Bovine virus diarrhoea-mucosal disease virus: pathogenicity for the fetal calf following maternal infection

Abstract

Fifteen pregnant, bovine virus diarrhoea-mucosal disease (BVD-MD) antibody-free Jersey heifers were infected experimentally with a mixture of 10 cytopathic strains of BVD-MD virus isolated from cattle in Britain. Each cow was inoculated intramuscularly on gestation day 100 with a high or a low dose of virus grown in primary calf testis tissue cultures. None of the cows showed clinical signs of illness following exposure, but all had seroconverted within six weeks. Six fetuses, including one set of twins, died in utero following infection. Of these five were aborted between days 136 and 154; the sixth one was mummified and still retained at day 300. The remaining 10 fetuses survived to term, but all showed evidence of intrauterine growth retardation with or without gross malformation and/or dysmyelination of the central nervous system. Three were clinically affected with congenital nervous disease. Of the 10 liveborn fetuses, two had specific serum antibodies to BVD-MD. Non-cytopathic BVD-MD virus was recovered from all of the remaining eight. When non-immune cows become infected with BVD-MD virus in mid gestation: transplacental infection of the fetus will probably result; apart from the risk of fetal death, with or without abortion, there is a high probability of fetal mal-development which may not always be clinically obvious; the immunological competence of the fetus may be impaired; congenital infection is likely in a substantial proportion of liveborn calves. About one in 16 bovine fetuses in British herds are estimated to be at risk from BVD-MD virus infection.

Bovine Viral Diarrhea Virus Cyclically Impairs Long Bone Trabecular Modeling in Experimental Persistently Infected Fetuses

“…5,9,17 NcpBVDV, by virtue of its ability to cross the placenta and infect the fetus at any stage of gestation, has been associated with a myriad of different manifestations, including early embryonic death, abortion, fetal PI, and congenital abnormalities. 2,10,11 The fetal consequences of transplacental infection appear to be primarily determined by the age of the fetus at the time of infection, although other factors may contribute, such as the pathogenicity of the infecting virus strain and the immune and health status of the dam. 4 Transplacental infection of the fetus by ncpBVDV prior to adaptive immune system development, which occurs during the second and third trimesters of gestation, is thought to enable PI and lifelong viral shedding by the animal due to development of highly virus-specific T-cell tolerance to the infecting strain.…”

“…10,26,27,32,38 The morphogenesis of these lesions and the mechanisms responsible for their development are unclear. Reduced bone and calcified cartilage core resorption would be the direct explanation, but contributions of other potential processes, including enhanced bone formation or physeal abnormalities leading to the production of thickened primary spongiosa, have not been investigated.…”

“…Taken collectively, most of the previous studies were limited by uncertainty in the time and course of infection, infection status (whether subject was persistently or transiently infected), and/or small numbers of affected animals. 10,26,27,32 This study was undertaken to characterize the morphogenesis of long bone lesions over the course of experimentally induced fetal PI with BVDV in an attempt to determine the processes and mechanisms responsible for the development of these lesions.…”

Genetic typing of bovine viral diarrhoea virus in cattle on Irish farms

“…Congenital defects develop in the foetus typically when infected during the mid-gestation stage (Radostits and Littlejohns 1988). CNS defects include cerebellar hypoplasia (Ward et al 1969), microencephalopathy, hydrocephalus and hydranencephaly (Badman et al 1981), while incidences of optic neuritis, alopecia (Yeruham et al 2001) and growth retardation have also been observed (Done et al 1980). …”

Prevalence of BVD infection in ruminants in Serbia

“…Major economic losses due to BVDV infection include reduced fertility, abortions, growth retardation and the generation of persistently viremic calves, which can develop fatal "mucosal disease" (Brownlie, 1990;Bielefeldt, 1995;Moennig and Liess, 1995). Placental infection with ncp virus in the first trimester of gestation can induce persistently viremic calves (Moennig and Liess, 1995), whereas fetal infection later in gestation often causes abortion, retarded development or results in healthy virus-free and seropositive offspring (Done, et al, 1980;Bielefeldt, 1995). Persistently infected lifelong virus carriers play a key role in BVDV epidemiology.…”