Things Every poultry Farmer Must know About Colibacillosis

Colibacillose is caused by infection with a pathogenic strain of Escherichia coli. Signs vary and may include acute fatal septicemia, airsacculitis, Pericarditis, perihepatitis, and lymphocytic depletion of the bursa and thymus. The diagnosis is made by isolating a pure culture of E. coli. Most bacterial isolates are resistant to multiple antibiotics, so it is recommended to prevent exposure through good management.

Colibacillose is a localized or systemic infection caused by avian pathogen Escherichia coli (APEC). It manifests in a variety of ways, including acute fatal septicemia, subacute pericarditis, airsacculitis, salpingitis, peritonitis, and cellulitis. It is one of the world’s most prevalent and economically devastating bacterial diseases in poultry.

Etiology and pathogenesis
Escherichia coli is a gram-negative, rod-shaped bacterium normally found in the intestines of poultry and other vertebrates. Although many E. coli are non-pathogenic, some have acquired virulence factors, greatly increasing their pathogenicity. , The majority of cases of colibacillosis appear to be due to E. coli acquiring a number of virulence genes grouped into plasmid-borne pathogenicity islands (PAIs). These PAI-containing plasmids are thought to be the defining feature of the APEC pathotype.

Other cases are due to infection with commensal E. coli given access to birds debilitated by a predisposing condition such as mycoplasmosis, infectious bronchitis, Newcastle disease, hemorrhagic enteritis, turkey bordetellosis, poor air quality, or other environmental exposures.
While the majority of APEC were previously assigned to the three main serogroups O1, O2 and O78, recent research has shown that there is great diversity in the APEC serogroups that cause colibacillosis. A high percentage of APEC isolates cannot be grouped using current methods. Therefore, it is likely that no single E. coli serogroup used as a bacterin provides complete protection against all serogroups that cause colibacillosis.
Virulence factors include possession of large virulence plasmids and the ability:

Resist phagocytosis and serum killing Acquire iron under iron-poor conditions Adhere iron to host structures under iron-poor conditions
APEC are generally non-toxic.
Large numbers of E. coli are maintained in the poultry house environment through fecal contamination. Initial exposure to APEC can occur at the hatchery through infected or contaminated eggs. The bacterial portal of entry into birds varies but may include the respiratory tract, skin lesions, cloaca, damaged intestinal mucosa, and navel. From these entry points, E. coli can spread locally or enter the bloodstream to cause colisepticemia, which can progress from acute septicemia to death. Infection can also extend to serous surfaces, causing subacute polyserositis and chronic granulomatous inflammation.

Clinical findings and lesions
Signs are nonspecific and vary with age, organs affected, and concomitant disease. Young birds dying of acute septicemia have few lesions other than an enlarged, hyperemic liver and spleen with excess fluid in the body cavities. Birds surviving septicemia develop subacute fibrinopurulent airsacculitis, pericarditis, perihepatitis, and lymphocytic depletion of the bursa and thymus (unusually pathogenic Salmonella 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 spread of serositis. Sporadic lesions include pneumonia, arthritis, osteomyelitis, peritonitis, and salpingitis.

Isolation of E. coli in pure culture
In contrast to pathogenic E. coli, which has been implicated in disease in other animal species, avian isolates on sheep blood agar (5%) are generally non-hemolytic. Isolation of a pure culture of E. coli from cardiac blood, liver, or typical visceral lesions in a fresh cadaver is indicative of primary or secondary colibacillosis. Predisposing infections and environmental factors should be considered. Pathogenicity of isolates is assessed using multiplex PCR panels for plasmid-mediated virulence genes or when parenteral inoculation of young chicks or chicks results in fatal septicemia or typical lesions within 3 days. Pathogenicity can also be demonstrated by inoculation of the allantoic sac of 12-day-old chick embryos. Resulting gross lesions include cranial and skin hemorrhages and encephalomalacia in embryos inoculated with virulent isolates.

treatment and control

Due to widespread resistance, antibiotics are not recommended
Prevention depends on good management to reduce exposure
Prevention of colibacillosis relies on good management to reduce exposure of birds to APEC and to reduce the effects of stress and predisposing infections on birds’ susceptibility to APEC infection. In addition, experimental and commercial vaccines of various types have been used to prevent mixed-effect colibacillosis. Treatment of colibacillosis with antimicrobials is problematic due to widespread multidrug resistance in APEC and limitations 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 being resistant to five or more antibiotics. The use of fluoroquinolones is now banned in many countries, including the United States. APEC also show widespread resistance to disinfectants, including certain heavy metal compounds, further complicating colibacillosis control.

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