Brain Lesions in Calves following Transplacental Infection with Bovine‐virus Diarrhoea Virus

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Abstract
Summary: In 33 calves and subadult cattle of the Holstein‐Friesian breed ranging from 1 to 210 days of age, the spectrum of brain lesions induced by intra‐uterine infection with bovine‐virus diarrhoea virus (BVDV) was retrospectively analysed. Of these, 27 animals originated from herds with a long history of BVD. Six calves were derived from dams vaccinated between the 90th and 118th day of gestation with a BVD live vaccine. The most frequent lesion was cerebellar hypoplasia, being present in 25 out of 33 (76%) of the animals. In most of these cases, cerebellar hypoplasia was associated with hydranencephaly, internal hydrocephalus, microencephaly or porencephaly. In cases with hydranencephaly, the fluid‐filled cavities were devoid of ependymal lining. The lumina of the lateral ventricles of these cases were surrounded by glial fibrillary acidic protein (GFAP)‐positive cells and a dense layer of immunoreactive cell processes. In the white matter adjacent to the dilated ventricular lumina, a reactive astrocytosis was present. Porencephalic cysts were surrounded by astrocytes with increased expression of GFAP and vimentin‐positive cells and cell processes. In hydranencephalic brains, staining for neuron‐specific enolase (NSE) revealed a marked reduction of NSE‐positive nerve cells in cortical areas. In all six experimental cases and in several field cases with hydranencephaly or internal hydrocephalus, small groups of heterotopic NSE‐positive neurons were present in the white matter of the cerebral hemispheres. In markedly hypoplastic cerebella, reduction of the cortical cell layers and degenerative changes in, and heterotopia of, Purkinje cells were found. In these cases, NSE‐ and neurofilament‐positive cell processes were either markedly diminished or only remnants of immunoreactive cell processes were present. In five animals without significant gross cerebellar abnormalities, degenerative changes of Purkinje cells were found.Immunohistochemical staining using antibodies against glial and neuron‐specific proteins on these brains, which represent postnatal end‐stage lesions of BVDV‐induced disturbances of the normal brain development, did not provide any insight into the possible pathogenetic mechanisms of these alterations. Application of immunohistochemistry, however, revealed changes, such as reactive astrocytosis and loss of nerve cell processes, which were not obvious on haematoxylin and eosin (H&E) stained sections.