A novel type D retrovirus was isolated by cocultivation of explants of fibromatous tissue from a rhesus monkey (Macaca mulatta) with immunodeficiency and retroperitoneal fibromatosis. This type D virus, isolated from a macaque with simian acquired immunodeficiency syndrome (SAIDS-D/Washington), is exogenous and is partially related to the Mason-Pfizer and the langur monkey type D viruses. The SAiDS-D virus can be distinguished from all other primate retroviruses by antigenicity and molecular hybridization. Nucleic acid hybridization studies reveal that the origin of the SAIDS-D isolate may reside in Old World monkey (subfamily Colobinae) cellular DNA.

Abstract. An epornitic of canary pox occurred in white-crowned sparrows (Zonotrichia leucophrys gambelli) , golden-crowned sparrows (Zonotrichia atricapilla) , and house sparrows (Passer domesticus), which had been caught in the wild and were being studied in laboratories. Of 900 exposed birds, 100 died naturally with the disease and 200 with clinical signs, and their 600 cage mates were killed. The earliest lesion was proliferative dermatitis around the eyes and beak. Next, severe ulcerative dermatitis, often with secondary bacterial and mycotic infections, developed under the wing; rhinitis, pneumonia, pleuritis, and peritonitis occurred in advanced cases. Histologically, there were eosinophilic, sudanophilic, cytoplasmic inclusions in epithelial cells and in subepidermal lymphoreticular cells. The isolated virus produced 100% mortality when inoculated into white-crowned sparrows, house sparrows, and canaries but only local cutaneous reactions in pigeons, turkeys, and chickens.Wild passerine birds are increasingly used in biomedical research. Among the potential diseases in such species, canary pox is probably the most serious threat, since it is highly infectious [3, 271, produces almost 100% mortality in affected birds [3,7, 231, and may occur in a latent form with the virus being shed from lesions for up to 13 months [18]. It may thus be introduced from the wild into stocks of laboratory-maintained birds, with devastating results.The canary poxvirus is one of the four major subgroups of the avian poxviruses ; the other three are fowl poxvirus, pigeon poxvirus, and turkey poxvirus [3,5,8, 13, 351. These three viruses usually cause a cutaneous disease of high morbidity but variable mortality [8]. Large pocks with umbilicated centers form on the skin. Within the cutaneous lesions, which are generally confined to the epidermis, there are pronounced hypertrophy and hyperplasia of epithelial cells. The cytoplasm of these cells often contains Bollinger bodies, that is, large eosinophilic inclusions composed of clusters of viral particles [8,24].

Spontaneous renal disease in the pigtailed macaque was evaluated in a prospective study of 20 apparently healthy monkeys that were killed and a retrospective study of 674 monkeys that died of spontaneous disease. Many apparently normal pigtailed macaques have a mesangioproliferative glomerulonephritis of slight to moderate severity. Deposition of immunoglobulin, particularly IgM, was common in renal glomeruli and did not seem to correlate with renal disease. Glomerulonephritis was found in 14% of the adult monkeys that died of spontaneous disease; in 4.2% it was severe enough to have caused renal failure. Tubular nephrosis was the most common renal lesion (22.6% of adults) and was usually a nephrotoxicity resulting from treatment of diarrhea with nephrotoxic antibiotics. Other lesions found were incidental or were secondary to disease processes in other organs. Pigtailed macaques that have been in our colony at least six months have a higher incidence of renal disease than is reported elsewhere in Old World monkeys.

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Mesangioproliferative glomerulonephritis was found in 28 of 113 pigtailed macaques (Macaca nemestrina) that died in 1977. In five it was considered severe enough to cause significant renal dysfunction; in two of these it was the cause of death. The basic lesion was a proliferation of mesangial cells and deposition of mesangial matrix in the mesangial stalk, resulting in various degrees of stalk expansion and increased lobulation of the glomerular tuft. Preliminary immunofluorescence and ultrastructural studies suggests the pathogenesis of the lesion may involve deposition of antigen-IgM immune complexes in the mesangial region.