Overview of Colibacillosis in Poultry

Escherichia coli is a gram-negative, rod-shaped bacterium normally found in the intestine of poultry and most other animals. Although most serotypes are nonpathogenic, a limited number produce extraintestinal infections. Avian pathogenic E coli (APEC) strains are commonly of the O1, O2, and O78 serogroups, but many others have also been associated with cellulitis and colibacillosis. There is considerable diversity of serogroups among clinical isolates, with a high percentage of APEC isolates being untypeable. Therefore, no single E coli serogroup used as a bacterin can provide full protection against all of the serogroups that cause infections. Virulence factors include possession of large virulence plasmids and the abilities to resist phagocytosis and serum killing, acquire iron in low iron conditions, and adhere to host structures. APEC are generally nontoxigenic and poorly invasive.

Large numbers of E coli are maintained in the poultry house environment through fecal contamination. Initial exposure to APEC may occur in the hatchery from infected or contaminated eggs. Although most E coli isolated from colibacillosis are well equipped with virulence factors that distinguish them from fecal commensal strains, systemic infection often involves predisposing environmental factors or infectious causes. Thus, mycoplasmosis, infectious bronchitis, Newcastle disease, hemorrhagic enteritis, and turkey bordetellosis, or exposure to poor air quality and other environmental stresses, may precede colibacillosis.

Systemic infection occurs when large numbers of APEC gain access to the bloodstream from the respiratory tract or intestine. Bacteremia progresses to septicemia and death, or the infection extends to serosal surfaces, pericardium, joints, and other organs.

Signs are nonspecific and vary with age, organs involved, and concurrent disease. Young birds dying of acute septicemia have few lesions except for an enlarged, hyperemic liver and spleen with increased fluid in body cavities. Birds that survive septicemia develop subacute fibrinopurulent airsacculitis, pericarditis, perihepatitis, and lymphocytic depletion of the bursa and thymus (unusually pathogenic salmonellae produce similar lesions in chicks). Although airsacculitis is a classic lesion of colibacillosis, it is unclear whether it results from primary respiratory exposure or from extension of serositis. Sporadic lesions include pneumonia, arthritis, osteomyelitis, peritonitis, and salpingitis.

Unlike pathogenic E coli associated with illnesses in other animal species, avian isolates are generally nonhemolytic on sheep (5%) blood agar. Isolation of a pure culture of E coli from heart blood, liver, or typical visceral lesions in a fresh carcass indicates primary or secondary colibacillosis. Consideration should be given to predisposing infections and environmental factors. Pathogenicity of isolates is established using multiplex PCR panels for plasmid-mediated virulence genes or when parenteral inoculation of young chicks or poults results in fatal septicemia or typical lesions within 3 days. Pathogenicity can also be detected by inoculation of the allantoic sac of 12-day-old chicken embryos. Resulting gross lesions include cranial and skin hemorrhages in addition to encephalomalacia in embryos inoculated with virulent isolates.

Treatment strategies include attempts to control predisposing infections or environmental factors and early use of antibacterials indicated by susceptibility tests. Most isolates are resistant to tetracyclines, streptomycin, and sulfa drugs, although therapeutic success can sometimes be achieved with tetracycline. In fact, 90% of clinical isolates are resistant to tetracycline, with 60% of isolates resistant to five or more antibiotics. Fluoroquinolone use is now banned in many countries, including the USA. Commercial bacterins administered to breeder hens or chicks have provided some protection against homologous E coli serogroups.