ISSN 2398-2977      

Escherichia coli

pequis

Synonym(s): E. coli


Introduction

Classification

Taxonomy

  • Family: Enterobacteriaceae.
  • GenusEscherichia.
  • Speciescoli.

Classification of enteritis-causing E. coli strains

Enteric E. coli are classified on the basis of serological characteristics and virulence properties.

  • Enterotoxigenic E. coli (ETEC): have fimbrial adhesins to bind to enterocyte cells in small intestines, produce heat-labile and heat-stable enterotoxin, non-invasive and do not cause inflammation, cause neonatal colibacillosis.
  • Enteropathogenic E. coli (EPEC): do not produce enterotoxins, lack fimbria, use an adhesion known as intimin to bind to host intestinal cells, moderately invasive and elicit an inflammatory response, cause enteritis/diarrhea and colisepticemia.
  • Enteroinvasive E. coli (EIEC): invade intestinal mucosa, release endotoxins, not reported in horses.
  • Enterohemorrhagic E. coli (EHEC): have fimbrial adhesins to bind to enterocyte cells in small intestines, produce shiga toxin, moderately invasive and elicit an intense inflammatory response, not reported in horses.
  • Enteroaggregative E. coli (EAEC): have fimbria which induce cellular aggregation in vitro, produce a hemolysin and heat stable enterotoxin, non-invasive, not reported in horses.
  • Verotoxigenic E. coli (VTEC): produce verotoxin and have fimbria, not reported in horses.
  • Diffusely adherent E. coli (DAEC): produce fimbria which induce diffuse cellular adherence in vitro.
  • Necrotoxigenic E. coli (NTEC): produce cytotoxic necrotizing factors, hemolysin and fimbria.
  • Uropathogenic E. coli (UPEC): produce cytotoxic necrotizing factors and fimbria.
  • Invasive E. coli (SePEC): produce cytotoxic necrotizing factors and fimbria.

Etymology

  • Escherichia: named after Theodor Escherich, who named the type species of the genus.
  • Gk: kolon - food, meat.

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Clinical Effects

Epidemiology

Habitat

  • Pathogenic and non-pathogenic strains of E. coli inhibit the lower gastrointestinal tract.
  • Also abundant in the environment of animals.

Lifecycle

  • Reproduces by binary fission, usually in the gastrointestinal tract of the host.
  • Conjugation may occur with other bacteria to allow exchange of plasmids, which may bear toxin genes, and other transposable elements.

Transmission

  • Fecal oral route.

Pathological effects

  • Immunologic defense via:
    • Prevention of attachment to host cells.
    • Destruction of bacteria.
    • Neutralization of toxins.
  • Colostral antibodies important in protection against neonatal septicemia Foal: neonatal septicemia syndrome; requires maternal exposure to the virulence determinants of the particular strain.
Predisposers
  • Insufficient passive (colostral) immunity in neonates Foal: failure of passive transfer (IgG)
  • Poor environmental hygiene → build-up of pathogenic strain → may overcome normal levels of passive immunity.
  • Intensive farming methods → rapid transmission of pathogenic strains.
  • Age - (<1 week old) because:
    • Normal flora not yet established.
    • Immature immune system.
    • Receptors for the adhesins of E. coli only present for first week of life (calves) and first 6 weeks of life (piglets).
  • Stress factors, eg changed environment and diet in recently weaned pigs.
  • Heavy grain diets - allowing massive colonization of enterotoxigenic K88 and K99 strains of E. coli.
  • Recent change in feed and period of rapid growth, eg edema disease in pigs.
  • Surgery or contamination of wounds with fecal material.

