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Description & Distribution

The Schmallenberg virus is a newly described virus affecting cattle, sheep and goats. It was first found infecting cattle in Germany in summer 2011. It was then recorded in the Netherlands affecting sheep. At the time of infection cattle suffer a mild clinical disease. Sheep may show no symptoms or may suffer diarrhoea.

In both countries, symptoms disappeared after a few days and the animals appeared to recover unaffected. However, in early December, a high number of congenital malformations occurred in newborn lambs and many were stillborn. Similar malformations have been reported in cattle. The Schmallenberg virus has since been reported in many other European countries (see below).

Sheep with lambs in East Sussex, UK
(Photo: InfluentialPoints)

Schmallenberg virus (SBV) was identified in Germany using metagenomic analysis. Virions were subsequently isolated from blood of affected animals. SBV is a previously unknown orthobunyavirus, most closely related to Akabane, Ainoa and Shamonda viruses (Hoffmann et al., 2012). These viruses are all in the Simbu-Serogroup, a subgroup not previously detected in Europe. They are known to cause developmental malformations of brain and articulations, in particular in ruminants. The Akabane, Ainoa and Shamonda viruses only infect cattle in Asia and Australia. It is unclear whether Schmallenberg virus has been newly introduced or whether it has been present undetected in ruminants in Europe for some time. Researchers have recently proposed that SBV is either a reassortant virus within the Simba serogroup viruses (Yanase et al., 2012) or that it should be reclassified as Sathuperi virus and is a possible ancestor of the reassortant Shamonda virus (Goller et al., 2012).

Because of the close relationship to Shamonda virus, and the absence of reports of clinical signs in humans, the risk to humans is currently considered low to negligible (European Center for Disease Prevention and Control, 2011). Nevertheless some members of the Simbu serogroup such as Oropouche virus are zoonotic, so clinical and serologic surveillance for Schmallenberg virus in humans is being conducted in regions with infected animals to update the risk assessments.

The map below (courtesy shows the distribution of cases at the end of January 2012, when the epidemic spread beyond mainland Europe. The white ring indicates Schmallenberg, where the first cases were found less than 6 months previously.

In February 2012 the true scale of the Schmallenberg epidemic was becoming clearer, with birth defects being reported throughout Germany, Belgium and the Netherlands and increasing numbers in France and England (see below). By 13 February 2012 in the UK it has been formally identified in 55 farms in Norfolk, Suffolk, Essex, Kent, Hertfordshire, East Sussex, West Sussex and most recently Surrey, Wiltshire and Cornwall. The West Sussex record was the first UK cattle infection. Early data from the UK, among breeding sheep, gave an apparent morbidity rate (% of animals sick) of 6.2% (OIE, 2012), but morbidity rate has since been shown to vary widely between farms.

Geographic distribution of Schmallenberg virus reports, Feb 2012 (courtesy of

By late March most of Western Europe was affected with cases in Luxembourg, Spain and Italy, and many cases in France and England.

Geographic distribution of Schmallenberg virus reports, Mar 2012 (courtesy of

During April the number of cases in sheep leveled off and there was little obvious change in distribution of the outbreaks. However, the number of cases in cattle increased, this lag reflecting the longer gestation period of cows compared to sheep.

Geographic distribution of Schmallenberg virus reports, Apr 2012 (courtesy of

It was recognized that there was little chance of the epidemic 'dying out' naturally and further spread of the epidemic was therefore expected in 2012-2013 (Driver, 2012). The virus may overwinter in the midge population or be present in lambs and calves in spring. There was also evidence that in the affected areas in 2011 many more animals were infected than had shown symptoms (van der Hoek, 2012). In those areas populations should have a good level of natural immunity, but many cases can be expected around the periphery of this area.

In 2012 midges were present from May to November with a peak in June and were again able to transmit the disease. By November 2012 the number of cases had started to increase again as sheep exposed to midges in the summer started to give birth.

Geographic distribution of Schmallenberg virus reports, Nov 2012 (courtesy of

In UK the Animal Health and Veterinary Laboratories Agency introduced enhanced surveillance in early to mid-2012 specifically to monitor the spread of the disease into previously unaffected counties. But by December cases or seropositives had already been reported in nearly all the counties of England and Wales with 976 holdings affected, (AHVLA, 2012). Since the disease could no longer spread any more in England and Wales, the enhanced surveillance was abandoned.


Clinical signs & Diagnosis

In dairy cows the initial clinical disease is characterized by increased body temperatures (>40C), impaired general condition, anorexia, and reduced milk yield by up to 50%. These symptoms are short-lived disappearing after several days. There may be no obvious clinical symptoms in sheep at the time of infection, or they may suffer diarrhoea. Foetal infections in both cattle and sheep result in stillbirths and severe congenital deformations such as twisted neck, abnormal curvature of the spine, and limb contractures (Health Protection Agency, 2012). The picture below shows one such congenital deformation in a lamb.

