Lack of Evidence for Zoonotic Transmission of Schmallenberg Virus

Chantal Reusken¹

, Cees van den Wijngaard¹, Paul van Beek, Martin Beer, Ruth Bouwstra, Gert-Jan Godeke, Leslie Isken, Hans van den Kerkhof, Wilfrid van Pelt, Wim van der Poel, Johan Reimerink, Peter Schielen, Jonas Schmidt-Chanasit, Piet Vellema, Ankje de Vries, Inge Wouters, and Marion Koopmans

Author affiliations: National Institute for Public Health and the Environment, Bilthoven, the Netherlands (C. Reusken, C. van den Wijngaard, P. van Beek, G.-J. Godeke, L. Isken, H. van den Kerkhof, W. van Pelt, J. Reimerink, P. Schielen, A. de Vries, M. Koopmans); Friedrich-Loeffler-Institut, Insel Riems, Germany (M. Beer); Central Veterinary Institute of Wageningen University and Research Centre, Lelystad, the Netherlands (R. Bouwstra, W. van der Poel); Bernhard Nocht Institute for Tropical Medicine, Hamburg (J. Schmidt-Chanasit); Animal Health Service, Deventer, the Netherlands (P. Vellema); and Institute for Risk Assessment Sciences, Utrecht, the Netherlands (I. Wouters)

Abstract

The emergence of Schmallenberg virus (SBV), a novel orthobunyavirus, in ruminants in Europe triggered a joint veterinary and public health response to address the possible consequences to human health. Use of a risk profiling algorithm enabled the conclusion that the risk for zoonotic transmission of SBV could not be excluded completely. Self-reported health problems were monitored, and a serologic study was initiated among persons living and/or working on SBV-affected farms. In the study set-up, we addressed the vector and direct transmission routes for putative zoonotic transfer. In total, 69 sheep farms, 4 goat farms, and 50 cattle farms were included. No evidence for SBV-neutralizing antibodies was found in serum of 301 participants. The lack of evidence for zoonotic transmission from either syndromic illness monitoring or serologic testing of presumably highly exposed persons suggests that the public health risk for SBV, given the current situation, is absent or extremely low.

In November 2011, scientists in Germany identified novel viral sequences in serum from cattle affected by a febrile syndrome that was reported during August–September 2011 in Germany and the Netherlands. Clinical signs included decreased milk production and diarrhea. The virus, named Schmallenberg virus (SBV), was isolated from blood of affected cattle, and similar clinical manifestations were observed in experimentally infected calves (1). In the Netherlands, SBV was detected retrospectively in serum from affected cattle in December 2011 (2).
Since the end of November 2011, an unusually high number of ovine and bovine congenital malformations were reported in the Netherlands. The main macroscopic findings included arthrogryposis; torticollis; scoliosis; brachygnathia inferior; hydranencephaly; and hypoplasia of cerebrum, cerebellum, and spinal cord. SBV genome was detected in the brain of malformed lambs and calves (3–5). These findings, together with detection of SBV RNA in multiple types of samples, e.g., amniotic fluid, meconium, and placenta remains from diseased lambs and calves, strongly pointed to SBV as the causative agent of the clinical manifestations (6). The teratogenic effects in ruminants are hypothesized to reflect virus circulation in late summer/early autumn 2011, leading to intrauterine infection with SBV during a specific period of gestation (4).
In June 2012, seven additional European countries (Belgium, Denmark, France, Italy, Luxemburg, Spain, and the United Kingdom) confirmed SBV in ruminants, accumulating to a total of 3,745 PCR-confirmed infected animal holdings (4,7). In the Netherlands 1,670 holdings were suspected to be affected by SBV on the basis of births of animals with malformations typical of SBV infection, of which 350 were confirmed by PCR as of June 12, 2012. The holdings with confirmed SBV comprise 237 cattle, 107 sheep, and 6 goat farms (8).
SBV has been identified as most related to Sathuperi virus, and for the small and large segments, Shamonda virus segments show the highest sequence identity. All those viruses are members of the Simbu serogroup, family Bunyaviridae, genus Orthobunyavirus, and known as arthropod-borne viruses that can cause illness in ruminants (9). The orthobunyaviruses comprise ≈170 virus isolates, assigned to 48 distinct species, arranged in 18 serogroups, including the Simbu serogroup. Serogroups within the genus are based on cross–hemagglutination-inhibition and antibody neutralization relationships. Phylogenetic relationships are consistent with the results of serologic relationships (10–12).
Because the family Bunyaviridae contains several medically relevant zoonotic viruses, of which Crimean-Congo hemorrhagic fever virus, Rift Valley fever virus, Sin Nombre virus, and sandfly fever Naples virus are examples, the emergence of SBV triggered a joint veterinary and public health response in the Netherlands to address the possible consequences to human health. We present the public health risk ascertainment of the emergence of SBV in ruminants in the Netherlands and most likely other European countries were SBV has emerged.