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

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.

Hypomyelination Associated With Bovine Viral Diarrhea Virus Type 2 Infection in a Longhorn Calf

“…Most fetal infections with BVDV result in persistent subclinical infection, fetal death, or defects such as cerebellar hypoplasia, hydranencephaly, internal hydrocephalus, microencephaly, and porencephaly. 5,10,14 Neuropathologic descriptions of natural in utero BVDV infection resulting in hypomyelination are limited. In a dairy farm in the Netherlands, an outbreak of BVD resulted in multiple calves being born with neurologic signs similar to those described here, and histologic findings included widespread loss of myelin staining, an increased number of microglia and astrocytes with enlarged vesicular nuclei, and mild mononuclear cell cuffing of blood vessels.…”

“…Types of BVDV-induced central nervous system (CNS) defects include cerebellar hypoplasia, spinal cord hypoplasia, microencephaly, porencephaly, hydranencephaly, internal hydrocephalus, and a variety of ocular changes. 2,10,14 Hypomyelination has been reported in calves congenitally infected with BVDV; 5,10,20,23 however, hypomyelination is a relatively uncommon outcome compared with intrauterine infections with BDV and CSFV strains in sheep and pigs, respectively. Here we describe the histologic, immunohistochemical, and ultrastructural findings in a calf with severe hypomyelination presumably induced by naturally acquired intrauterine infection with a virus specifically genotyped as BVDV type 2.…”

Infectious Agents

“…Defects of the CNS include cerebellar hypoplasia (Figure 60.2), hydranencephaly, hydrocephalus, porencephaly, microencephaly, spinal cord hypoplasia, and a variety of ocular changes such as cataracts, optic neuritis, retinal degeneration, and microphthalmia. 150,176,177 Less commonly, congenital BVDV infection can cause CNS hypomyelination, which has been reported with both species of BVDV. 178,179 In addition to CNS abnormalities, congenital BVDV infections can result in brachygnathism, osteopetrosis, thymic aplasia, hypotrichosis, hair coat abnormalities, pulmonary hypoplasia, and growth retardation.…”

The chasm between public health and reproductive research: what history tells us about Zika virus

“…Vertical transmission of hepatitis C virus, a virus of the Hepacivirus genus, from mother to child is known to occur in up to 10 % of pregnancies. BVDV, a member of the Pestivirus genus, does not infect humans but is known for its vertical transmission in cattle [1][2][3][4][5]. BVDV infection at different stages of gestation may lead to a spectrum of adverse pregnancy outcomes, including pregnancy loss and neurologic manifestations (including deformations such as hydrocephalus and microcephaly) in the offspring.…”