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Schmallenberg virus
Schmallenberg virus circulation in Belgium in 2012
  1. C. Bayrou,
  2. M-M. Garigliany,
  3. D. Cassart,
  4. S. Jolly and
  5. D. Desmecht
  1. Department of Pathology, Faculty of Veterinary Medicine, University of Liège, B-4000 Liège, Belgium
  1. e-mail: daniel.desmecht{at}

Statistics from

IN Belgium, the end of 2011 and beginning of 2012 were characterised by numerous reports of births at term of calves with neurological signs or malformations of the head, spine or limbs that were subsequently assigned to the emerging Schmallenberg virus (SBV) (Garigliany and others 2012a). Further, the large-scale cross-sectional serological surveys conducted in cattle during spring 2012 concluded that almost all Belgian cattle had already been in contact with the virus (Garigliany and others 2012b, Méroc and others 2013). As the immunity raised by the cow against close phylogenetic relatives of the newcomer prevents subsequent infection of the fetus (Anon 2008), it seemed likely to most studying the virus that the teratogenic infection due to SBV would disappear in 2012.

Field veterinarians refer approximately 2200 dead animals per year for postmortem examination to the University of Liège's Faculty of Veterinary Medicine. For cattle, a dedicated shuttle runs daily throughout southern Belgium to remove and transport the carcases from the farms to the faculty, allowing for postmortem examination to take place within 12 to 48 hours in over 90 per cent of cases. In January and February, 2013, 50 calves less than one week old were referred and we sought the new virus in the tissues of all animals belonging to one or more of the following categories: calves with reported neurological signs antemortem; calves displaying musculoskeletal deformities; and calves that died spontaneously soon after birth and in which no unequivocal cause of death was identified at postmortem examination.

Among the 12 suspect animals, SBV genetic material was detected in three by RT-qPCR. As all attempts to retrieve the genetic material of bluetongue virus type 8 and bovine viral diarrhoea viruses from the tissues of these SBV-positive cases failed, and because none of them was carrying the mutation characteristic of the cleft palate/arthrogryposis syndrome that is responsible for virtually all non-infectious cases of arthrogryposis in the local livestock, we attributed their malformations to SBV infection in utero. The first showed a torticollis and the other two displayed joint fixation of one or all joints, which is referred to as arthrogryposis. Joint fixation was always symmetric. The double fore/hindlegs involvement was observed in the most severe case and only the hindlimbs were involved in the second. In addition, in one case, the cross-sectional area of the lumbar spinal cord was dramatically reduced (micromyelia) and the ependymal canal was duplicated (myelodysplasia).

These field and laboratory observations suggest that SBV was circulating in Belgium during the summer 2012 despite a very high herd immunity. Further studies will be conducted to determine whether we are observing the last cases of this epizootic or if the above calves announce a transition to endemicity.


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