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A large commercial flock of Hungarian partridge (Perdix perdix) experienced elevated mortality associated with a wasting disease in May 1998. Postmortem examination of females consistently revealed a distended crop and abnormal gray-white tissue infiltrating the wall of the crop and thoracic esophagus. Neoplasia in male partridge was observed in the liver. Microscopic examination of the crop and thoracic esophagus revealed transmural masses of immature lymphocytes with frequent mitotic figures. Similar cells were observed in the liver of affected males. Virus particles consistent in size and morphology with reticuloendotheliosis virions were observed in neoplastic lymphoid cells via electron microscopy. Reticuloendotheliosis virus was isolated from each of four blood samples. This disease has not previously been reported in Hungarian partridges. Hungarian partridge may represent a potential reservoir of infection for other gamebirds, including prairie chickens.

Reticuloendotheliosis in captive greater (Tympanuchus cupido pinnatus) and Attwater's (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 AM 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 Attwater's 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, Attwater's 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 Attwater's prairie chickens for reticuloendotheliosis is recommended prior to translocation or release.

An emaciated wild turkey (Meleagris gallopavo) exhibiting neurologic signs was found on Ossabaw Island, Chatham County, Georgia (USA) on 11 April 1989. The neurologic abnormalities observed included ataxia, drooping wings, head tremors, torticollis, and circling. At necropsy, discrete yellowish-white nodules, varying in size from 2 to 5 mm, were present in the spleen. White nodular lesions approximately 2 mm in diameter were observed beneath the mucosal surface of the distal esophagus. Histopathologic examination of the splenic nodules disclosed large numbers of primitive lymphoreticular cells with leptochromatic nuclei and abundant, slightly basophilic cytoplasms. The mitotic index in these cells was moderate to high. Similar neoplastic cells composed the masses observed in the esophagus. Multifocal, mild perivascular cuffing with mononuclear cells was found in the lumbar spinal cord, brain, and brain stem. Reticuloendotheliosis virus, subtype 3, was isolated from samples of the spleen and liver.

A moribund wild turkey (Meleagris gallopavo) died shortly after it was discovered in Martin County, North Carolina (USA). The 4.3-kg female turkey appeared in good condition with no visible external lesions or evidence of injury. There were 2- to 5-mm yellow-white plaques on the mucosal surfaces of the oral cavity and mid-esophagus. The liver had large, multifocal, irregular pale areas on cut and uncut surfaces. The spleen contained multifocal, pale, hard, nodules. Microscopic changes in the liver consisted of large multifocal coalescing areas of necrosis. Occasional spherical 10 to 15 microns in diameter organisms consistent with Histomonas meleagridis were present in the necrotic areas. Viable hepatic parenchyma contained multifocal infiltrations of numerous mononuclear cells interpreted as neoplastic cells resembling lymphoblasts and plasma cells. Similar neoplastic cell infiltrates, consistent with the lymphoproliferative disease reticuloendotheliosis, were present in spleen, lung, and esophageal and oral mucosa. Reticuloendotheliosis virus, subtype 2, was isolated from samples of liver and spleen.