Introduction

Classification

Taxonomy

• Family: Enterobacteriaceae.
• Genus: Escherichia.
• Species: coli.

Classification of enteritis-causing E. coli

• Strains:
  • Enterotoxigenic E. coli (ETEC): have fimbrial adhesins, produce enterotoxin, cause neonatal colibacillosis.
  • Enteropathogenic E. coli (EPEC): do not produce enterotoxins or Shiga-like toxins, cause enteritis/diarrhea and colisepticemia by other mechanisms.
  • Enteroinvasive E. coli (EIEC): invade intestinal mucosa, release endotoxins, cause colisepticemia.
  • Enterohemorrhagic E. coli (EHEC): colonize small intestine, attach to target cells and kill them, Shiga-like toxins, isolated from calves and rabbits with enteric disease.

Etymology

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

Active Forms

Clinical Effects

Epidemiology

Habitat

• Pathogenic and nonpathogenic strains of E. coli inhabit 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. Requires maternal exposure to the virulence determinants of the particular strain.

Predisposers

• Insufficient passive (colostral) immunity, ie neonates.
• 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 enterotoxigenic 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

• Capsular polysaccharide (K antigen).
• Endotoxin (Lipid A) associated with septicemia and the toxemia in coliform mastitis.
• Certain fimbriae are protein adhesins.
• Alpha- and beta-hemolysins.
• Siderophores.
• Heat-labile and heat-stable enterotoxins. (LT enterotoxin is antigenically related to the cholera toxin.)
• Cytotoxic necrotizing factors.
• Verotoxin or Shiga-like toxins - inhibit protein synthesis in host cells. Important in edema disease and in neonatal calves and piglets.

Opportunistic infections

• E. coli strains, normally regarded as non-pathogenic can cause opportunistic infections, eg mastitis Mastitis and metritis.

Other Host Effects

• Predominant facultative species in large intestine.

Diseases associated with E. coli

Dog and cat

• Neonatal colisepticemia.
• Pyometra Pyometra.
• Urinary tract infection Cystitis.

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.
• Coliform mastitis.

Poultry

• Omphalitis.
• Colisepticemia.
• Coligranuloma (Hjarre's disease).

Other species

• Colibacillosis and colisepticemia.

Control

Control via animal

• Sound husbandry - the dam should be exposed to the local strains before parturition.
• Some vaccines are available.
• Maternal exposure to E. coli, either natural or artificial, 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 Therapeutics: antimicrobial drug to treat the diarrhea is controversial.

Vaccination

• Some are available.

Diagnosis

Further Reading

Publications

Refereed papers

• Recent references from PubMed and VetMedResource.
• Cullor J S (1995) Escherichia coli O157-H7 - the silent danger. Vet Med 90 (1), 74-82 VetMedResource.
• Dorn C R (1995) Escherichia coli O157-H7. JAVMA 206 (10), 1583-1585 PubMed.
• Whipp S C, Rasmussen M A & Cray W C Jr. (1994) Animals as a source of Escherichia coli pathogenic for human beings. JAVMA 204 (8), 1168-1175 PubMed.
• Hart C A, Embaye H, Getty B et al (1990) Ultrastructural lesions to canine intestinal epithelium caused by enteropathogenic Escherichia coli. JSAP 31 (12), 591-594 VetMedResource.
• Levine M M (1987) Escherichia coli that cause diarrhea - enterotoxigenic, enteropathogenic, enteroinvasive, enterohemorrhagic and enteroadherent. J Infect Dis 155 (3), 377-389 PubMed.
• Olson P, Hedhammar A, Faris A et al (1985) Enterotoxigenic Escherichia coli (ETEC) and Klebisella pneumoniae isolated from dogs with diarrhea. Vet Microbiol 10 (6), 577-589 PubMed.