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Published on: October 11, 2018
Pathomorphological studies of polyserositis in commercial caged layer chicken
Palani Srinivasan1, Gurusamypalayam Amirthalingam Balasubramaniam1, Thippichettipalayam Ramasamy Gopala Krishna Murthy2
1Department of Veterinary Pathology, Veterinary College and Research Institute, Namakkal, Tamil Nadu State, India.
Objective:
To detect etiological agents and pathological changes associated with polyserositis in commercial layer chicken.
Methods:
Ten commercial layer flocks which had a sudden increase in mortality and a drop in egg production with lesions suggestive of colisepticemia were investigated. Flock details and pathological changes were recorded in affected flocks to assess the prevalence and impact of polyserositis on commercial layer chicken. Trachea, heart blood, liver, oviduct, cloacal swab, poultry house environment samples, water and feed samples were screened for bacteriological agents. Pooled tissue (trachea, lung, spleen, caecal tonsil, kidney and oviduct) samples from colisepticemia cases were screened for viral agents. Serum samples collected from affected flocks were screened for Newcastle disease virus, infectious bronchitis virus and egg drop syndrome-76 virus by haemagglutination inhibition test, and for Mycoplasma gallisepticum and Mycoplasma synoviae by enzyme linked immunosorbent assay.
Results:
On necropsy examination of dead birds, fibrinous polyserositis and congestion of various visceral organs were noticed. Microscopically, deciliation and hypertrophy of mucus glands showed in the tracheal epithelium. Vascular derangements and infiltration of inflammatory cells showed in the lungs and air sac. Fibrinous polyserositis, focal necrosis and infiltration of inflammatory cells showed in parenchyma of heart and liver. Inflammatory changes were observed in the ovary and oviduct. Escherichia coli (E. coli) was isolated as a pure culture from 108 birds and from the poultry house environment of the ten affected flocks. Among the eight E. coli serotypes, identified serotypes O78 and O111 were predominant. In colisepticemia affected flocks egg production drop and mortality varied from 3%-10% and 2%-5%, respectively and occured during the peak egg production (21 to 40 weeks) and southwest monsoon season (June to September).
Conclusions:
The present study revealed that the colisepticemia inducing E. coli isolates were derived from the layer house environment. Hence, the incidences of colisepticemia can be minimized by effectively reducing the bacterial load in the layer house environment through appropriate biosecurity measures.
