• Cause: colibacillosis is caused by a gram-negative bacillus belonging to the Enterobacteriaceae family and genus Escherichia. The Escherichia coli (E. coli) species is ubiquitous to the environment and the lower gastrointestinal tract of birds and mammals.
• Avian colibacillosis refers to any localized or systemic infection caused entirely or partly by avian pathogenic E. coli (APEC). This is in contrast to colibacillosis in mammals, where infection is most often primary enteric or in the urinary tract.
• E. coli is transmitted via the fecal-oral route. Poultry may become infected by direct contact with dirty litter and hatchers or contaminated eggshells.
• Avian colibacillosis most often occurs in poultry raised under a low standard of sanitation, poor environmental conditions.
• Strains of E. coli that cause disease outside the intestinal tract of any species share common characteristics and are called extraintestinal pathogenic E. coli (ExPEC). Most APEC are ExPEC and share characteristics with mammalian ExPEC.
• Signs: non-specific.
• Diagnosis: bacterial culture and postmortem examination findings.
• Treatment: combination of antibiotic treatments.
• Prognosis: guarded.
• Lesions alone should not be used to infer an E. coli infection without the descriptor “coli” or “coliform” being added, because other opportunistic bacteria can behave similarly to E. coli in secondary infections.

• Depression.
• Dehydration.
• Decreased appetite.
• Diarrhea.
• Lameness.
• Lethargy.
• Ruffled feathers.
• Respiratory signs.

• Respiratory distress.
• Sudden death.

• Worldwide.

• Young poultry.

• Male.

• Poultry has not been a significant source of shigatoxin producing E. coli (STEC) in human disease. However, continued vigilance is recommended because STEC has been isolated from birds and poultry products.
• There are remarkable similarities between APEC and human ExPEC. This has led to a hypothesis about the possibility that APEC‐contaminated poultry and eggs are a foodborne reservoir of ExPEC, leading to human extraintestinal diseases.
• Virulence plasmids of APEC may harbor multidrug resistance encoding genes. Previous work has indicated that transmission of resistant organisms and/or plasmids from poultry to people can occur. For instance, similar antibiotic resistance patterns were found in E. coli isolated from poultry slaughter workers and birds.

• Colibacillosis is the most common infectious bacterial disease of poultry, leading to significant economic losses.

• The APEC serogroup is determined by the O (somatic) antigen. The serotype is determined by the H (flagellar) and sometimes the K (capsular) antigens.  There are 180 O antigens, 60 H antigens and 80 K antigens.
• The lipopolysaccharide (LPS) in the cell wall is also known as endotoxin. The antigenic portion of LPS is known as the O (somatic) antigen. The most common serotypes associated with disease in poultry are O1, O2, O18, O35, O36, O78 and O111. The K antigens most often associated with disease infections are K1 and K80. Some strains are untypeable.
• Other infectious agents and non-infectious factors usually predispose a bird to infection or contribute to the severity of the disease.
• Two additional Escherichia species, Escherichia fergusonii and Escherichia albertii, have been isolated from birds and are capable of causing disease or are of public health significance:
  • E.  fergusonii has been shown to cause disease in day‐old chicks and acute death in adult ostriches. It also exhibits a broad range of antimicrobial resistances.
  • E. albertii causes gastroenteritis in people and in birds; infections range from asymptomatic to severe intestinal disease and mortality.
• There are many different types of E. coli, some that produce toxins and cause signs of disease, and others that are not toxic and don’t usually cause any signs of disease:
  • For instance, enterotoxigenic E. coli (ETEC), enteroinvasive E. coli (EIEC), and enterohemorrhagic E. coli (EHEC) all lead to colibacillosis through the production of toxins.
  • Enteropathogenic E. coli (EPEC), on the other hand, does not produce toxins and leads to enteritis and colisepticemia by other mechanisms.

Specific

• Avian colibacillosis often occurs as a secondary infection in poultry with weakened immune systems. Previous health issues and disease, high levels of stress, low standards of sanitation and poor environmental conditions can predispose poultry of APEC.
• In immature females, coliform salpingitis Salpingitis can occur when there is involvement of nearby air sacs. Infectious bronchitis virus infection Infectious bronchitis of the oviduct may also be an important predisposing factor in juvenile coliform salpingitis.

