David L. Graham

RETICULOENDOTHELIOSIS IN CAPTIVE GREATER AND ATTWATER'S PRAIRIE CHICKENS

Reticuloendotheliosis in captive greater (Tympanuchus cupido pinnatus) and Attwaters (T. cupido attwateri) prairie chickens is reported for the first time. Between September 1993 and August 1994, two adult female wild-caught greater prairie chickens housed at Texas A&M University (College Station, Texas, USA) were observed with multiple subcutaneous nodules. Both birds were euthanatized. Complete necropsy examinations revealed lesions limited to the skin of each bird. Histopathologic examination of lesions revealed pleomorphic lymphoreticular cells suggestive of reticuloendotheliosis and reticuloendotheliosis virus (REV) was demonstrated in tumor tissue by polymerase chain reaction and virus isolation. Between September 1994 and June 1995, five additional greater prairie chickens and two Attwaters prairie chickens were euthanatized or found dead with evidence of lymphoreticular neoplasia in multiple organ systems. Initial testing of the captive flock in December 1994 for evidence of viremia and antibody to reticuloendotheliosis virus revealed over 50% of the tested birds were viremic, but none developed antibodies. Subsequent testing between January 1995 and January 1996 indicated that once infected with reticuloendotheliosis virus, Attwaters prairie chickens tended to remain outwardly healthy despite persistent viremia compared to infected greater prairie chickens which had higher morbidity and mortality rates within 60 to 90 days after initial detection of viremia and did not usually develop persistent viremia. Antibodies to REV were detected in only three captive greater prairie chickens and only in 1995. Six of the nine birds that were euthanatized or found dead due to reticuloendotheliosis developed viremia prior to death; three birds were not tested prior to death. Testing of free-ranging greater and Attwaters prairie chickens for reticuloendotheliosis is recommended prior to translocation or release.

INCLUSION BODY DISEASE (HERPESVIRUS INFECTION) OF FALCONS (IBDF)

Inclusion body disease of falcons (IBDF) is caused by a herpesvirus. The clinical course is short, 24 to 72 hours in duration, and is characterized by mild to severe depression and weakness often accompanied by anorexia. The disease is invariably fatal. The virus has a marked affinity for the reticuloendothelial system and hepatocytes, producing focal to diffuse necrosis of infected tissues accompanied by the formation of intranuclear inclusion bodies. The virus is pathogenic for American kestrels (Falco sparverius) and great horned owls (Bubo virginianus) in which typical lesions of IBDF are reproduced. The lesions of IBDF are similar to those produced by some herpesvirus infections in other avian species.

EPIZOOTIOLOGY AND PATHOLOGIC FINDINGS ASSOCIATED WITH A NEWLY DESCRIBED ADENOVIRUS IN THE RED SQUIRREL, SCIURUS VULGARIS

An infectious disease caused by Squirrelpox virus has contributed to the decline of red squirrels, Sciurus vulgaris, in the British Isles. Because of the heightened disease surveillance activity in red squirrels, adenovirus infection with associated mortality has been detected. Adenoviral disease is described in other rodent species usually associated with stressors. Here we 1) describe the pathologic findings in red squirrels found dead with adenoviral infection and gastrointestinal disease, and 2) investigate the epizootiology of the disease through pathologic investigation, scanning surveillance, and virologic studies. Ten red squirrels involved in conservation studies were diagnosed with adenoviral infection by electron microscopy or PCR. All squirrels exhibited diarrhea and small intestinal inflammation or hemorrhage was evident in seven cases. Lesions indicative of splenic lymphocytolysis were observed in one squirrel and leukocytic hepatitis in another. No adenovirus was detected in grey squirrels, Sciurus carolinensis, inhabiting the same forest area, but previous serologic studies showed that grey squirrels cannot be discounted as a reservoir of the virus. Scanning surveillance showed that 12% of 493 red squirrels had diarrheal disease and two of 13 free-living red squirrels with diarrheal disease had adenovirus infection. Adenoviral disease in declining free-living wild red squirrel populations in the British Isles occurs at a detectable frequency and its impact on the conservation of this species deserves further attention.

EXPERIMENTAL RABIES IN A GREAT HORNED OWL

A great horned owl (Bubo virginianus) was fed the carcass of an experimentally infected rabid skunk. The bird developed antibody titer to rabies, detected by passive haemagglutination, 27 days after oral inoculation by ingestion. The owl suppressed the infection until corticosteroid administration, after which a maximum antibody titer was attained. Evidence of active rabies viral infection was seen by fluorescent antibody staining of oral swabs, corneal impression smears and histologic tissue smears, by suckling mouse inoculation of oral swab washings, and by transmission electron microcopy. No clinical signs of rabies virus infection were observed.

Pathogenicity and Host Range of the Falcon Herpesvirus

The falcon herpesvirus (FHV) is a pathogen of birds of the family Falconidae in which it causes inclusion body disease of falcons (IBDF), an invariably fatal disease. The virus has been isolated from natural cases of IBDF in the prairie falcon (Falco mexicanus) the peregrine falcon (F. peregrinus) and the red-headed falcon (F. chicquera). The disease has also been diagnosed on the basis of its characteristic le-sions in the gyrfalcon (F. rusticolis). Experi-mental inoculation with FHV resulted in fatal IBDF in a prairie falcon and two other falcon species, the American kestrel (F. sparverius) and the merlin (F. columbarius). A fatal disease clinically and pathologically indistinguishable from IBDF resulted from FHV inoculation of the following species representing 7 families; Swain-son’s hawk (Buteo swainsoni) Cooper’s hawk (Accipiter cooperi) sharp-shinned hawk (A. striatus) great horned owl (Bubo virgianus) screech owl (Otus asio) snowy owl (Nyctea scandiaca) American coot (Fulica americana) green heron (Butorides virescens) budgerigar (Melopsittacus undulatus) Amazon parrot (Amazona ocrocephala) ring-necked dove (Streptopelia risoria) and baby muscovy ducks (Cairina moschata). Representatives of 15 avian species and 5 mammalian species were shown to be refractory to FHV.

Clinical and Pathological Aspects of Inclusion body Disease (Herpesvirus Infection) of Falcons (IBDF)

Inclusion body disease of falcons (IBDF) is caused by a herpesvirus. The clinical course is short, 24 to 72 hours in duration, and is characterized by mild to severe depression and weakness often accompanied by anorexia. The disease is invariably fatal. The virus has a marked affinity for the reticuloendothelial system and hepatocytes,producing focal to diffuse necrosis of infected tissues accompanied by the formation of intranuclear inclusion bodies. The virus is pathogenic for American kestrels (Falco sparverius) and great horned owls (Bubo virginianus) in which typical lesions of IBDF are reproduced. The lesions of IBDF are similar to those produced by some herpesvirus infections in other avian species.