E. Coli Flashcards
Enterobacteriaceae (general features)
Gram Negative bacilli of enteric tract
facultative anaerobes
mostly found in the lower GI tract
ferment sugars (different types used for distinguishing between species)
usually motile–> have flagellae all around surface
ETEC
epi and clinical presentation
Enterotoxigenic E. Coli
important in developing countries– diarrhea in children and travelers
watery diarrhea
short duration (usually 1-5 days)
25% of patients can have nausea, vomiting, malaise, anorexia, cramping
rarely fatal
fecal-oral transmission
ETEC– Virulence Factors
1) Colonization Factor Antigens (pili)
2) Heat-labile enterotoxin
ADP-ribosylation causes activation of adenylate cyclase–> increase in cAMP—> opening of CFTR–> Cl secreted into lumen of gut and water follows
3) heat-stable enterotoxin
small peptide –> binds gunaylate cyclase –> increase in cGMP–> activation of CFTR–> Cl secretion into gut
Pili + heat-labile enterotoxin + heat-stable entertoxin
ETEC
EPEC
Epi and clinical presentation
Enteropathogenic E. Coli
important in infants in developing countries
person to person transmission
only requires small inoculum
watery diarrhea AND vomiting
often fever
usually short duration but can be protracted
rare but can be deadly
vomiting makes re-hydration therapy difficult in non-IV accessible countries
EPEC– virulence factors
adherence via plasmid-encoded pilus
Bundle-forming pilus which causes aggregation into microcolonies
attaching and effacing via type 3 secretion system encoded on pathogenicity island (LEE)
inject Tir into host membrane using T3SS which acts as a receptor for Intimin to bind
Attaching and effacing mechanisms
EPEC
EHEC
epi and clinical presentation
Enterohemorrhagic E. Coli –> O157:H7
reservoir is cattle and most common contaminated food is ground beef, produce, and unpasteurized juice- also drinking water and swimming pools
can be transmitted person to person
LOW inoculum required for illness
day cares, petting zoos, etc.
Severe cramps and abdominal pain, bloody diarrhea (can be copious amounts that are mistaken for GI bleed), no or low-grade fever, inflammation/edema of ascending and transverse colon
Complication: HUS in young children and elderly (~4% of cases)
EHEC– virulence factors
Attaching/effacing AND Shiga toxins
Shiga toxins-
encoded by bacteriophages
induced by SOS response (could be caused by antibiotics, oxidative stress)
leads to protein synthesis inhibition and cell lysis
MOST COMMON SEROTYPE is O157: H7
EAEC
epi and clinical presentation
Enteroaggregative E. Coli
childhood diarrhea in developing countries – can be persistent and associated with growth retardation
traveler’s diarrhea
watery diarrhea with mucous and/or blood
growth retardation
EAEC– virulence factors
pili –> aggregative adherence
damage to intestinal cells
toxins (pet and EAST)- nonShiga
ExPEC
Extra-intestinal Pathogenic E. Coli
causes neonatal meningitis and UTIs (#1 cause)
K1 capsule, fimbriae, invasive
Proteus mirabilis
Gram negative bacilli
swarming motility- fimbriae
urease producers–> catalyzes hydrolysis of urea
alkaline urine
precipitates resulting in stones
kidney calculi (stag horn) form in renal pelvis and cannot properly treat bacterial infection until clear blocks
unlike all other GNB, proteus is resistant to tigecycline and polymixin
Ampicillin, TMP-SMX, cephalosporins, or fluoroquinolones
ETEC treatment
Oral rehydration
can treat with anti-motility agents
antimicrobials can shorten duration, but usually seen as not worth using–> fluroquinolone or rifaximin
EPEC treatment
rehydration
supportive care
high levels or resistance to anti-microbials and not proven useful
NO anti-motility agents