• Healthy birds are resistant to virulent E. coli compared to birds with immunocompromised immune systems.
• E. coli enters host tissues following mucosal colonization or directly through breaks or openings in the skin. Virulent strains are capable of traversing the mucosa, although the exact mechanism is poorly understood.
• Once E. coli becomes extra mucosal there is an acute inflammatory response in the host.
• The inflammation, paired with endotoxin in the circulation causes decreased feed consumption, body weight and breast meat yield. In addition, it compromises tibial bone health, increases mortality and liver weight. Vascular permeability increases, leading to the accumulation of exudate in the tissues.
• Exudate undergoes caseation to form a firm, dry, yellow, irregular, cheese‐like mass. The heterophilic granulomatous exudate consists of embedded but viable bacterial colonies surrounded by multinucleated giant cells and macrophages. The fibrin-rich exudate is eventually converted to scar tissue.
• Gross lesions are inversely related to virulence. Highly virulent strains cause mortality so quickly that gross lesions have little time to develop, whereas birds infected with less virulent strains survive longer and develop more extensive lesions.
• Infections with APEC serve as a model for studying the molecular aspects of host–pathogen interactions of ExPEC infections.

• E. coli are part of the normal intestinal microbiota of animals.
• A small percentage of the E. coli present in the intestinal tract are pathogenic.
• Birds are constantly exposed to APEC in their environment, with most healthy birds having high levels of resistance.
• Localized infections generally result in fewer and milder clinical signs than systemic infection.
• Localized colibacillosis infections include coliform omphalitis, coliform cellulitis, swollen head syndrome, diarrheal disease, venereal colibacillosis, coliform salpingitis, coliform peritonitis, coliform orchitis, and coliform epididymitis.
• Systemic or generalized presentations of colisepticemia are categorized as respiratory origin, enteric origin, hemorrhagic septicemia, neonatal, layer and duck. Sequelae of colisepticemia include meningitis, encephalitis, panophthalmitis, osteomyelitis, spondylitis, arthritis, synovitis, juvenile salpingitis, chronic fibrosing pericarditis and sternal bursitis. Systemic infection can also present as coligranulomas.
• The most important form of transmission is at the hatchery. Exposure to APEC at the hatchery often starts with contamination of eggshells through a dirty setter, feces-covered eggs, or excessive moisture during storage.  E. coli can then penetrate the shell and membranes of the egg. Exposure at the hatchery during incubation or after hatching can result in coliform omphalitis – swollen, red, and crusted navels, newly hatched birds.
• Hens can also shed E. coli onto the egg. Some of these embryos die late during incubation or soon after hatching. If they survive, they can become a source of E. coli for the rest of the flock.
• E. coli can also be introduced into the flock through contaminated water, food, and rodents. Free living birds, darkling beetles and houseflies can also be sources of APEC.
• While birds of any age can develop avian colibacillosis, young birds are affected more often, and often present with more severe clinical signs.
• Factors known to increase susceptibility APEC include:
  • Infection with other infectious agents, including viruses and protozoa.
  • Toxins such as ammonia and mycotoxins.
  • Environmental factors such as dusty conditions, temperature extremes and overcrowding.
  • Nutritional factors such as hypervitaminosis A, hypervitaminosis E or vitamin A deficiency Nutritional conditions overview.
• Respiratory presentation of APEC in juvenile birds is often preceded by infection with primary respiratory infectious agents such as mycoplasma Mycoplasma gallisepticum infection Mycoplasma synoviae infection, Newcastle disease Newcastle disease, or infectious bronchitis Infectious bronchitis.
• Affected birds are typically undersized for the age and size of the flock. Affected birds are commonly found at the ends of the poultry house, along the side walls, or under feeders or waterers.
• Affected birds that are lethargic and unable to ambulate may become victims of cannibalism Feather / vent pecking / cannibalism by other birds.
• Diarrheal disease due to APEC infection is rare in poultry. When present, it is due to infection with ETEC, EIEC, and EHEC or EPEC Diarrhea / vent pasting.

Refereed papers

• Recent references from PubMed and VetMedResource.

Other sources of information

• Morishita T Y & Porter R E Jr (2021) Gastrointestinal and Hepatic Diseases. In: Backyard Poultry Medicine and Surgery. A Guide for Veterinary Practitioners. 2nd edn. Wiley-Blackwell, USA. pp 289-312.
• Nolan L K, Vaillancourt J-P, Barbieri N L & Logue C M (2020) Colibacillosis. In: Diseases of Poultry. 14th edn. Eds: Swayne D E, Boulianne M, Logue C M et al. Wiley-Blackwell, USA. pp 770-808.

_{Reproduced with permission from Cheryl B Greenacre & Teresa Y Morishita: Backyard Poultry Medicine and Surgery. A Guide for Veterinary Practitioners. © 2021, and David E Swayne: Diseases of Poultry. © 2020, published by John Wiley & Sons.}