No abstract

Between November 1984 and February 1985, a serious outbreak of pyrexia, diarrhoea, agalactia, metritis and severe weight loss affected most of the recently calved cows in a 183-cow dairy herd in Norfolk. Fifteen cows died and 20 were culled. Forty cows aborted during or after the outbreak, and many of them produced mummified fetuses; 18 calves were stillborn and three others died soon after birth. Necropsy of three affected cows revealed ulceration of the gastrointestinal tract similar to that seen in cases of mucosal disease. Bovine virus diarrhoea virus was isolated from the intestines of one cow that died soon after the onset of illness. The virus was also isolated from the blood of four acutely ill cows and seroconversion was demonstrated in three of those that survived. The virus was isolated from three aborted fetuses, a stillborn calf and a live neonatal calf. Body fluids from two aborted fetuses were seropositive for the virus as were sera from all the aborting cows tested. In addition to widespread seroconversion to bovine virus diarrhoea virus during the outbreak, there was serological evidence of recent infection with Leptospira interrogans serovar hardjo and Coxiella burnetii in a high proportion of cows. It was concluded that this was primarily an acute outbreak of bovine virus diarrhoea but its unprecedented clinical severity was probably associated with the concurrent introduction of L hardjo and C burnetii into an immunologically naive herd during the main calving period. Epidemiological analysis suggested that the source of the virus and L hardjo was down-calving heifers returning from communal marsh grazing.

Two Friesian cows, half-sibs by a common dam, produced four bull calves with severe congenital hypotrichosis and incisor anodontia and three normal heifers by six unrelated Holstein, Friesian, Devon and Hereford bulls. The two dams, and their dam, had coats of a short, stubbly nature and the pigmented areas appeared rusty grey rather than black. Pathological examination of skin samples taken from multiple standardised sites from two of the affected calves showed a reduction in the number of large first-formed hair follicles. Smaller calibre hair follicles were present but, unlike those of normal neonatal calves, all were in the telogen (inactive) phase. Although the herd was infected with bovine virus diarrhoea virus there was no convincing evidence that the virus was implicated in the pathogenesis of these cases of congenital hypotrichosis with incisor anodontia. The family breeding information on the few severely affected and normal progeny and mildly affected and normal parents may be explained by the genetic hypothesis of an X-linked incompletely dominant gene.

Following the recurrence of classical swine fever in the United Kingdom in 1986, a virus isolated from a single outbreak was studied. A major factor in the spread of this disease is considered to be the presence of infectious virus in tissues taken from animals at certain stages of infection, although their condition may escape detection by routine inspection either before or after slaughter. Intranasal inoculation of the isolate into eight-week-old pigs reproduced the acute form of the disease. The pigs were killed or died between seven and 25 days after inoculation. The virus concentration was determined in a wide range of tissues taken at different stages of infection. Infectious virus was present at high concentrations in all the tissues taken and at all stages of infection. Any porcine tissue is therefore a potential source of infection even when it is taken either before the animal displays detectable signs of disease of after it develops serum neutralising antibodies.

Five calves were given live intranasal vaccine against bovid herpesvirus 1 (BHV1) two days after intranasal inoculation of bovine pestivirus (BVDV). Another 5 were vaccinated in the absence of BVDV. Control unvaccinated groups were also maintained. All calves were challenged with virulent BHV1. The unvaccinated calves developed signs of infectious bovine rhinotracheitis (IBR) and both vaccinated groups showed a similar degree of clinical protection from IBR. Those given BVDV before vaccination shed up to 140 times more BHV1 (P less than 0.01) in the nasal mucus following challenge than those which had received BHV1 vaccine alone. The epidemiological significance of this is discussed.