Colibacillosis in Poultry
Colibacillosis is a localized or systemic infection caused by avian pathogenic Escherichia coli (APEC). It manifests in diverse ways, including as acute fatal septicemia, subacute pericarditis, airsacculitis, salpingitis, peritonitis, and cellulitis . It is one of the most commonly occurring and economically devastating bacterial diseases of poultry worldwide.
Escherichia coli is a gram-negative, rod-shaped bacterium normally found in the intestine of poultry and other vertebrates. Though many E coli are not pathogenic, some have acquired virulence factors, greatly increasing their pathogenicity. , The majority of cases of colibacillosis appear to be due to E coli that have acquired a number of virulence genes clustered together in plasmid-borne pathogenicity islands (PAIs). These PAI-containing plasmids are said to be the defining feature of the APEC pathotype. Other cases are due to infection with commensal E coli that gain access to birds weakened by some predisposing condition such as mycoplasmosis, infectious bronchitis, Newcastle disease, hemorrhagic enteritis, turkey bordetellosis, poor air quality, or other environmental stresses.
Whereas the majority of APEC were previously assigned to three main serogroups, O1, O2, and O78, more recent research has shown that there is great diversity in the serogroups of APEC causing colibacillosis. A high percentage of APEC isolates cannot be grouped using current methods. Therefore, no single E coli serogroup used as a bacterin is likely to provide full protection against all of the serogroups that cause colibacillosis.
Virulence factors include possession of large virulence plasmids and the abilities to:
APEC are generally nontoxigenic.
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. The bacterial portal of entry into birds varies but can include the respiratory tract, skin trauma, cloaca, damaged intestinal mucosa, and navel. From these entry sites, E coli can extend locally or gain access to the bloodstream to cause colisepticemia, which may progress from acute septicemia to death. Infection can also extend to serosal surfaces to cause subacute polyserositis and chronic granulomatous inflammation.
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.
Prevention of colibacillosis relies on good management to decrease exposure of birds to APEC and lessen the impact of stress and predisposing infections on the susceptibility of birds to APEC infection. In addition, experimental and commercial vaccines of various types have been used to prevent colibacillosis, to mixed effect. Treatment of colibacillosis with antimicrobial agents is problematic due to widespread multidrug resistance among APEC and restrictions on antimicrobial use in poultry imposed by regulation and public concern. Most isolates are resistant to tetracyclines, streptomycin, and sulfa drugs, although therapeutic success can sometimes be achieved with tetracycline. However, the vast majority of clinical isolates are resistant to tetracycline, with most APEC isolates resistant to five or more antibiotics. Fluoroquinolone use is now banned in many countries, including the USA. APEC also show widespread resistance to disinfectants, including certain heavy metal compounds, further complicating control of colibacillosis.
Colibacillosis is a major cause of morbidity, mortality, and economic loss for all types of poultry worldwide.
Avian pathogenic E coli (APEC), the causative agent of colibacillosis, encompass a diverse grouping of E coli, most of which harbor large virulence plasmids.
Control of colibacillosis is problematic due to widespread antibiotic resistance among APEC, restrictions on use of antimicrobial agents in poultry, and lack of vaccines to provide protection against all types of APEC causing colibacillosis.