Fowl aviadenovirus serotype 1 confirmed as the aetiological agent of gizzard erosions in replacement pullets and layer flocks in Great Britain by laboratory and in vivo studies.

An investigation into the aetiology and pathogenesis of adenoviral gizzard erosion has been conducted following three natural outbreaks affecting one flock of 6-week-old replacement pullets and two consecutive placements of free range layers at the age of 21 and 23 weeks. Affected flocks showed increased mortality (0.12-0.30% per week), and gizzard lesions were consistent with fowl aviadenovirus (FAdV) involvement. To substantiate the initial findings, a selection of archived formalin-fixed paraffin-embedded gizzard samples from another 12 pullet and layer flocks, for which macroscopic and histopathological diagnosis of the disease were recorded in Great Britain during the period 2009-2016, were also investigated. In situ hybridization (ISH), virology and/or PCR confirmed the presence of FAdV species-A, serotype-1 (FAdV-A, FAdV-1) DNA in gizzard samples of all 15 cases investigated. Co-infections with additional FAdV serotypes including FAdV-8a were detected by serology and/or virology in two of the pullet flocks. However, species-specific in situ hybridization revealed that pathological changes of affected gizzards were only associated with the detection of FAdV-A. A subsequent in vivo study infecting 21-day-old SPF pullets with FAdV-1 or FAdV-8a strains isolated from the 6-week-old replacement pullets revealed characteristic pathomorphological changes only in the gizzards from birds infected with FAdV-1. While infection with FAdV-8a was confirmed by virology and serology, infected SPF birds did not develop pathomorphological changes. Therefore, the aetiological involvement of the isolated FAdV-8a in the development of adenoviral gizzard erosion in commercial pullets has been ruled out.

Avian leukosis virus subgroup J-associated myelocytoma in a hobby chicken.

The avian leukosis viruses (ALVs) are a major group of retroviruses associated with neoplastic diseases in poultry. The ALV-J strain was identified as a cause of myelocytomas in broiler breeder and broiler chickens in the UK in the 1980s; however, following eradication of the virus,commercial broilers have remained free of infection since the early 2000s. A pet chicken was submitted to Animal and Plant Health Agency (APHA) in 2013 with a history of croaking respirations, abnormality of the left eye and apparent paralysis. Postmortem examination of the bird showed widespread tumour-like infiltration of many organs, including the pectoral muscles, internal organs, sternum and ribs. Histopathological examination of the affected tissues revealed myelocytoma formation typical of the lesions associated with ALV-J, and the virus was confirmed by PCR testing and sequencing. Virus was not detected in blood samples in the other five chickens remaining in the flock. The source of infection was not established. This was the first time ALV-J had been seen in the UK since its eradicationand the case highlights the importance of continued surveillance of backyard and hobby chickens to detect potential new and re-emerging disease threats, such as ALV-J, which may be of significance to the wider poultry population.