 20

Shigella

Answer 20

most common cause of dysentry and persistent diarrhea

Question 21

shigella properties

Answer 21

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)

Question 22

shigella species

Answer 22

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)

Question 23

shigella incubation time

Answer 23

symptoms begin 1-2 days after exposure

Question 24

shigella clinical symptoms

Answer 24

abdominal cramps, diarrhea, fever, bloody stools

Question 25

shigella sonnei/shigella flexneri

Answer 25

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

Question 26

s. dysenteriae virulence

Answer 26

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

Question 27

shigella pathogenesis

Answer 27

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

Question 28

s. sonnei pathogenesis

Answer 28

has the same invasion process as other species, but with no dysentery only watery diarrhea

Question 29

s. dysenteriae type 1

Answer 29

most sever possibly due to intensity of inflammatory response

Question 30

s. flexneri

Answer 30

causes severe illness with dysentery and bloody diarrhea; has no genes for shiga toxin

Question 31

salmonella characteristics

Answer 31

non-motile, gram-negative, non-spore-forming rod

Question 32

solmonella enterica sources of infection

Answer 32

contact with animals; ingestion of contaminated water, food; by fecal-oral contact in children

Question 33

enteric fever

Answer 33

typhoid fever

Question 34

typhoid fever

Answer 34

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

Question 35

gastroenteritis

Answer 35

more common disease of salmonella infections; more acid sensitive than shigella; septicemia in pediatric and geriatric patients