Experimental production of fatal mucosal disease in cattle

Abstract

Three outbreaks of mucosal disease were investigated. Careful examination of 47 cattle that were persistently viraemic with bovine virus diarrhoea virus (BVDV) revealed no clinical disease, no or low levels of BVDV antibody and only non-cytopathic virus in their blood. The four animals with mucosal disease all showed clinical disease and both cytopathic and non-cytopathic virus in their blood. Following post mortem examination, there were particularly high levels of cytopathic virus in gut tissue. A hypothesis for the induction of mucosal disease is suggested. It states that animals become persistently infected with non-cytopathic virus following in utero infection and when, in post natal life, they become superinfected with a cytopathic virus, then mucosal disease ensues. The experimental reproduction of mucosal disease in support of this hypothesis is described.

Retrospective genome analysis of a live vaccine strain of bovine viral diarrhea virus

“…The first vaccines were aimed at reducing the severity of clinical symptoms of postnatal BVD. After elucidation of the pathogenesis of persistent infection and MD in the mid 1980s [6,8], and the role of PI cattle in the disease, the main goal of modern BVDV vaccines is to prevent foetal infections.…”

“…PI animals are immunotolerant against the respective ncp virus. After superinfection with an antigenically closely related cp strain, which is either of exogenous origin or develops by genetic alterations of the resident ncp virus, the PI animals are predisposed to develop early onset of MD [6,8], whereas superinfection of PI animals with an antigenically different cp BVDV can result in the late onset of MD [16,35].…”

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

“…There is also evidence to suggest that MD may develop due to the super infection of an animal persistently infected with ncp BVDV becoming infected with a secondary cp BVDV (Bachofen et al 2010). This process has been demonstrated experimentally with both ncp and cp BVDV isolated from MD infected animals (Brownlie et al 1984;Bolin et al 1985). The cp virus is unchallenged by the host immune system as the host is BVDV immunotolerent due to the ncp persistent infection (Brownlie et al 1998).…”

“…PI animals act as the main reservoir of BVDV as they shed a large amount virus continuously throughout their life time (Brownlie et al 1984). …”

“…The cp virus is unchallenged by the host immune system as the host is BVDV immunotolerent due to the ncp persistent infection (Brownlie et al 1998). Post-mortem analysis of MD infected animals typically reveals mucosal lesions and cytopathicity of the lymphoid tissue in the gastrointestinal tract (Liebler et al 1995;Brownlie et al 1984). Both biotypes have been isolated from chronically infected animals which presented with mucosal disease.…”