Abstract

Bovine viral diarrhoea (BVD) virus is maintained in the environment by persistently infected animals [8]. The BVD virus in an immunocompetent pregnant animal is capable of crossing the placental barrier and invading the foetus [12,9]. The principal determinant of foetal response to infection is the age of the foetus at the time of infection [1], and the differing ability of different strains of BVD virus to produce congenital defects [11,19]. Breed variation and immune status of the host may also be important factors in determining the foetal effect. The possible outcomes of foetal infection include foetal resorption, abortion, mummification, congenital malformations, birth of weak and undersized calves, birth of calves persistently infected with BVD virus, and birth of normal calves. Foetopathology caused by BVD virus infection during the first trimester has been well documented [13,7,20,4,3,9,21,2,17,18]. The following congenital defects have been described: cerebellar hypoplasia, hydrocephalus, hydranencephaly, with or without cranial deformation, dysmyelination of the spinal cord, lenticular cataracts, microphthalmos, chorioretinopathy, alopecia, brachygnathia, intrauterine growth retardation and thymus hypoplasia. This report describes an unusual congenital malformation in a calf, where there was serological evidence of foetal BVD virus infection. The male calf was born to a 3.5-year-old dairy cow after a prolonged gestation (294 days), and 15 min after the calving the animal died. The first female calf born to this cow, one year previously, was normal. The well managed dairy cattle herd (Israeli-Holstein breed), comprising 40 lactating cows, was kept under a zero-grazing management system in open barns, all the year round, with a rolling herd milk production average of 9,000 kg. The herd had not been routinely vaccinated against BVD infection. This unusual malformation was one-off occurrence, and there were no other indications of BVD virus – associated in this herd. Serological survey by ELISA test showed a prevalence of 89% for BVD virus in this particular herd. Pre-colostral serum from heart blood of the newborn calf and a blood sample from the dam were collected for detection of neutralizing antibodies and for virus isolation.

Highlights

  • Cerebellar hypoplasia, hydrocephalus, hydranencephaly, with or without cranial deformation, dysmyelination of the spinal cord, lenticular cataracts, microphthalmos, chorioretinopathy, alopecia, brachygnathia, intrauterine growth retardation and thymus hypoplasia

  • The spotted sample was incubated with diluted bovine anti-Bovine viral diarrhoea (BVD) virus antiserum in a humid chamber for 30 min at 37 °C, washed 3 times with carbonate/bicarbonate buffer, incubated with diluted goat anti-bovine IgG/ FITC in a dark humid chamber for 30 min at 37°C

  • If inhibition of the cytopathic effect was observed at any dilution, the serum was considered to be negative for BVD virus-neutralizing antibodies

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Summary

Introduction

Cerebellar hypoplasia, hydrocephalus, hydranencephaly, with or without cranial deformation, dysmyelination of the spinal cord, lenticular cataracts, microphthalmos, chorioretinopathy, alopecia, brachygnathia, intrauterine growth retardation and thymus hypoplasia. Sera were heated at 56°C for 30 min and examined in a neutralization assay in microtitre plates, using a 1-h incubation at 37°C with cytopathogenic BVD virus isolate (100 TCID50 per well) and serial twofold serum dilutions. If inhibition of the cytopathic effect was observed at any dilution, the serum was considered to be negative for BVD virus-neutralizing antibodies.

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