Avian metapneumovirus (AMPV) causes an upper respiratory tract infection in turkeys leading to turkey rhinotracheitis. In other avian species, including chickens, it is also involved in the aetiology of multifactorial diseases such as swollen head syndrome. Sensitivity of wild birds to AMPV and their role in maintaining and spreading the virus to poultry is still a matter of debate. Recently the sensitivity of pigeons to AMPV of subtype A or B has been claimed, based on very limited PCR detections from wild or experimentally infected birds. In order to have conclusive evidence regarding the sensitivity of pigeons to AMPV of subtype B and its role in spreading the virus to turkeys, two experimental trials were planned in secure isolation conditions. In trial 1 two isolators were modified to host turkeys and pigeons in the same environment, separated only by a net. Drinkers were shared between groups. 16 Pigeons were infected with AMPV and housed in one isolator with naïve turkeys. Similarly turkeys were infected and housed with naïve pigeons. Additional turkeys and pigeons were kept in different isolators as uninfected controls. Post-infection clinical signs, virus shedding and immune response were assessed for three weeks. In trial 2, commercial two-weeks old turkeys were divided in two groups of ten and housed in two different isolators. Birds in isolator A were challenged as previously described. Four days post-infection, five 7 weeks old naïve pigeons were introduced in the isolator A and kept with the infected turkeys for 24 hours, then removed, sprayed with 0,5 % of Wirkon S solution. After 10 minutes, pigeons were rinsed with water, dried, and introduced in the isolator B, where 10 naïve turkeys were housed. Clinical sign were monitored for 10 days. Pigeons were found refractory to AMPV experimental infection and neither able to spread the virus to naïve turkeys. Our paper shows that pigeons are highly unlikely to play any relevant role in the environmental spread of subtype B AMPV. Pigeons are not biological vector or reservoir species for AMPV subtype B.
Catelli E., Lupini C., Listorti V. , Marziali A., De Matteo P., Naylor C.J., et al. (2012). THE PIGEON (COLUMBA LIVIA) IS NOT SENSITIVE TO AVIAN METAPNEUMOVIRUS SUBTYPE B AND DOES NOT PLAY ANY ROLE IN VIRUS SPREAD IN EXPERIMENTAL CONDITIONS.. WETTER : Druckerei Schroder.
THE PIGEON (COLUMBA LIVIA) IS NOT SENSITIVE TO AVIAN METAPNEUMOVIRUS SUBTYPE B AND DOES NOT PLAY ANY ROLE IN VIRUS SPREAD IN EXPERIMENTAL CONDITIONS.
CATELLI, ELENA;LUPINI, CATERINA;LISTORTI, VALERIA;DE MATTEO, PATRIZIA;
2012
Abstract
Avian metapneumovirus (AMPV) causes an upper respiratory tract infection in turkeys leading to turkey rhinotracheitis. In other avian species, including chickens, it is also involved in the aetiology of multifactorial diseases such as swollen head syndrome. Sensitivity of wild birds to AMPV and their role in maintaining and spreading the virus to poultry is still a matter of debate. Recently the sensitivity of pigeons to AMPV of subtype A or B has been claimed, based on very limited PCR detections from wild or experimentally infected birds. In order to have conclusive evidence regarding the sensitivity of pigeons to AMPV of subtype B and its role in spreading the virus to turkeys, two experimental trials were planned in secure isolation conditions. In trial 1 two isolators were modified to host turkeys and pigeons in the same environment, separated only by a net. Drinkers were shared between groups. 16 Pigeons were infected with AMPV and housed in one isolator with naïve turkeys. Similarly turkeys were infected and housed with naïve pigeons. Additional turkeys and pigeons were kept in different isolators as uninfected controls. Post-infection clinical signs, virus shedding and immune response were assessed for three weeks. In trial 2, commercial two-weeks old turkeys were divided in two groups of ten and housed in two different isolators. Birds in isolator A were challenged as previously described. Four days post-infection, five 7 weeks old naïve pigeons were introduced in the isolator A and kept with the infected turkeys for 24 hours, then removed, sprayed with 0,5 % of Wirkon S solution. After 10 minutes, pigeons were rinsed with water, dried, and introduced in the isolator B, where 10 naïve turkeys were housed. Clinical sign were monitored for 10 days. Pigeons were found refractory to AMPV experimental infection and neither able to spread the virus to naïve turkeys. Our paper shows that pigeons are highly unlikely to play any relevant role in the environmental spread of subtype B AMPV. Pigeons are not biological vector or reservoir species for AMPV subtype B.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
