Schmallenberg disease was first observed in adult dairy cattle during the summer of 2011 in North Rhine-Westphalia. The initial clinical signs of the affected animals included pyrexia, decreased milk production and diarrhoea. Pooled blood samples from affected individuals were initially screened using metagenomic methods which highlighted seven orthobunyavirus-specific sequences. Phylogenetic analyses of these sequences highlighted that this was a novel virus (named tentatively as Schmallenberg virus) within the Simbu serogroup. Members of this serogroup have a wide global distribution (although they are not present in northern Europe) and are largely vector-borne. While some related viruses within this serogroup do have an impact on human health, (e.g. Oropouche virus), the most closely related viruses to SBV (e.g. Shamonda virus: SHV), do not pose this risk, and in the absence of any epidemiological evidence of human infection, the zoonotic potential of SBV is considered to be very low to negligible (Chantal and others 2012).
Following the initial identification of clinical disease in adult dairy cattle, it became increasingly clear that the main clinical impact of SBV infection lay in its affect upon the developing foetus in cattle and sheep. Subsequent to the observation of clinical signs in adults, SBV was isolated in newborn lambs in the Netherlands that had congenital malformations. It soon became clear that these malformations were associated with large quantities of SBV, partly localised in the central nervous system of affected individuals. The appearance of these clinical signs led to the retrospective discovery of SBV transmission in Belgium, France, Italy, Luxembourg and the United Kingdom (Gubbins and others 2014).
SBV has been confirmed by PCR or virus isolation in cattle, sheep, goats, bison and roe deer. In contrast, only serological evidence of SBV infection has been detected in red deer, alpacas, mouflons and wild boar (Barlow and others 2013) (Mouchantat and others 2015).
SBV is spread by Culicoides midges; like BTV, infection is very efficient midge-to-animal, but unlike BTV is also spread very efficiently from animal-to-midge. This means that disease spread can be very rapid within and between herds and flocks, even though the period an animal carries the virus (viraemia) is only 5-7 days compared to 14 days in BTV. Sheep, goats and cattle are affected.
Unlike BTV, the clinical signs of SBV infection of adult animals are mild, unless high levels of virus are generated, and more severe signs are seen in cattle than sheep.
Adult cattle develop a fever, acute drop in milk production (up to 50 per cent of the previous production which is recovered over about a week), and in some cases profuse diarrhoea that can affect anywhere from a few animals to a large proportion of the herd. This acute infection passes through the herd in about three weeks, after which production recovers. There are also anecdotal reports of drops in fertility (for example, increased number of services per conception).
The other main clinical signs are seen in near-term lambs and calves. The virus is teratogenic and causes damage to the growing foetus resulting in arthrogryposis (twisted limbs and spine) and can lead to abortion or still births. Hydranencephaly (in which the brain’s cerebral hemispheres are absent to varying degrees and the remaining cranial cavity is filled with cerebrospinal fluid) can lead to stillbirth or in some cases ‘dummy’ calves. Transplacental infection occurs more frequently in lambs and less frequently in calves. Typically, small numbers of lambs and calves are affected.
The use of synchronised breeding in some sheep flocks to achieve early lambing, led in a few cases to incidents where up to 30 per cent of lambs were affected due to infection during the early part of pregnancy. The European Food Safety Authority commissioned a multi-country research programme, which has been published (EFSA 2014) and is a useful source of further information http://www.efsa. europa.eu/en/efsajournal/pub/3681.
SBV is endemic in much of northern Europe and has spread as far north as Finland. It has been detected in England, Wales, Ireland and in very localised areas of Scotland. During 2014, there was limited evidence that aroused the suspicion of there being acute disease in areas of southwest England and the Welsh borders.
However, there is clear evidence from mainland Europe that even though SBV may be endemic in an area, not all flocks or herds have been infected, nor have all animals within herds and flocks been infected. Therefore, as time goes on, and the proportion of replacement animals lacking immunity to SBV increases, so the potential for reinfection will increase.
There is no legal requirement to report SBV disease; hence there is a low level of reporting across Europe, although most countries have had cases. Recently, pre-export testing of heifers of breeding age from Holland detected sero-conversion (ie. the production of antibodies), and in some cases the virus was also detected, indicating that these animals had become infected. This is the type of animal which is very likely to be imported into Great Britain; there is, therefore, a very low risk (given the short incubation period) of importation of animals carrying the virus, but a higher risk of animals carrying deformed calves.
Those considering importing animals, especially potentially pregnant animals from mainland Europe, should consider carefully from where they source their animals, and should also ensure that in addition to the official testing required prior to importation or post-import of quarantined animals, consideration is also given to appropriate testing for other diseases.
Two SBV vaccines were available in Great Britain but, despite warnings, due to the lack of uptake neither is currently available. Although these vaccines could be brought back into production relatively quickly, there will be a lag during which animals will not be able to be vaccinated.
Cattle, sheep and goat owners are strongly advised to consult their veterinary surgeon to ensure that they have an active, up-to-date flock or herd health plan which includes provision for SBV, and that advice is sought to determine what their flock or herd SBV status is and what might be done to protect livestock from disease.
During 2015 and 2016 APHA Veterinary Investigation Centres have continued to look for evidence of SBV in all lambs submitted for investigation of abortion presented with arthrogryposis. To date, it has not been identified.
The University of Liverpool has also carried out a serological surveillance study for SBV in sheep in the South of England, and the results are anticipated in the near future.
BARLOW, A., GREEN, P., BANHAM, T. & HEALY, N. (2013) Serological confirmation of SBV infection in wild British deer. Veterinary Record 172, 429
CHANTAL, R., CEES VAN DEN, W., PAUL VAN, B., MARTIN, B., RUTH, B., GERT-JAN, G., LESLIE, I., HANS VAN DEN, K., WILFRID VAN, P., WIM VAN DER, P., JOHAN, R., PETER, S., JONAS, S.-C., PIET, V., ANKJE DE, V., INGE, W. & MARION, K. (2012) Lack of Evidence for Zoonotic Transmission of Schmallenberg Virus. Emerging Infectious Disease journal 18, 1746
GUBBINS, S., RICHARDSON, J., BAYLIS, M., WILSON, A. J. & ABRAHANTES, J. C. (2014) Modelling the continental-scale spread of Schmallenberg virus in Europe: Approaches and challenges. Prev Vet Med 116, 404-411
MOUCHANTAT, S., WERNIKE, K., LUTZ, W., HOFFMANN, B., ULRICH, R. G., BÖRNER, K., WITTSTATT, U. & BEER, M. (2015) A broad spectrum screening of Schmallenberg virus antibodies in wildlife animals in Germany. Veterinary Research 46, 99.