Introduction

Classification

Taxonomy

• Family: enterobacteriaceae.
• Genus: escherichia.
• Species: coli.

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.
• 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.
• Enteroaggregative E. coli (EAEC):
  • Have fimbria which induce cellular aggregation in vitro, produce a hemolysin and heat stable enterotoxin, non-invasive.
• Verotoxigenic E. coli (VTEC):
  • Produce verotoxin and have fimbria.
• 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.

Active Forms

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 Disease transmission.

Pathological effects

• Immunologic defence via:
  • Prevention of attachment to host cells.
  • Destruction of bacteria.
  • Neutralization of toxins.
• Colostral antibodies important in protection against neonatal septicemia Colostrum: overview.

Predisposers

• Insufficient passive (colostral) immunity in 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 E. coli only present for first week of life (calves) and first 6 weeks of life (piglets).
• Stress factors, eg changed environment and diet.
• Heavy grain diets - allowing massive colonization of enterotoxigenic K88 and K99 strains of E. coli.
• 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

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

Other Host Effects

• Predominant facultative species in large intestine.

• Predominant facultative species in large intestine.

Diseases associated with E. coli

• Scour.
• Colisepticemia.
• Joint ill.
• Coliform mastitis.

Control

Control via animal

• Some vaccines are available Mastitis: vaccines.
• Maternal exposure to E. coli, allows for antibodies to be produced by the dam and secreted into the colostrum and milk. Newborn animals should be provided with access to colostrum.
• 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.
• Calves with neonatal diarrhea should be provided with fluids. Fluid therapy
• Bovine gammaglobulin can be provided to calves with hypogammaglobulinemia.

Control via environment

• Hygiene at parturition, including provision of a clean environement.

Vaccination

• Commercial vaccines do exist.

Diagnosis

Further Reading

Publications

Refereed papers

• Recent references from PubMed and VetMedResource.
• Saeedi P, Yazdanparast M, Behzadi E, Salmanian A H, Mousavi S L, Nazarian S & Amani J (2017) A review on strategies for decreasing E. coli O157:H7 risk in animals. Microb Pathog 103, 186-195 PubMed.
• Ekong P S, Sanderson M W & Cernicchiaro N (2015) Prevalence and concentration of Escherichia coli O157 in different seasons and cattle types processed in North America: A systematic review and meta-analysis of published research. Prev Vet Med 121 (1-2), 74-85 PubMed.
• Munns K D, Selinger L B, Stanford K, Guan L, Callaway T R & McAllister T A (2015) Perspectives on super-shedding of Escherichia coli O157:H7 by cattle. Foodborne Pathog Dis 12 (2), 89-103 PubMed.
• Smith D R (2014) Vaccination of Cattle against Escherichia coli O157:H7. Microbiol Spectr 2 (6) PubMed.
• Vande Walle K, Vanrompay D & Cox E (2013) Bovine innate and adaptive immune responses against Escherichia coli O157:H7 and vaccination strategies to reduce faecal shedding in ruminants. Vet Immunol Immunopathol 152 (1-2), 109-20 PubMed.
• Ferens W A & Hovde C J (2011) Escherichia coli O157:H7: animal reservoir and sources of human infection. Foodborne Pathog Dis 8 (4), 465-87 PubMed.
• Cullor J S (1995) Escherichia coli O157-H7 - the silent danger. Vet Med 90 (1), 74-82.
• Dorn C R (1995) Escherichia coli O157-H7. JAVMA 206 (10), 1583-1585 PubMed.
• 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.
• Levine M (1987) Escherichia coli that causes diarrhea - enterotoxigenic, enteropathogenic, enteroinvasive, enterohemorrhagic and enteroadherent. J Infect Dis 155, 377 PubMed.