Changes

====Acute Infections: Pregnant Animals====

====Acute Infections: Pregnant Animals====

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 also 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.

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>39, 40</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.

Infection at the time of insemination may result in reduced conception rates, and that shortly after increases loss of embryos (Carlsson et. al, 1989; McGowan et. al, 1993). Foetal infection in the first trimester (50-100 days) can cause death, although expulsion of the foetus may 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 degeneration⁴¹. Weak, stunted calves may also be produced by BVDV infection in the second trimester.

 

Transplacental infection between days 100 and 150 may result in congenital defects. At this stage the immune system is in the final phase of development, and mounts an inappropriate inflammatory response to BVDV to cause these effects (Duffell and Harkness, 1985). Growth defects in organs such as the thymus, and central nervous system pathologies such as cerebellar hypoplasia, often arise (Brownlie, 1985). Calves with cerebellar hypoplasia are ataxic, reluctant to stand and may suffer tremors (Baker, 1995). Infection at this point may also cause visual problems, including blindness and cataracts. Virus may localise to the vascular endothelium, causing vasculitis and associated inflammation, oedema, hypoxia and cellular degeneration (Brownlie, 2000). Weak, stunted calves may also be produced.

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.

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.