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Clinicians and Pathologists
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Clinicians and Pathologists
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Consecutive Inclusion Body Hepatitis Outbreaks on Two Broiler Farms in Alberta D. Onderka Provincial Veterinary Laboratory
A broiler farm in East Central Alberta had inclusion body hepatitis in three consecutive flocks. This resulted in mortality between 3 and 5% from this disease in each cycle. The farm houses a single broiler flock in one barn averaging between 5200 and 7200 birds. This operator has a second barn in which he raises commercial turkeys. Flock 1 At 16 days of age, mortality was low at 5-7 birds per day, but was submitted for examination to the laboratory. Inclusion body hepatitis was diagnosed based on gross and histologic criteria. All birds were from one hatchery that has its own breeder flock.
Flock 2 At 13 days of age, the barn experienced a mortality rate of 40 birds per day. Again IBH was diagnosed. Histologically there was no evidence of IBD although some bursal changes consistent with an infectious disease challenge were noted. On April 16 at 32 days of age, a follow-up submission showed no histologic or serologic evidence of IBD. Because adenoviruses are readily egg transmitted, the breeder flock was tested, but found to be negative for adenovirus exposure using immune diffusion test. Cleanout procedures between flocks did no seem ideal and the owner was advised to do a more thorough cleanout for the next cycle.
Flock 3 At 4 days of age, a small sample of birds were submitted and diagnosed with the usual mixture of problems associated with early chick mortality. However, on May 25, at 14 days of age, this flock experienced a mortality rate of 85 birds per 24 hours as a result of inclusion body hepatitis. Again, there was no histologic evidence of infectious bursal disease. At 17 days of age, sick birds were resubmitted and adenovirus was isolated and identified by EM. This isolate was used for pathogenicity study. At 32 days of age, the flock was negative for IBD histologically and serologically.
Pathogenicity study The adenovirus was grown in a cell culture with standard cell culture fluid. Broiler chicks were obtained from a young breeder flock with known high IBD titres. Six, six-day-old chicks were inoculated intraperitoneally with 1 ml of adenovirus suspension. Plaque forming units were not quantitated, but each chick received at least 105 pfu. Four chicks were inoculated with cell culture medium only and served as controls. Prior to inoculation, all ten birds were bled to form a combined sample for adenovirus serology. Six days post inoculation; there were no clinical signs. Tow of the infected birds were necropsied and had no gross lesions. Ten days post inoculation; the feed was removed for 48 hours to apply some stress to these birds. At twelve days post inoculation, two more birds were necropsied again with no gross lesions. At that time, blood was collected for serology. Nineteen days post inoculation (25 days of age), the remaining two birds were necropsied together with the four control birds. In none of the birds were there any gross lesions. Again, blood was collected for serology. Serology, using immunodiffusion, showed all chicks to be negative on the preinoculation sample. By 12 days p.i, two of four birds were adenovirus positive. Control birds remained serologically negative although they were housed in adjacent compartments in electrically heated brooders. Inclusion body hepatitis has been reported to occur sporadically without known or identifiable underlying immunosuppressive disease. In this case infectious bursal disease was carefully considered and eliminated. Also, chick anemia agent was considered as the possible underlying cause. In that case the breeder flock would have had to become infected and transmit the virus through the egg to the chicks. This could be a plausible scenario for the first flock; however, subsequent flocks should be resistant to chick anemia agent challenge as the breeder flock now should transmit protective antibodies. It does not appear that the adenovirus involved had any unusual pathogenicity as experimental infections failed to produce any lesions. Although the breeder flock could not be incriminated based on the laboratory findings, the owner chose to switch suppliers and flock 4 was obtained from a different hatchery. At the same time, however, a more thorough cleanout of the premise was undertaken and as of this date, inclusion body hepatitis has not recurred on this premise.
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