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Starting in 2006, bluetongue virus serotype 8 (BTV8) was responsible for a major epizootic in Western and Northern Europe. The magnitude and spread of the disease were surprisingly high and the control of BTV improved significantly with the marketing of BTV8 inactivated vaccines in 2008. During late summer of 2011, a first cluster of reduced milk yield, fever, and diarrhoea was reported in the Netherlands. Congenital malformations appeared in March 2012 and Schmallenberg virus (SBV) was identified, becoming one of the very few orthobunyaviruses distributed in Europe. At the start of both epizootics, little was known about the pathogenesis and epidemiology of these viruses in the European context and most assumptions were extrapolated based on other related viruses and/or other regions of the World. Standardized and repeatable models potentially mimicking clinical signs observed in the field are required to study the pathogenesis of these infections, and to clarify their ability to cross the placental barrier. This review presents some of the latest experimental designs for infectious disease challenges with BTV or SBV. Infectious doses, routes of infection, inoculum preparation, and origin are discussed. Particular emphasis is given to the placental crossing associated with these two viruses.

Schmallenberg virus was detected in cattle and sheep in northwestern Europe in 2011. To determine whether wild ruminants are also susceptible, we measured antibody seroprevalence in cervids (roe deer and red deer) in Belgium in 2010 and 2011. Findings indicated rapid spread among these deer since virus emergence ≈250 km away.

To determine prevalence of antibodies against Schmallenberg virus in adult cows and proportion of infection transmitted to fetuses, we tested serum samples from 519 cow/calf pairs in Belgium in spring 2012. Of cattle within 250 km of location where the virus emerged, ≈91% tested positive for IgG targeting nucleoprotein. Risk for fetal infection was ≈28%.

Ireland lost its official freedom from Schmallenberg virus (SBV) in October 2012. The route of introduction is uncertain, with long-distance displacement of infected Culicoides, biting midges, by suitable wind flows considered to be the most likely source. The authors investigated the potential introduction of SBV into Ireland through a Culicoides incursion event in the summer of 2012. They conducted SBV serology on archived bovine sera to identify the prospective dispersal window, then used atmospheric dispersion modelling during periods around this window to identify environmental conditions the authors considered suitable for atmospheric dispersal of Culicoides from potential infected source locations across Southern England. The authors believe that there was one plausible window over the summer of 2012, on August 10-11, based on suitable meteorological conditions. They conclude that a potential long-range transportation event of Culicoides appears to have occurred successfully only once during the 2012 vector competent season. If these incursion events remain at a low frequency, meteorological modelling has the potential to contribute cost-effectively to the alert and response systems for vectorborne diseases in the future.

Objective The present study aimed to estimate and compare the economic impact of Schmallenberg virus (SBV) in different sheep production holdings using partial budget and gross margin analyses in combination with production models. Participants The sheep production types considered were lowland spring lambing, upland spring lambing and early lambing flocks in the UK, and grass lamb flocks of the Centre and West of France, extensive lambing flocks and dairy sheep flocks in France. Methodology Two disease scenarios with distinct input parameters associated with reproductive problems were considered: low and high impact. Sensitivity analyses were performed for the most uncertain input parameters, and the models were run with all of the lowest and highest values to estimate the range of disease impact. Results The estimated net SBV disease cost per year and ewe for the UK was £19.65–£20.85 for the high impact scenario and £6.40–£6.58 for the low impact scenario. No major differences were observed between the different production types. For France, the net SBV disease cost per year and ewe for the meat sheep holdings was £15.59–£17.20 for the high impact scenario and £4.75–£5.26 for the low impact scenario. For the dairy sheep, the costs per year and ewe were £29.81 for the high impact scenario and £10.34 for the low impact scenario. Conclusions The models represent a useful decision support tool for farmers and veterinarians who are facing decisions regarding disease control measures. They allow estimating disease impact on a farm accounting for differing production practices, which creates the necessary basis for cost effectiveness analysis of intervention strategies, such as vaccination.

