E. Coli Flashcards
E.coli- general characteristics
Many strands of E. coli are commensals of mammalian gut
Ferment lactose
indole positive (produce indole from tryptophan)
Most strains are flagellated
some strains have capsules–> cause extra-intestinal disease, usually hemolytic on blood agar
some strains have beta hemolysis on sheep blood agar
E. coli causing septicemia are hemolytic
E. coli- diseases it can cause
Neonatal and post-weaning diarrhea- many species
Neonatal septicemia- many species
Mastitis- many species–> 25-30% of mastitis caused by e.coli
UTI- many species
Hemorrhagic colitis and hemolytic uremia syndrome in humans (E. coli O157)
Oedema disease- pigs
Watery mouth- lambs–> overwhelming e.coli septicemia
Infection of existing lesions- many species–> mixed infection in gut.
E. coli pathogens
Enterotoxigenic E. coli–> ETEC- animals and humans
Enteropathogenic E. coli–> EPEC, AEEC- animals and humans
Verotoxigenic E. Coli–> VTEC/STEC- animals and humans (no symptoms in animals)
(Enterohemorrhagic E. Coli EHEC in man)
Enteroaggregative E. coli (EAEC), Diffusely adherent e. coli (DAEC), enteroinvasive E. coli (EIEC) all in humans
Extra-intestinal pathogenic e. coli ExPEC- animals and humans
-non-enteric infections- UTIs, mastitis, septicemia, meningitis
NB: generally strains that cause disease in animals don’t cause disease in humans (c.f. salmonella which as broad host range serotypes).
EXCEPTION: E. coli O157 is zoonotic, but animals are asymptomatic.
Virulence factors of Enterotoxigenic E. coli (ETEC)
heat labile enterotoxin (LT), heat stable enterotoxin (ST), particular fimbriae (allow targeting of gut tissue)
Virulence factors of Enteropathogenic E. coli
pathogenicity island (LEE), TTSS, intimin, particular fimbriae
Virulence factors of Enterohemorrhagic E. coli (O157)
pathogenicity island (LEE), TTSS, intimin, fimbriae and also acquired toxins (verotoxins/shiga-like toxins).
Virulence factors of Extra-intestinal pathogenic e. coli (ExPEC)
causes septicemia, UTIs–> hemolysin, iron-uptake systems, particular fimbriae and capsules–> genes required for an extra-intestinal life style
Mastitis has no particular virulence factors- perhaps it’s just an opportunist infection.
ExPEC infections of animals
Cows and Pigs: mastitis and septicemia
Dogs and Cats: UTIs, pyometra and septicemia
Poultry: air sacculitis, septicemia, cellulitis, yolk sac infection
Relation between commensal e. coli, septicemic pathogens and enteric pathogens
If you look at commensals of E. coli in gut, we see the same strains that cause septicemia and UTIs. ExPEC e. coli are carried in the gut, but don’t cause pathology there. intestinal pathologic e. coli must be acquired from another animal.
ExPEC virulence factors
Capsule- K antigen- survival within tissue/blood
Fimbriae (Pili): particularly imp. in UTI–> adhere to kidney/organ to avoid being flushed away
Toxins:1) hemolysin- effect on RBCs and WBCs
2) Cytotoxic necrotizing factor 1
Siderophores for scavenging iron
1) Enterochelin (enterobactin) found in pathogenic and commensal E. coli- produced by all E. coli strains; genes found on chromosomes
2) aerobactin: not all E. coli strains produce; genes found on plasmid.
Enterochelin vs. Aerobactin Siderophores
Enterochelin has a greater affinity for iron than aerobactin in vitro, but it’s suggested that pathogenic organisms ALL use aerobactin. Why? Enterobactin is bound by serum albumin, which inactivates it. Therefore, it can’t scavenge/return iron back to the bacterium. Anti-enterochelin ABs are produced. At a lower pH, aerobactin has a higher affinity for iron than enterochelin. No ABs are produced for aerobactin.
Enterotoxigenic E. Coli (ETEC)
non-invasive: just sit on mucosal surface–> that’s their mechanism of disease
Non-inflammatory, watery diarrhea
non-zoonotic: human strains don’t infect animals and vice versa
acute diarrhea in young animals–> life threatening. die d/t dehydration.
Mulitfactorial virulence of ETEC
one plasmid carries the toxin which causes diarrhea, and one plasmid carries the fimbriae which help colonize. To have disease occuring, must have both. Toxins result in not only water NOT getting absorbed, but also results in active secretion of water.
E. coli fimbriae
E. coli fimbriae action is SPECIFIC. it recognized species-specific receptors K88=F4--> pigs K99=F5--> pigs, sheep, calbes F6= pigs and calves F41= pigs and calves Human ETEC have different fimbriae.
