Congenital BVDV type 1 infection in a group of lambs: a shaky situation

Rebecca Egan, Davor Ojkic, Jim Fairles, John Van Ostaaijen, Jocelyn Jansen

Animal Health Laboratory, University of Guelph, Guelph, ON (Egan, Ojkic, Fairles), Eldale Veterinary Clinic (Van Ostaaijen), OMAFRA (Jansen).

AHL Newsletter 2021;25(2):11.

Over a two-week period, an Ontario sheep flock had approximately 10 lambs born with tremors and weakness (see video link below), and a diagnostic investigation was carried out to investigate the cause.  Clinically, the tremors seemed to worsen when the lambs were excited, and while some of the stronger lambs were able to nurse, weaker lambs succumbed to the disease.  In the month leading up to lambing, the pregnant ewes had been sheared, deloused and vaccinated against clostridial diseases, and the dams were generally in good health leading up to and following lambing.  An important piece of clinical history was provided as well: young Holstein calves sourced from various regions of Ontario and Quebec were being brought in and raised at this farm, and these animals were not vaccinated against BVDV prior to arrival.  In addition to sharing airspace in the barn, some calves were housed in a pen directly beside a group of pregnant ewes.  There was a solid cement partition wall with a shared waterer, which could have been a source of viral transmission via saliva.  Additionally, there was potential transmission via the movement of staff and equipment.

An affected 1-day-old lamb was submitted to the AHL for postmortem examination.  The lamb was in thin body condition with partial depletion of fat stores.  Subtle changes were observed in the brain.  In the cerebral cortex, the interface between the grey and white matter of gyri appeared slightly darker than usual, and the adjacent white matter tracts were slender.  The cerebellum appeared normal in size with equivocal flattening of folia noted in some areas.  Congenital copper deficiency (swayback) can cause similar neurologic signs stemming from lesions in the white matter of the CNS, and therefore, a liver sample was submitted for assessment of copper level which was found to be sufficient.  Histologically, the distinction between grey and white matter in the brain and spinal cord was less well-defined than normal, the white matter tracts were slender (compatible with hypomyelination, which could be highlighted with a special Luxol fast blue stain), and there was prominent gliosis.  Immunohistochemistry was pursued and identified immunoreactivity for bovine viral diarrhea virus (BVDV) in multiple organs.   These included brain, intestine, urinary bladder, spleen, and liver, with involvement of multiple tissue elements such as neurons, glia, mural ganglia, epithelial cells, vascular smooth muscle, and interstitial macrophages/dendritic cells (Fig. 1).  The abundance of viral antigen and immunohistochemical staining pattern supported persistent viral infection in this lamb.  It is important to note that anti-BVDV antibody will also recognize Border Disease virus antigen, a closely related pestivirus; however, in this case, PCR testing of spleen and ileum detected BVDV type 1.

In sheep, infection with Border disease virus (BDV) can result in abortions, stillbirths, and small weak-born lambs, some of which may have arthrogryposis, mandibular brachygnathism, thymic hypoplasia, and hairy fleece and tremors (known as ‘hairy-shaker’ lambs), with the latter stemming from CNS lesions. This virus is very closely related to BVDV, with both viruses belonging to the Flaviviridae family, thus it is not surprising that infection of sheep by BVDV types 1 or 2 are capable of producing Border Disease syndrome in sheep.

Ruminants persistently infected (PI) with BVDV shed the virus and are the main source of spread among herds.  A  recent study showed that in addition to direct contact, BVDV transmission may occurs as a result of aerosol transmission as well (3).  In the current case, BVDV screening was pursued to identify and remove infected animals, and implementation of additional biosecurity measures were recommended to prevent similar cross-species transmission in the future.  BVDV screening can be done via PCR testing (EDTA blood or serum, tissues) which will identify both acutely infected and PI animals.  Serum samples can be pooled into groups of 5, but samples should be submitted individually so that animals can be tested individually in the event that the pooled sample is positive.  Furthermore, a positive PCR result on a single sample cannot distinguish between an acutely infected animal and a PI animal, so positive animals must be re-tested at least 3 weeks following the initial test, at which point PI animals will still have detectable virus and animals that have recovered from acute infection should not.  For more information, see AHL LabNote 1 Summary of bovine viral diarrhea virus (BVDV) testing at the AHL.    AHL

 neuron cell bodies (D,E - arrows), ganglia (F) and peripheral nerves (*).  IHC

Figure 1.  Congenital BVDV type 1 infection in a lamb.  Cerebral cortex (A-C) with white matter that displays reduced myelination (A - arrowhead) and gliosis (B).  Neuron cell bodies are indicated (C - arrows).  H&E stain.  Positive immunostaining for BVDV in brain (D-F): neuron cell bodies (D,E - arrows), ganglia (F) and peripheral nerves (*).  IHC


1. Cantile C, Youssef S. Nervous System. In: Jubb, Kennedy & Palmer’s Pathology of Domestic Animals, 6th ed. Maxie MG, ed. Elsevier, 2016; vol 1:280-283.

2. Nettleton P, Willoughby K.  Border Disease Virus. In: Encyclopedia of Virology, 3rd ed. Mahy BWJ, Van Regenmortel MHV, eds.  Academic Press, 2008:335-341.

3. Hou P, et al. Detection of bovine viral diarrhea virus genotype 1 in aerosol by a real time RT-PCR assay. BMC Vet Res 2020; 16(1):114.