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Malignant catarrhal fever (MCF) is a herpesvirus disease syndrome of ruminants. The microscopic pathology of MCF is characterized by lymphoid proliferation and infiltration, necrotizing vasculitis and epithelial necrosis. Because previous attempts to detect viral antigen or nucleic acids in lesions have been unsuccessful, the pathogenesis of the lesions in acute MCF has been speculated to involve mechanisms of autoimmunity and lymphocyte dysregulation. In this study, the vascular lesions in the brains of a cow and a bison with acute MCF were evaluated by in situ PCR and immunohistochemistry. The results demonstrated that the predominant infiltrating cell type in these lesions was CD8(+) T lymphocytes and that large numbers of these cells were infected with ovine herpesvirus 2. The lesions also contained macrophages, but no detectable CD4(+) or B lymphocytes.

An outbreak of malignant catarrhal fever (MCF) resulted in the deaths of 12 cattle in a herd of 77 animals during seven weeks in 1999; in addition, one cow developed a milder disease which was confirmed as MCF by PCR for ovine herpesvirus 2 DNA and an immunofluorescent antibody test for antibodies to the virus, but recovered. Further PCR and serological testing revealed the infection in three other animals, none of which developed clinical disease. Hypocuprosis and the possibility of a genetic predisposition were identified as factors which may have contributed to the outbreak.

This paper describes the first cases of malignant catarrhal fever (MCF) in pigs in which the diagnosis was verified aetiologically by polymerase chain reaction (PCR) and DNA analysis and by the demonstration of antibodies. Three pigs on two separate premises showed clinical signs, gross pathological and histopathological lesions which were in many respects similar to those of MCF in ruminants. The pigs were housed adjacent to sheep and DNA of ovine herpesvirus-2 (OHV-2) was detected by PCR in tissues of all the pigs. In addition, antibody to alcelaphine herpesvirus-1 was detected in the serum of the pigs and in five in-contact sheep. It is concluded that the disease described is MCF of pigs caused by OHV-2.

Acute malignant catarrhal fever (MCF) was diagnosed in 10 bison from 6 herds and ranging from 1 to 6 years of age. The pattern of clinical signs and morphologic lesions differed among bison. Combinations of corneal opacity, lacrimation, nasal discharge, depression, excess salivation, anorexia, diarrhea, melena, and hematuria were observed. Vasculitis characterized by lymphoid infiltrates in the adventia with variable extension into media and intima was found in multiple tissues in each animal. Fibrinoid vascular necrosis was rare. Ulceration in the alimentary tract was found in 9/10 bison, and ulceration or hemorrhage in the urinary bladder was found in 8/10 bison. Lymphoid infiltrates were present in 7 of 9 livers and 9 of 9 kidneys examined histologically. Hyperplasia of lymph nodes was observed in 5 bison. Chronic MCF was diagnosed in 1 bison with an 80-day course of illness that began with lacrimation, corneal opacity, mucoid nasal discharge, depression, and anorexia. These signs ceased after 15 days but circling and blindness developed on day 76. Chronic vascular lesions characterized by endothelial cell hypertrophy, intimal thickening, fragmentation of the internal elastic membrane, smooth muscle hypertrophy, and adventitial infiltrates of lymphocytes and plasma cells were found in many organs. The retinal arteries had chronic inflammation and acute transmural fibrinoid necrosis. The retinas were infarcted. Polymerase chain reaction technique for amplification of ovine herpesvirus 2 sequences was performed on formalin-fixed tissues, and viral sequences were detected in 1-7 tissues from each animal. These viral sequences were not found in tissues of 4 bison not affected by MCF.

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.

Enzootic pneumonia was diagnosed in 160 of 225 bullocks in a livestock fattening unit. Within the first 10 weeks, 51 of those affected contracted the disease a second time after the symptoms had vanished. Acute catarrhal bronchopneumonia were most common (49.3%) during the first outbreak, whereas acute catarrhal purulent bronchopneumonia (39.2%) and chronic pneumonia (29.4%) were most common during the second. Arterial blood gas analysis was undertaken for 33 clinically healthy bullocks and 100 bullocks with clinically diagnosed acute bronchitis, acute catarrhal bronchopneumonia, acute catarrhal purulent bronchopneumonia and chronic pneumonia. The pO2, SATO2 and A-aDO2 levels found in blood from the abdominal aorta of all diseased animals differed significantly from those of healthy animals. The values for animals with distinct catarrhal bronchopneumonia and catarrhal purulent bronchopneumonia showed the greatest differences.

Malignant Catarrhal Fever was diagnosed in an Indian Gaur (Bos gaurus gaurus), a Barasingha Deer, (Cervus duvauceli duvauceli), and four Javan Banteng (Bos javanicus javanicus) at the San Diego Wild Animal Park between July, 1976 and January, 1979. Three of the four Banteng lived adjacent to an exhibit in which wildebeast were born at 29.68 and 82 days prior to the Banteng's deaths. The disease was characterized by pyrexia, conjunctivitis, diarrhea, dyspnea and rhinitis. Mortality was 100%. Post mortem lesions in the respiratory, digestive, lymphoid and nervous systems were erosions, ulcers, necrosis and hemorrhage. Microscopic lesions included lymphoid necrosis, reticuloendothelial hyperplasia and diffuse vasculitis. All virus isolation attempts were negative.

Rabbits pretreated with cyclophosphamide for 7 days (CY+) and control rabbits (CY-), were infected with cell-associated malignant catarrhal fever virus (MCFV), and CY treatment of the CY+ group was continued to day 20 p.i. The time of onset and degree of antibody formation to bovine serum albumin was significantly suppressed in the CY+ group whilst the humoral antibody response to MCFV appeared to be delayed rather than suppressed. Although incubation periods of the disease were comparable in the CY+ and CY- groups, the disease course was much shorter in the CY- group, 100% mortality occurring within a mean of 4.5 days, as opposed to a mean of 15 days in CY+ animals. Mortalities did not occur in the CY+ group until a mean of 5.5 days following withdrawal of CY. In further experiments it was shown that pre-existing antibody to MCFV had no effect on the incubation period and course of MCF in rabbits. The results thus suggest that MCF may not be an immune complex disease.