ETEC toxins- mechanisms of LT and ST
action of heat labile (LT) and heat stable toxins (ST)
LT binds to receptor and modulates expression of G-protein. Transfers ADP ribose–> turns on/up-regulates adenylate cyclase–> increases cAMP-> activates protein kinase A–> opens channels for fluid secretion.
ST binds to receptor to up-regulate guanylate cyclase–> increase cGMP which prevents water absorption.
Can have one, or the other, or both toxins produced by a strain of E. coli
LT toxin
highly immunogenic. 1A subunit with enzyme ADP-ribosyltransferase and 3 B subunits which bind receptors
V. similar to cholera toxin
ST toxin
non-immunogenic d/t small size. small, single peptide
2 types: 1) STa produced by human and animals strains 2) STb produced by porcine e. coli strains
Genes for both types of toxins are carried on plasmids.
Diarrhea: ETEC vs. Salmonella species
E. coli: remain extra-cellular–> non-inflammatory diarrhea
Salmonella: invade cells- intracellular location –> inflammatory diarrhea.
Enteropathogenic E. coli (EPEC)
Diarrhea in young animals
Attaching and Effacing lesions- characterizing histopathological lesion.
Actin pedestals–> pilus attaches to gut, TTSS induces actin pedestals.
Microvilli effaced/ disappear- very localized.
Get diarrhea due to loss of microvill and some of the effector proteins injected by TTSS alter electrolyte absorption.
EPEC virulence factors
pathogenicity island–> locus of enterocyte effacement (LEE), TTSS
E. Coli O157- VTEC/STEC/EHEC- general characteristics
EHEC important in humans, VTEC/STEC important in animals.
certain VTEC/STEC strains with vero toxin/shiga-like toxin cause hemorrhagic colitis in humans (EHEC)
Shiga-like/vero toxin
SLT causes hemolytic uremic syndrome.
VT/SLT toxins
both are AB subunit toxins
A subunit= enzymatic N-glycosidase–> inhibits protein synthesis, kills cells–> removes an adenine residue from the 3’ end of 28S rRNA. Prevents binding of aminoacyl t-RNA to the ribosome.
B= binding gangliosides Gb3 and Gb4–> main target=endothelial cells of BVs–> causes edema, hemorrhage and thrombosis.
Gangliosides Gb3 and Gb4 are present on renal cells and endothelium of BVs. SLT and VT are responsible for hemolytic uremic disease seen in EHEC in humans
Hemorrhagic colitis
(more than 90% of EHEC cases) -sudden onset of severe cramps and abdominal pain bloody diarrhea after about 3 days nausea or vomiting little or no fever
Hemolytic uremic syndrome
most commonly occurs in infection in children (50% of kids with HUS have to get dialysis).
15% of E. coli O157 infected people develop HUS due to SLT getting into blood
Causes: hemolytic anemia, thrombocytopenia, renal failure.
ABX may make HUS worse due to lysing of bacteria and release of even more toxin
E. Coli O157
first isolated in 1982 in canada
found in hamburgers, raw potatoes, raw milk, unpasteurized fruit juices and cider, lettuce/alfalfa sprouts/salads and possibly sea eels in japan.
Around 100 organisms in healthy human is infectious dose.
EHEC reservoirs
Mostly in last 5cm of cattle rectum
chickens, deer sheep and pigs
carrier animal isn’t sick
meat becomes contaminated during slaughter process
bacteria on cow’s udders and equipment can contaminate milk
EHEC in certain countries
occurs more in developed countries (advanced foor production system); all other e.coli more often occur in developing countries.
Evolution of E. Coli O157 and VT
E. coli O157 is like an EPEC that also produces VT. Where does the VT come from? Lysogenic phages.
Virulence factors
LEE (locus of enterocyte effacement) is the pathogenicity island
VT1=shiga toxin
VT2 shares 56% homology with VT- often associated with severe e.coli but we don’t know why.
EHEC pathogenesis
EPEC infection plus a toxin-induced infection. Displacement of microvilli, lesions cause diarrhea. The toxins produce HUS and hemorrhagic enteritis.
Oedema disease in pigs
SLT/VT-2e, F18 fimbriae causes oedema (due to systemic release of SLT from gut) of forehead, stomach, LI and mesentery. No consistent evidence of enteritis, no LEE
Not zoonotic
Unique fimbriae bind to tissue.
E. coli outbreak Germany 2011
May-July 2011
4000 people, mainly adults
20% of people infected came down with HUS
found to be E. coli O104:H4
different serotype- hybrid of 2 pathotypes
Hypothetically enteroaggregative E. coli plus VT genes
EAEC+ VT genes
EAEC pathogenic in humans- causes chronic diarrhea in kids. This strain E. coli O104:H4 has acquired ST/VT from a phage. Get a number of organisms adhering, delivering lots of toxins which cause severe disease.
