ABSTRACT
One-day-old poults or two-week old chicks were infected oculonasally with avian pneumovirus. Cloacal swabs were collected for virus isolation as were selected tissues (Harderian gland, turbinates, trachea, lungs and kidneys) from birds killed at regular intervals up to 33 days post infection (p.i.) for poults, and up to 40 days p. i. for chicks. In an attempt to induce virus re-excretion, the T-cell-suppressor cyclosporin A (CSA) was given for 12 days starting from three weeks p.i. in poults and from four weeks p.i. in chicks. Birds were sampled for virus isolations up to day 12 post CSA treatment. Virus was recovered only up to day nine p.i. in poults, and day five p.i. in chicks during the acute phase of the infection. Despite T-cell suppression, there was no evidence of re-excretion of the virus, and hence no evidence for the persistence of virus in the tissues examined.
Subject(s)
Cyclosporine/pharmacology , Immunosuppressive Agents/pharmacology , Pneumovirus Infections/veterinary , Pneumovirus/isolation & purification , Poultry Diseases/physiopathology , Aging , Animals , Chickens , Cloaca/virology , Harderian Gland/virology , Kidney/virology , Lung/virology , Pneumovirus/physiology , Pneumovirus Infections/immunology , Pneumovirus Infections/physiopathology , Poultry Diseases/immunology , Time Factors , Trachea/virology , Turbinates/virologyABSTRACT
Poults were infected with avian pneumovirus (APV) at 1-day-old, followed by Mycoplasma synoviae (Ms) 3 days later. Dual infection did not cause an increase in severity of clinical disease, or gross and microscopic lesions due to APV. The patterns of virus and Ms isolations from tracheal swabs or tissues from single and dual infected groups were similar. Ms infection did not induce Ms antibodies, nor did it affect seroconversion to APV in the dual infection.
ABSTRACT
The pathogenicity of avian pneumovirus (APV) for the chicken oviduct was studied in vitro using oviduct organ cultures (OOC), in vivo in young chicks with artificially enlarged oviducts and in adult female chickens. The OOCs were prepared from artificially enlarged oviducts of young chicks induced by oestrogen treatment and from normal oviducts of adult hens. The pathogenicity of APV for OOCs in vitro and oviducts in vivo were assessed by virus titrations and immunofluorescence. While in vitro experiments revealed an intrinsic susceptibility of oviduct epithelium to APV infection, in vivo studies failed to show APV replication in the hen oviduct, even after intravenous inoculation.
