Western Meeting of Poultry

 Clinicians and Pathologists 

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In the winter and early summer of 2005 two non-sequential flocks of broilers on a Vancouver Island farm experienced high mortality. Mortality increased to 0.4 to 0.6% per day starting at day 30 and continued until slaughter. These flocks were separated by a flock which experienced normal mortality for this farm. Gross post mortems of numerous birds revealed several abnormalities including colibacillosis, kinky back, tibial dyschondroplasia, dermatitis and enteritis but none of these conditions accounted for such high mortality.

This farm has multi-aged broilers with processing of on and off-farm birds which compromises health through a constant disease challenge. This results in naïve birds being exposed to a multitude of potential infectious agents which can complicate a definitive diagnosis.

Routine vaccination for Marek’s and IBD occurred at the hatchery. As well, two previous flocks were vaccinated for IBD with a coarse spray at 10 days of age.

Histology of brains from the initial laboratory submission revealed prolific lesions with larger lymphoid-type cell infiltrates and smaller lymphocytes which did not have a homogenous appearance. Random cells appeared to be in mitosis with clear rosettes or equatorial plates observed. This suggested a neoplastic rather than an inflammatory infiltrate. The changes seen were marked and resembled a Type A Marek’s lesion. Brain histology of a submission from the second affected flock did not show this lesion but instead was suggestive of viral encephalitis, most probably Avian Encephalitis as the etiological agent.

Birds from both affected flocks which survived beyond 40-days of age began to show skin lesions compatible with Marek’s. The clinical signs and associated mortality pattern were very consistent with a diagnosis of Marek’s. All other gross and laboratory findings were not imaginary and no doubt contributed to the health and performance of these flocks but none but Marek’s could totally explain what we saw and experienced.

This case illustrates that multi-age flocks compromised by poor biosecurity compounded with exposure to foreign birds are insulted with a multitude of pathogens and pathologic conditions. Although all these insults can result in disease and mortality, at least in the first flock, one etiology, Marek’s, was ultimately responsible for a majority of the loss. Clinically, the two affected flocks were similar, but AE, not Marek’s was diagnosed from histology of brain tissue from the second flock. This observation was made in spite of the fact that no clinical signs or mortality were observed in the first two weeks of age which is usually consistent with AE.

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Last modified: 5/28/2009