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Title: The pathogenicity of avian metapneumovirus subtype C wild bird isolates in domestic turkeys

Author
item Cha, Ra Mi
item Yu, Qingzhong
item Zsak, Laszlo

Submitted to: Virology Journal
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/25/2013
Publication Date: 1/30/2013
Publication URL: http://handle.nal.usda.gov/10113/61421
Citation: Cha, R., Yu, Q., Zsak, L. 2013. The pathogenicity of avian metapneumovirus subtype C wild bird isolates in domestic turkeys. Virology Journal. 10:38 DOI: 10.1186/1743-422X-10-38.

Interpretive Summary: Avian metapneumovirus (aMPV) is an important avian pathogen that can cause serious respiratory disease in poultry, resulting significant economic losses to the poultry industry worldwide. In the United States outbreaks of aMPV infection have occurred in a seasonal pattern (spring and fall), and wild migratory birds have been implicated in the spread of the disease. The role of wild birds in the epidemiology of the disease and transmission of the virus between commercial turkey farms is not clear. In the present study, we isolated avian metapneumoviruses from wild birds samples collected in 2000 from Georgia, South Carolina and Arkansas. Sequence analysis of virus isolates from oral swabs of American coots (AC) and Canada geese (CG) confirmed that these viruses belong to subtype C aMPV. Our data clearly demonstrate that both AC and CG wild bird viruses were fully pathogenic in specific pathogen free and commercial turkeys. Following experimental inoculation, aMPV subtype C specific clinical signs, virus replication and shedding in the upper respiratory tract were indistinguishable in AC and CG virus infected birds from those observed in group of turkeys inoculated with virulent reference virus aMPV subtype C. This finding provides further and more definite reason of maintaining high biosecurity standard in the poultry industry.

Technical Abstract: Avian metapneumovirus subtype C (aMPV/C) causes severe upper respiratory disease in turkeys. Previous report revealed the presence of aMPV/C in wild birds in the southeast regions of the United States. In this study, aMPV/C positive oral swabs from American coot (AC) and Canada goose (CG) were passaged three times in the respiratory tract of specific pathogen free (SPF) turkeys and used as aMPV/C P3 virus isolates in subsequent studies. Wild bird P3 isolates showed similar growth characteristics when compared to virulent aMPV/C in chicken embryo fibroblast cell cultures and their glycoprotein G gene sequence was closely related to the G gene of aMPV/C Colorado reference virus. Three-day-old commercial or SPF turkeys were inoculated oculonasally with wild bird aMPV/C P3 isolates. At 5 and 7 days post-inoculation (DPI), severe clinical signs were observed in both of the AC and CG virus-exposed groups. Viral ribonucleic acid was detected in tracheal swabs by reverse transcriptase-polymerase chain reaction. In addition, immunohistochemistry showed virus replication in the nasal turbinate and trachea. All virus exposed turkeys developed positive antibody response by 14 DPI. Our data demonstrate that aMPV/C wild bird isolates induced typical aMPV/C disease in the domestic turkeys.