CASE NOTES
SCHMALLENBERG VIRUS—WHAT IS ALL OF THE FUSS ABOUT?
PD Kirkland, Virology Laboratory, EMAI, Camden NSW
Posted Flock & Herd April 2013
Introduction
Animal health authorities were astounded by the incursion of bluetongue viruses into Western Europe. However, few expected another vector borne virus to emerge so quickly and close to the focus of emergence of BTV-8. While there was initially a high level of concern as the newly discovered virus was characterised, attitudes and responses quickly changed. The global economic situation was clearly a contributing factor but the disease also played a part. The commentary that follows provides a current perspective on the biology and impact of Schmallenberg virus (SBV) in Europe, comparisons with the Simbu viruses in Australia and global reactions.
THE VIRUS AND ITS ORIGINS
In August 2011 a transient mild febrile illness, sometimes with diarrhoea and usually a drop in milk production, was observed in a small proportion of cattle in herds in the region close to where BTV serotype 8 (BTV-8) was first detected in The Netherlands and Germany. Application of modern molecular "bug hunting" techniques soon led to the identification and isolation of SBV. Since that time, this virus has been characterised as a novel virus belonging to the Simbu serogroup of orthobunyaviruses - the same group that contains a number of Australian Culicoides borne arboviruses - including Aino, Akabane, Douglas, Peaton and Tinaroo. Despite full sequencing of the SBV genome, its origins remain obscure but it is clearly a previously unrecognised virus.
EPIDEMIOLOGY
During serological surveys to assess the spread of SBV, there was concern about the high prevalence of antibodies being detected. An incidence of >90% was detected in many Dutch and German herds. Because of this high prevalence, the possibility of lateral transmission was proposed. Experimental studies have excluded this possibility. However, similar levels are frequently encountered with Akabane virus - and the lack of disease in Australia is a direct outcome of this high level of herd immunity. Subsequent research identified that up to 30% of Culicoides (the same species as were spreading BTV-8) were infected with the virus. Compared to BTV it was also known that only small midge populations were needed because of the high infection rates and efficient transmission. The capacity of midges belonging to the C. obsoletus/pulicaris and C. dewulfi groups to withstand cold conditions is considered to have been the main reason for SBV to overwinter - with widespread transmission early in the northern Spring of 2012 and also for clear evidence of transmission even during late winter in some locations. Consequently, since its initial recognition, in less than 2 years SBV has spread throughout much of Europe- west into Poland, southwards into Switzerland and northern Italy, west into England and north into the Scandinavian countries.
OCCURRENCE OF DISEASE
The very mild acute disease first observed in adult cattle has been a characteristic of the entry of SBV into a naive population. In Switzerland, when the virus first appeared, >90% of adult cattle presenting with a sudden onset of diarrhoea and milk drop were shown to be infected with SBV by real time PCR. These signs have not previously been reported with a Simbu virus but there are few instances of one of these viruses entering a large naive population. A similar situation would arise when Akabane extends south and west beyond its normal range but it is considered unlikely that much attention would be given to these mild transient signs under Australian conditions, if indeed they were detected. Identification of SBV as a Simbu virus generated considerable concern for the possibility of an outbreak of congenital defects in both cattle and the many small ruminants in the affected areas.
Defects of the predicted range were subsequently observed at the expected times - firstly with cases of concurrent arthrogryposis (AG) and hydranencephaly (HE) in sheep and goats, and then progressively, in cattle cases of AG followed later by calves affected with HE. However, this is really the only similarity between Akabane and SBV - the pathology and pathogenesis of foetal infections are almost identical but the virulence/pathogenicity is substantially different. While up to 30% of lambs have been affected in some flocks where early, synchronised breeding was practised, across the affected populations, where about 5,000 farms have reported cases, the incidence of defects in lambs whose dams have been infected is <2% and in cattle 0.5-1%. In contrast, average rates of abnormalities in cattle with Akabane are about 25-30% and in some instances, as high as 50%.
COMPARISON WITH AUSTRALIAN SIMBU VIRUSES
While SBV has been classified as a Simbu virus, it is most closely related to Douglas virus. In Australia, this virus has not been associated with any disease, despite being regularly transmitted in NSW. Transmission of Douglas virus is detected in sentinel herds in NSW as frequently as Akabane. Testing at EMAI of sera from cattle and sheep infected with SBV has shown extensive cross reactivity with Douglas virus and to a lesser extent with some of the other Simbu viruses. Similarly, Douglas virus RNA is detected in a qRT-PCR for SBV. Consequently, the levels of cross reactivity by serology and PCR would make it difficult to distinguish between SBV and Douglas virus. However, once virus isolates are sequenced and compared, these viruses are clearly different and not directly related.
GLOBAL RESPONSES
Following the discovery and identification of SBV, many countries banned importation of all animals and reproductive material from Europe. Australia placed restrictions on the importation of semen for collections made during the period when SBV may have been transmitted but unrecognised. Subsequently, there are requirements for collection of semen that aim to exclude importation from animals that have been infected around the time of semen collection.
DIAGNOSTIC CAPABILITIES AND VACCINES
Both EMAI and AAHL have a capacity to detect SBV by qRT-PCR and by specific VNT serology. The development of a commercial inactivated vaccine for SBV is advanced but the viability of this product is uncertain. Unlike this situation with bluetongue, Government sponsored vaccination for SBV has been discounted. Although SBV and Akabane are related, it is unlikely that a vaccine for SBV would provide protection against Akabane virus.
LATEST DEVELOPMENTS
In late December 2012, the detection of SBV in bovine semen by qRT-PCR was reported in a small number of bulls. It is not yet known whether this represents the presence of infectious virus. If this virus is shown to be infectious by virus isolation in cell culture or by calf inoculation, to assess the significance, in turn it will be necessary to determine whether cows become infected after insemination with SBV infected semen.