To the Editor: From the end of August through the end of October 2011, a clinical syndrome involving adult cattle and the fetuses of pregnant cows emerged in the border area between the Netherlands and North Rhine-Westphalia, Germany (1). The syndrome was characterized by nonspecific clinical signs (fever, decreased milk production), severe diarrhea, and some abortions. A metagenomic analysis was conducted on pooled samples from cattle with acute signs on a farm in the city of Schmallenberg, Germany. The analysis detected nucleotide sequences homologous to arthropod-borne Akabane, Aino, and Shamonda viruses, all belonging to the family Bunyaviridae, genus Orthobunyavirus, and Simbu serogroup (1). Real-time PCR detected the genomic RNA of the new and emerging virus, tentatively designated Schmallenberg virus (SBV), in the blood of adult cattle, abdominal fluid of a stillborn calf, and brains of lambs born with birth defects on dozens of farms in the Netherlands, Germany, and Belgium. No data are yet available to predict how the emerging virus might affect the cattle industry. We report the case of a 1-week old calf with severe central nervous system (CNS) lesions probably caused by in utero infection with the new virus. In Belgium in January 2012, a Belgian Blue multiparous cow gave birth to a 45-kg female calf that was morphologically normal but hypertonic and hyperreflexic. Pregnancy had proceeded uneventfully and lasted 9 months and 4 days. Spontaneous reflexes such as sucking, swallowing, micturition, defecation, and crying were completely preserved, but the calf was unable to stand, and its consciousness alternated from mild to severe depression. It was obviously blind and showed ventrolateral strabismus, but the pupils functioned normally. Muscle tone was permanently increased, as indicated by tetanus-like erection of the ears and by a violent but brief startle response to the slightest acoustic or tactile stimulation (Figure). When the calf was placed upright, loss of conscious proprioception was obvious; it maintained its position only a few seconds before collapsing. Altogether, the clinical signs suggested severe dysfunctions of the cerebral cortex, basal ganglia, and mesencephalon. The calf drank from a bottle twice a day for a week, but then was euthanized for humane reasons (infected decubital ulcers). Figure A 7-day old, female, Schmallenberg virus–positive calf showing severe central nervous system dysfunctions (A–C) and lesions (D–E). A) Spontaneously lying down; B–C) standing with assistance; D–G) porcencephaly, ... At necropsy, the cerebellum, brainstem, and diencephalon appeared normal in shape and volume (Figure). However, the cerebral hemispheres were replaced by 2 thin-walled, fluid-filled cysts with some floating islets and peninsulae corresponding to preserved cortex. There was variable preservation of the cerebrum, total liquefaction of occipital lobes, and irregular preservation of the outer layers of some parts of the temporal and frontal lobes. Altogether, the picture was compatible with severe porencephaly or hydranencephaly. The spine showed no sign of scoliosis, and movement of the limb joints was not restricted (i.e., no arthrogryposis). Samples were removed from the remnants of the cerebrum, diencephalon, and organs (thymus, lung, myocardium, jejunum, ileum, mesenteric lymph node, liver, spleen, kidney, and striated muscle), and 3 independent real-time PCR protocols were conducted to detect genomes of bovine viral diarrhea/mucosal disease virus, bluetongue virus serotype 8, and the novel SBV. Initial retrotranscription of the RNA genomes was followed by quantitative (real-time) PCR. The process was conducted by using our procedures (2) and, for SBV, by following the protocol and using recently developed control reagents as described (1). The SBV genome was detected in only CNS samples (quantification cycle value 28.8); bovine viral diarrhea/mucosal disease virus and BTV-8 genomes were not detected. The new virus genome load was 1.61 × 104 copies per gram of cerebrum sample. Taken together, the above data suggest that, like other Simbu serogroup viruses, the new virus crosses the placenta, contaminates the bovine fetus, infects the fetus’ CNS, and causes necrosis and/or developmental arrest of the cerebral cortex. Unlike the viruses mentioned above (3,4), and provided this case is not an exception, the SBV genome seems to persist in the infected fetus and is detectable after birth by real-time reverse transcription PCR, despite gestation length. Although reliable reagents for detecting seroconversion are temporarily unavailable, the persistence of the new virus in fetal tissue should greatly facilitate the epidemiologic monitoring of the emergence and spread of the new virus. When calves from experimentally infected dams are infected with the closest phylogenetic relative to SBV, Akabane virus, porencephaly develops during gestational days 62–96 (5). If the same is true for the new virus, the above calf was probably infected during June 9–July 13, 2011. Therefore, it is hypothesized that infected arthropods were already circulating in the village of Hamois-in-Condroz (50°24′56′′N, 5°8′7′′E), which is ≈240 km southwest of Schmallenberg (51°8′42′′N, 8°17′18′′E), ≈2 months before the emergence of the clinical syndrome that led to the identification of the new virus.