Lamb affected by arthrogyroposis (persistent flexion of the joints)
(Photo: courtesy of DEFRA under the Open Government Licence)

The Friedrich-Loeffler-Institut has developed a detection method that has been made available to institutions in Belgium, France, England, the Netherlands, Italy and in Switzerland (Kupferschmidt, 2012). Disease is currently confirmed on the basis of a polymerase-chain reaction (PCR) test for viral RNA. Adiavet has produced a commercial PCR detection kit. Serological tests for Schmallenberg virus are currently being developed in several countries. Once available, they will provide information about current and past infection as well as exposure in humans.



The related Akabane, Ainoa and Shamonda viruses are mainly transmitted by insect vectors, mostly midges (Culicoides), but possibly also by other insects such as mosquitoes. On this basis it seemed likely that Schmallenberg virus would be transmitted by Culicoides midges or possibly mosquitoes.

This is Culicoides sonorensis, a known vector of Oropouche virus
(Photo: courtesy of Scott Bauer, U.S. Agricultural Research Service)

The Schmallenberg virus (SBV) has now been identified in two species of midges - Culicoides obsoletus and Culicoides dewulfi (van den Bergh et al., 2012) and according to some reports Culicoides pulicaris. All of these are found, often together, throughout North Europe, including the UK. Researchers in Belgium took pools of midges collected in September and October 2011 by light trap. Only the heads of the midges were tested thus avoiding testing the blood meal. Reverse transcription polymerase chain reaction (RT-PCR) tests suggested Schmallenberg virus was present in the salivary glands, indicative of active vector transmission, although actual transmission has yet to be demonstrated. Rasmussen (2012) also demonstrated the presence of SBV RNA in C. obsoletus group midges caught in Denmark during October 2011. Note Culicoides obsoletus is the primary vector of bluetongue virus in northern Europe.

Further evidence that Culicoides midges are responsible for much of the transmission is given by some predictive modeling carried out in UK (DEFRA, 2012). The figure below shows the probability of midge 'plumes' (estimated on the same basis as plumes of e.g. volcanic dust) carrying potentially infected midges from Europe to the UK in autumn 2011.

Plumes for 13 November 2011, and comparative risk of vector incursion into the UK from July to November 2011.
Plumes suitable for vector incursion occurred on less than 20% of days during this period.
(Figure: courtesy of DEFRA, 2012 under the Open Government Licence)

The initial occurrence of the virus in lambs born in eastern England in January 2012 was consistent with the hypothesis that it was transmitted by Culicoides midges blown there from affected areas in northern mainland Europe the previous autumn. It is now clear that the high risk areas extended further east into France, and even into Spain. This put the southwest of the UK at risk, and indeed cases have since occurred throughout the south west.

Despite numerous press rumors, we can find no credible evidence that livestock movement has contributed to the spread of this disease.


Prevention, Control and Origins

At present there is no treatment is available for Schmallenberg virus, and currently no vaccination. Culling of infected livestock has not been attempted, and would anyway be futile. One possible option is to control the vector Culicoides by direct application of a pour-on formulation of a synthetic pyrethroid insecticide to the animal, possibly supplemented with treatment of animal housing and reduction of local breeding sites (Carpenter et al., 2008). The cost of such vector control is offset if it also reduces other Culicoides-transmitted diseases, for instance bluetongue (another invasive virus disease of sheep, cattle and deer). Bluetongue is currently mainly controlled by vaccination, but the presence of multiple vector-borne diseases increase the case for vector control. However, it must be said that where the challenge is high, control of midges with pour-on has been dramatically unsuccessful with no noticeable reduction in the density of biting midges (Bauer et al., 2009). In UK the Animal Health and Veterinary Laboratories Agency has noted that control of midges is unlikely to be effective given that they are very widespread, and appear to be very effective at spreading the virus. (AHVLA, 2013) Hence transmission may still occur even when challenge levels are very low.

Fortunately the prospects for developing a vaccine in the near future do appear to be very good. Merck Animal Health (also known as MSD) have announced that they have produced a vaccine based on inactivated wild-type Schmallenberg virus, which should soon be available for use. Ironically the main question about vaccine deployment is how widely the vaccine will used, and hence whether the cost of vaccine development will be recouped. Exposure to the virus in affected areas seems to be close to 100% (see for example Méroc (2012) in Belgium), and widespread natural immunity may make vaccination uneconomic.

The sudden appearance of a 'new' disease like Schmallenberg inevitably prompts rather wild discussion of why such diseases have arisen. A good example can be obtained by looking at the discussion following an article by Carrington (2012) in the Guardian which suggested that the emergence of the Schmallenberg virus was the direct result of global warming. Whilst many distributional changes of diseases and vectors are occurring because of warming in the northern hemisphere, there is no evidence that global warming was the primary cause of the emergence of Schmallenberg virus.

Instead it could easily have resulted from something that people seem just as reluctant to believe in as global warming - namely evolution. Pathogens evolve in response to a host of changing factors such as greatly increased host mobility, rapidly changing farming practices, climate change, drug use and so on. Any one of these factors, or a combination of them, may have led to emergence of a new virus strain. After all we did not invoke global warming to explain the sudden appearance of the AIDS virus, nor the 1918 influenza serotype! It is, however, a reminder of just how rapidly a new disease can spread!


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Last Updated 3 January 2013