Changes

When acute BVDV infection occurs during pregnancy, the dam may show any of the clinical manifestations that are seen in non-pregnant animals. BVDV is able to cross the placenta and infect the developing foetus and so there may be additional outcomes of infection that depend on the stage of gestation. If infection becomes established at the time of insemination, conception rates may be reduced, and early embryonic death is increased when the virus is introduced at a slightly later stage<Sup>40, 41</sup>.  Foetal infection in the first trimester (50-100 days) may also result in death, although expulsion of the foetus often does not not occur until several months later.

When acute BVDV infection occurs during pregnancy, the dam may show any of the clinical manifestations that are seen in non-pregnant animals. BVDV is able to cross the placenta and infect the developing foetus and so there may be additional outcomes of infection that depend on the stage of gestation. If infection becomes established at the time of insemination, conception rates may be reduced, and early embryonic death is increased when the virus is introduced at a slightly later stage<Sup>40, 41</sup>.  Foetal infection in the first trimester (50-100 days) may also result in death, although expulsion of the foetus often does not not occur until several months later.

Congenital defects can arise from transplacental infection between days 100 and 150. This is caused by an inappropriate inflammatory response mounted to BVDV by the immune system, which is undergoing the final phase of development at this stage³³. Examples of common congenital abnormailites include defects of the thymus, occular changes and cerebellar hypoplasia³⁴. Calves with cerebellar hypoplasia ataxic, reluctant to stand and may suffer tremors³⁵, and occular pathology often causes blindness and cataracts. Localisation of virus to the vascular endothelium gives vasculitis, leading to oedema, hypoxia and cellular degeneration. Weak, stunted calves may also be produced by BVDV infection in the second trimester.

Congenital defects can arise from transplacental infection between days 100 and 150. This is caused by an inappropriate inflammatory response mounted to BVDV by the immune system, which is undergoing the final phase of development at this stage³³. Examples of common congenital abnormalities include defects of the thymus, ocular changes and cerebellar hypoplasia³⁴. Calves with cerebellar hypoplasia ataxic, reluctant to stand and may suffer tremors³⁵, and ocular pathology often causes blindness and cataracts. Localisation of virus to the vascular endothelium gives vasculitis, leading to oedema, hypoxia and cellular degeneration. Weak, stunted calves may also be produced by BVDV infection in the second trimester.

Infection in the third trimester trimester (over 180-200 days) elicits a response from the fully-developed immune system, giving rise to normal but seropositive calves. An additional effect of foetal infection before 120 days gestation is the birth of persistently infected calves.

Infection in the third trimester trimester (over 180-200 days) elicits a response from the fully-developed immune system, giving rise to normal but seropositive calves. An additional effect of foetal infection before 120 days gestation is the birth of persistently infected calves.