Infectivity of cell-free malignant catarrhal fever virus in rabbits and cattle

Malignant catarrhal fever was induced in cattle and rabbits inoculated intranasally with cell-free wildebeest-calf nasal and ocular secretions. This method of reproducing the disease is similar to that occurring in nature and should prove useful as a means of challenging experimentally induced immunity.     

The development of delayed cutaneous hypersensitivity in rabbits infected with the herpesvirus of malignant catarrhal fever

Delayed-type hypersensitivity (DTH) was demonstrated in malignant catarrhal fever (MCF) virus-infected rabbits intradermally injected with homologous viral antigens.The response was first detected four days post-infection (pi) and was maximal on day 7 pi. DTH could not be demonstrated after the onset of pyrexia. The abrogation of DTH in MCF virus-infected rabbits is discussed in relation to the pathogenesis of the disease.     

Target cells for malignant catarrhal fever virus in rabbits

Lymphocytes from lymph nodes and spleens of malignant catarrhal fever virus (MCFV) infected rabbits were tested for MCFV infectivity in secondary calf thyroid cell monolayers. Most infectivity was demonstrated in the lymphocytes. Some infectivity was also detected in macrophages/monocytes. It was thus concluded that lymphocytes form the major target cell for the herpesvirus of malignant catarrhal fever in rabbits.     

Malignant catarrhal fever in cattle experimentally inoculated with a herpesvirus isolated from a case of malignant catarrhal fever in Minnesota USA

A malignant catarrhal fever (MCF)-like syndrome was experimentally induced in three steers, which were under immunization trials with a herpesvirus previously isolated from a case of MCF in a cow in Minnesota USA. The clinical signs observed in the three steers, and the pathological and histological lesions observed in two of these steers which succumbed to the disease syndrome were indistinguishable from those described for MCF. Although seroconversion was readily demonstrated in the three animals, virus was not re-isolated from the blood leucocytes, secretions and tissues obtained from the two animals which succumbed to the syndrome during the course of the disease and after death. However, a herpesvirus which showed cell rounding cytopathic effects (cpe) in bovine thyroid cells (Bth), was re-isolated from the one steer which survived the disease.     

Vitamin D status in cattle with malignant catarrhal fever

The aim of the present study was to determine the vitamin D status in cattle with malignant catarrhal fever (MCF). Twelve cattle diagnosed as MCF and 6 healthy cattle (controls) were used in the study. Serum 1,25-dihydroxyvitamin D(3) (1,25-D), 25-hydroxyvitamin D(3) (25-D), calcium, phosphorus and parathyroid hormone (PTH) levels were determined as 96.83 pg/ml, 30.0 ng/ml, 2.19 mmol/l, 1.57 mmol/l and 15.21 pg/ml in MCF group and 42.33 pg/ml, 37.0 ng/ml, 2.43 mmol/l, 1.96 mmol/l and 36.08 pg/ml in controls, respectively. Although serum 1,25-D level in the MCF group was increased (P<0.01), serum calcium (P<0.01) and PTH (P<0.05) levels were decreased compared to the controls. The results suggest that there might be an interaction between vitamin D status and MCF.     

Antibody response in cattle and rabbits to early antigens of malignant catarrhal fever virus in cultured cells.

Cytosine arabinoside (Ara-C) inhibited the production of late antigens and of infectious virus in monolayers of bovine kidney cells infected with the high-passage, WC-11 strain of malignant catarrhal fever virus. Early antigens were not affected. Using hyperimmune and acute-phase sera from cattle and rabbits in indirect immunofluorescence tests, it was shown that Ara-C treated cultures contained two early antigens; one was diffuse and distributed throughout the cells, the other was particulate and intranuclear. Antibody to early antigens developed later and attained lower titres in infected animals, especially rabbits; only hyperimmune sera reacted with the diffuse early antigen.     

Antibodies to malignant catarrhal fever virus antigens in the sera of normal and naturally infected cattle in Kenya

Six different serological tests were used to examine Kenyan cattle sera for antibodies to the herpesvirus of malignant catarrhal fever. Significantly higher levels of indirect immunofluorescent antibody to early and late virus antigens and of complement fixing antibody were found in the sera of 13 naturally infected cattle than in 482 sera collected from four different groups of normal cattle. Virus neutralising and immunoprecipitating antibodies were also found in some infected cattle sera but not in normal cattle sera. Many non-specific reactions occurred using counterimmunoelectrophoresis. These preliminary results indicate that the serological diagnosis of wildebeest-associated malignant catarrhal fever may be possible.     

Large outbreak of malignant catarrhal fever in cattle

The prevalence of clinical malignant catarrhal fever (MCF) is low in the Netherlands, and at a farm level the disease is usually restricted to a single animal. This casereport describes an outbreak of MCF that killed 18 animals (39% of the cattle on the farm). The probable source of infection were 10 hand-reared lambs that were on the farm for a few months.     