Virulence factors of pathogenic E. coli strains

  • Certain fimbriae are protein adhesions and stimulate intestinal cell inflammatory pathways.
  • Alpha and beta hemolysins - pore-forming toxins.
  • Outer membrane proteins (OMPs) involved in bacteria-cell and bacteria-bacteria adhesion.
  • Type 3 secretion system involved in provoking the disappearance of enterocyte microvilli.
  • Siderophores - bind iron required by bacteria.
  • Heat-labile and heat-stable enterotoxins (LT enterotoxin is antigenically related to the cholera toxin).
  • Cytotoxic necrotizing factors - induce re-organization of cellular actin microfilaments in eukaryotic cells.
  • Verotoxin or Shiga-like toxins - inhibit protein synthesis in host cells.

Opportunistic infections

Other Host Effects

  • Predominant facultative species in large intestine.
  • Predominant facultative species in large intestine.

Diseases associated with E. coli

Horse

Dog and cat
  • Neonatal colisepticemia.
  • Pyometra.
  • Urinary tract infection.
Pig
  • Neonatal diarrhea.
  • Colisepticemia.
  • Piglet meningitis.
  • Edema disease.
  • Coliform mastitis.
  • Mastitis-metritis-agalactia (MMA) syndrome.
Cattle
  • White scour.
  • Colisepticemia.
  • Joint ill.
  • Coliform mastitis.
Sheep
  • Colibacillosis and colisepticemia.
  • 'Watery mouth'.
  • Coliform mastitis.
Poultry
  • Omphalitis.
  • Colisepticemia.
  • Coligranuloma.
  • Cellulitis.
Other species
  • Colibacillosis.
  • Colisepticemia.

Control

Control via animal

  • Some vaccines are available.
  • Maternal exposure to E. coli, allows for antibodies to be produced by the dam and secreted into the colostrum and milk.
  • Commercially produced preparations containing monoclonal antibodies to adhesins can be given orally to the neonate.

Control via chemotherapies

  • Most E. coli strains are sensitive to a wide range of antibiotics but resistance, often plasmid-mediated, is frequently encountered.

Antimicrobial susceptibility pattern often unpredictable.

  • The use of antimicrobials to treat diarrhea is controversial.

Control via environment

  • Exposure of mare to local strains.
  • Hygiene at parturition.

Vaccination

  • Some are available (not for horses).

Diagnosis

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Williams A et al (2013) Antimicrobial resistance changes in enteric Escherichia coli of horses during hospitalisation: resistance profiling of isolates. Vet J 195 (1), 121-126 PubMed
  • Maddox T W et al (2012) Cross-sectional study of antimicrobial-resistant bacteria in horses. Part 1: Prevalence of antimicrobial-resistant Escherichia coli and methicillin-resistant Staphylococcus aureusEquine Vet J 44 (3), 289-296 PubMed.
  • Maddox T W et al (2012) Cross-sectional study of antimicrobial-resistant bacteria in horses. Part 2: Risk factors for faecal carriage of antimicrobial-resistant Eschericia coli in horses. Equine Vet J 44 (3), 297-303 PubMed.
  • Mapes et al (2007) Comparison of five real-time PCR assays for detecting virulence genes in isolates of Escherichia coli from septicemic nenoatal foals. Vet Rec 161 (21), 716-718 PubMed.
  • Raisis A L, Hodgson J L & Hodgson D R (1996) Equine neonatal septicemia - 24 cases. Australian Vet J 73 (4), 137-140 PubMed.
  • Dorn C R (1995) Escherichia coli O157-H7. JAVMA 206 (10), 1583-1585 PubMed.
  • Cullor J S (1995) Escherichia coli O157-H7 - the silent danger. Vet Med 90 (1), 74-82.
  • Whipp S C, Rasmussen M A & Cray W C (1994) Animals as a source of Escherichia coli pathogenic for human beings. JAVMA 204 (4), 1168-1175.
  • Hirsch D C, Kirkham C and Wilson W D (1993) Characteristics of Escherichia coli isolated from septic foals. Vet Microbiol 34 (2), 123-130 PubMed.
  • Levine M (1987) Escherichia coli that causes diarrhea - enterotoxigenic, enteropathogenic, enteroinvasive, enterohemorrhagic and enteroadherent. J Infect Dis 155, 377 PubMed.

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