Epizootic spread of Schmallenberg virus among wild cervids, Belgium, Fall 2011.

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.

Schmallenberg virus in domestic cattle, Belgium, 2012.

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%.

Schmallenberg virus: a new Shamonda/Sathuperi-like virus on the rise in Europe.

In the summer-fall of 2011, a nonspecific febrile syndrome characterized by hyperthermia, drop in milk production and watery diarrhea was reported in adult dairy cows from a series of farms located in North-West Europe. Further, in November 2011, an enzootic outbreak of abortion, stillbirth and birth at term of lambs, kids and calves with neurologic signs and/or head, spine or limb malformations emerged throughout several European countries. Both syndromes were associated with the presence in the blood (adults) or in the central nervous system (newborns) of the genome of a new Shamonda-Sathuperi reassortant orthobunyavirus provisionally named Schmallenberg virus after the place where the first positive samples were collected. The clinical, pathological, virological and epidemiological facts that were made publicly available during the first 6 months after the emergence are presented here. Current knowledge of the epidemiology of the phylogenetically closest relatives of the newcomer (Shamonda, Sathuperi, Aino and Akabane viruses) is not exhaustive enough to predict whether the current outbreak of Schmallenberg virus is the prelude to endemicity or to a 2 years long outbreak before the infection burns out when serologically naïve animals are no longer available. In the future, cyclic epizootic reemergences are a possibility too, either synchronized with a global decrease of herd immunity or due to antigenic variants escaping the immunity acquired against their predecessors. The latter hypothesis seems unlikely because of the wide array of biologic constraints acting on the genome of viruses whose life cycle requires transmission by a vector, which represses genetic drift. The remarkable stability of the Shamonda virus genome over the last forty years is reassuring in this regard.