Pathogenesis of 'sheep-associated' malignant catarrhal fever in rabbits

Pathogenesis studies of experimentally produced sheep-associated malignant catarrhal fever (MCF) in laboratory rabbits are described. Animals were examined at intervals after inoculation. The principal change was a proliferation of lymphoid cells which began as soon as three days and became quite pronounced by 13 days after inoculation. The appendix, mesenteric lymph node and spleen were most obviously affected. The reason for this was a progressive increase in T-lymphocytes, which appeared to be a hyperplasia rather than neoplasia in T-dependent areas of these organs. Lymphoid cells also accumulated in interstitial spaces of non-lymphoid organs. The use of cyclosporin-A suppressed the lymphoid proliferation but rabbits still developed clinical MCF after a similar incubation period. It is suggested that the agent of MCF might produce its effect by infecting and causing a dysfunction of lymphoregulatory cells, resulting in benign polyclonal T-lymphocyte proliferation. Terminal necrosis could be due to natural killer cell activity.     

Immunoglobulins,haemolytic complement and serum C3 in cattle infected with malignant catarrhal fever herpesvirus

Serum levels of the third component of complement (C3) were reduced only in the terminal stages in malignant catarrhal fever (MCF) virus-infected steers. Haemolytic complement and immunoglobulin (IgM, IgG₁ and IgG₂) levels were not altered. C3 and immunoglobulin deposits were also not demonstrated in the vascular lesions induced by MCFV. MCF virus infection of cattle is probably not a typical immune complex-mediated disease as previously suggested.     

Neutralising antibodies to wildebeest-derived malignant catarrhal fever virus in African wildlife

A total of 2,722 sera collected between 1963 and 1983, from 43 different species of wildlife in 11 African countries was examined for neutralising antibodies against the wildebeest-derived strain of malignant catarrhal fever (MCF) virus. Antibodies were demonstrated in 10 species of Bovidae which included eight species from the sub-family Hippotraginae and one species each from Bovinae and Antilopinae. Neutralising antibodies were also recorded in hippopotamus. It is suggested that the high prevalence of antibodies recorded in sera from waterbuck and reedbuck indicate infection with MCF. However, titres in other species may be due to antigenically related viruses.     

Outbreak of wildebeest-associated malignant catarrhal fever in Ankole cattle

During an outbreak of malignant catarrhal fever in a herd of Ankole cattle in a zoological collection, two adult cows and one adult bull from a herd of 15 died or were euthanased between July and November 2004. The clinical, gross postmortem and histological findings were typical of the disease in uk native domestic cattle. The diagnosis was confirmed by serology in two animals, and by pcr in all three; the pcr provided evidence of alcelaphine herpesvirus type 1 infection in all three animals and also of ovine herpesvirus type 2 infection in one.     

Course of malignant catarrhal fever in immunosuppressed and immunostimulated rabbits

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.     

Changes in blood coagulation parameters of red deer (Cervus elaphus) experimentally infected with malignant catarrhal fever

Changes in blood coagulation parameters were followed in four red deer (Cervus elaphus) experimentally infected with malignant catarrhal fever (MCF) of deer. Blood platelet counts, activated partial thromboplastin time (APTT), one-stage prothrombin time (OSPT), activated clotting time (ACT), plasma anti-thrombin III (ATIII) activity, fibrinogen degradation production (FDP) and fibrinogen levels were measured. Inoculated deer became pyrexic after 17 or 19 days. Thereafter they developed watery diarrhoea which rapidly became haemorrhagic. The course of the clinical disease ranged from four to six days before the animals were killed or died. All inoculated deer developed abnormalities in laboratory parameters of blood coagulation. These varied within and between animals, but the coagulation profiles of all four animals remained abnormal until death. Post-mortem findings included extensive systemic petechiation, severe haemorrhage in the alimentary canal and vasculitis with disseminated thrombosis. Abnormal coagulation parameters included extension of APTT and OSPT, increased FDP, decreased ATIII and platelet counts and increased fibrinogen levels. The increases in fibrinogen were compatible with the acute phase response. The other coagulation abnormalities and haemorrhage and thrombosis were indicative of disseminated intravascular coagulation (DIC) with consumption coagulopathy, ACT remained normal in all deer although final clot quality was considered poor.     

Malignant catarrhal fever. I. Response of American cattle to malignant catarrhal virus isolated in Kenya.

Fifty-three American cattle were inoculated with malignant catarrhal fever virus isolated from a wildebeest in Kenya. Three animals showed the mild form of the disease and recovered, and 47 showed the severe form of the disease. The other three did not react. Of the 47 cattle, 28 died, 16 were killed for the collection of specimens and three recovered. The incubation period for the 47 cattle ranged from 16 to 29 days and the course of the fatal disease for 28 cattle averaged three to 23 days. Virus titration of specimens from nine infected steers yielded a mean titer of 10(4)/TCID50 per gm for lymph nodes, 10(3) TCID50 per mL for buffy coats and 10(2.3) TCID50 per gm for spleens. Smaller amounts of virus were found in the liver, kidneys, adrenals and thyroids. Malignant catarrhal fever virus was also found in nasal secretions and saliva of viremic cattle. Viral infectivity was shown in bovine buffy coat cells stored at 4 degrees C for two days but was immediately destroyed upon freezing even when glycerine or dimethylsulfoxide was added. Viral particles were not found in infected animal tissues by electron microscopy. The disease was successfully transmitted in steers by intratracheal intubation and by aerosol inhalation but not by contact.