A virus was isolated from an adult goat with chronic arthritis and shown to belong to the retrovirus group by electron microscopy and biochemical methods. Inoculation of the virus into cesarean-derived specific-pathogen-free goats' kids produced arthritic lesions similar to those in the spontaneous disease. Vrus was reisolated from the experimentally induced lesions.

Malignant catarrhal fever (MCF) is traditionally regarded as a disease with a short clinical course, low morbidity and high case fatality rate. Owing to the limitations of the assays used for laboratory diagnosis. It was difficult in characterise the clinical spectrum of sheep-associated MCF, particularly when the cattle recovered from an MCF-like clinical syndrome. Over a period of three years, 11 cattle that survived MCF for up to two-and-a-half years were identified on four premises. A clinical diagnosis of MCF was confirmed by the detection of ovine herpesvirus-2 DNA in peripheral blood leucocytes using a polymerase chain reaction (PCR) assay that detects a specific 238 base-pair fragment of viral genomic DNA. Of the 11 cattle examined, six recovered clinically with the exception of bilateral corneal oedema with stromal keratitis (four animals) and unilateral perforating keratitis (one animal). The 10 animals available for postmortem examination had disseminated subacute to chronic arteriopathy. Recovery was associated with the resolution of the acute lymphoid panarteritis that characterises the acute phase of MCF, and with the development of generalised chronic obliterative arteriosclerosis. Bilateral leucomata were due in part to the focal destruction of corneal endothelium secondary to acute endothelialitis. Formalin-fixed tissues and/or unfixed lymphoid cells from all 11 cattle were positive for sheep-associated MCF by PCR. These observations indicate that recovery and chronic disease are a significant part of the clinical spectrum of MCF and that such cases occur with some frequency in the area studied. The affected cattle remain persistently infected by the putative sheep-associated MCF gammaherpesvirus.

Abstract.A subacute disease presenting primarily as alopecia and weight loss occurred in 2 white-tailed deer (Odocoileus virginianus) on farms in Minnesota and in Texas. A presumptive diagnosis of malignant catarrhal fever (MCF) was made on the basis of histological lesions. Antibody against an epitope conserved among the MCF group viruses was detected in the serum of both deer. DNA samples from the deer were subjected to a variety of PCR amplifications. Alignment of the amplified sequences from the diseased animals revealed that they were 100% identical to each other and to the same DNA fragment from the newly recognized member of the MCF virus group endemic in domestic goats (Capra hircus), provisionally named caprine herpesvirus 2 (CpHV-2). A seroprevalence survey from one of the deer farms showed a high rate of subclincal infection in the deer population. This study provides further confirmation that CpHV-2 is a pathogen, at least for deer, and emphasizes the risk of loss from MCF when mixing cervids with goats.Malignant catarrhal fever (MCF) is a viral disease syndrome primarily of ruminants, caused by a group of closely related rhadinoviruses. The disease is characterized primarily by lymphoproliferation, mucosal inflammation, and vasculitis. 13 Its clinical course ranges from peracute to chronic. 15,19 Of several closely related MCF viruses, only one has been propagated in vitro and partly characterized. 4,18 This virus, endemic in the wildebeest, is known as alcelaphine herpesvirus 1 (AIHV-1). It causes the classic 'African' form of MCF, also known as wildebeestassociated MCF (WA-MCF). 17 The virus known as ovine herpesvirus 2 (OvHV-2) is the major MCF virus worldwide. This virus is endemic in sheep and causes sheep-associated MCF (SA-MCF) outbreaks in various ruminant species. OvHV-2 has never been propagated in vitro.Recently, 2 additional members of the MCF virus group were reported, both of which were associated with clinical disease. One caused classical MCF in white-tailed deer (Odocoileus virginianus) 7 ; the reservoir host for this virus has not been identified. The other, endemic in domestic goats (Capra hircus), provisionally termed caprine herpesvirus 2 (CpHV-2), 2,8 was associated with chronic alopecia in Sika deer (Cervus nippon). 3 This report describes 2 outbreaks of CpHV-2-induced MCF in white-tailed deer.Case No. 1 occurred on a deer farm in Minnesota. The farm contained more than one hundred animals, including white-tailed deer, Sika deer, fallow deer, pygmy goats (Capra hircus), and a variety of nonruminant species. Five white-tailed deer had died the previous year with similar clinical symptoms. A 6-year-old female white-tailed deer was frequently found recumbent over the previous 4-week period. Examination revealed significant weight loss, large areas of alopecia around the mouth and eyes, on both sides of the body, and on the legs. Vision appeared to be impaired. The animal was bled, euthanized, and tissue samples collected at necropsy. Gross skin lesions included severe and widespr...

Abstract.A fatal enteric syndrome was identified in American bison (Bison bison) at a large feedlot in the American Midwest in early 1998. An estimated 150 bison died of the syndrome between January 1998 and December 1999. The syndrome was identified as malignant catarrhal fever (MCF), primarily the alimentary form. Clinical onset was acute, and most affected bison died within 1-3 days; none recovered. Consistent lesions were hemorrhagic cystitis, ulcerative enterotyphlocolitis, and arteritis-phlebitis. Vasculitis was milder and more localized than that in cattle with MCF, and in contrast to the situation in cattle, lymphadenomegaly was minimal. Virtually all affected bison examined were positive for ovine herpesvirus 2 (OvHV-2) by polymerase chain reaction (PCR) assay. A retrospective study of archived tissues established that MCF occurred in the yard as early as 1993. A prospective study was undertaken to establish the importance of MCF relative to other fatal diseases at the feedlot. The fate of a group of 300 healthy male bison in a consignment of 1,101 animals was followed for up to 7 months to slaughter. At entry, 23% (71/300) of bison were seropositive for MCF viruses, and 11% (8/71) of these seropositive bison were PCR positive for OvHV-2. Forty seronegative bison were selected at random from the group, and all were PCR negative for OvHV-2. There was no change in seroprevalence in the group during the investigation. The minimum infection rate for MCF virus was 36.3% (93/256). Twenty-two (7.3%) of the 300 bison in the feedlot died. Of these, 15 had MCF, 4 had acute or chronic pneumonia, and 3 were unexamined. Losses in the entire consignment were higher (98/1,101; 8.8% death loss); 76% of deaths were attributable to MCF. The study failed to reveal a relationship between subclinical infection and development of clinical disease.

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