Schmallenberg Orthobunyavirus (SBV)
This is a fairly recently discovered disease and at this point has no other name
Description
During the summer and autumn of 2011, farmers and veterinarians in Germany (in North Rhine-Westphalia) and the Netherlands reported a previously unidentified disease in dairy cattle and sent samples to animal health authorities and diagnostic laboratories. The affected cows had fever, decreased milk production and diarrhea, but these signs were of short duration and the cattle recovered.
All previously known endemic and emerging viruses with similar signs were excluded as the causative agent. To identify the cause of the apparently new disease, Germany’s leading animal health research institute, the Friedrich Loeffler Institute (FLI), used genomic analysis to test pooled blood samples from affected cattle with acute signs.
This led to detection of genomic sequences related to the genomic sequences of Shamonda, Aino and Akabane virus — viruses of serogroup Simbu in the genus Orthobunyavirus. The newly discovered virus was named Schmallenberg virus (SBV), according to the location in Germany where the samples originated.
Starting in December 2011, sheep farms in the Netherlands reported births of congenitally malformed lambs on a growing number of farms throughout the country. Using the RT-PCR test obtained from the FLI, the Dutch Veterinary Research Institute in Lelystad was able to detect the virus in tissues of malformed lambs and samples from cattle that had suffered from clinical disease, enabling them to conclude that the same virus was involved in both syndromes and species.
This conclusion was supported by a preliminary experimental infection trial in cows, carried out by the FLI in Germany. This trial demonstrated viral propagation with a short-lived viremia (virus present in the bloodstream) on days 2 to 5 post-inoculation. The clinical signs observed included elevated temperature for 1 day and moderate diarrhea.
Malformed lambs, calves and kids were born throughout Germany and Belgium during that December, and later in France, southern United Kingdom, Luxembourg and one case in north Italy. Many of these cases were confirmed as SBV by the RT-PCR test.
The new disease quickly spread to the rest of the continent, with wind playing a role in transmission of the virus; infected midges were found to be vectors, and they are easily carried on air currents.
By mid-March, 2012 the total number of affected PCR-confirmed farms in 8 countries was about 2,500, of which 81% were sheep farms, 16.5% cattle farms and 2.5% goat farms. The actual number of affected cattle farms was assumed to be much higher since malformed calves seem to have tested PCR-negative more than 5 months after infection.
The results of a Dutch study suggested that the prevalence of antibodies against SBV in the dairy cattle population in the Netherlands was about 70%.
The researchers assumed that the virus was spread during summer and autumn by infected gnats/midges (Culicoides). The vector season ended in December, but taking into consideration the fact that closely related viruses, such as Akabane, are known to cause hydranencephaly in cattle, particularly during the third month of pregnancy, such cases may still occur until May, since the average gestation in cattle is 280 days.
The cold winter season did not eradicate the virus; new cases were observed in ruminants in Germany in June 2012. In late 2014, SBV outbreaks in cattle and sheep were again seen in the Netherlands. In 2016, an increase in SBV-specific antibody titers and prevalence in heifers was noted in the Netherlands. Additionally, the detection of SBV genomic sequences in aborted calves in Belgium in 2015 was a further indication of SBV circulation in the area.
Although there were several years of limited to no circulation of the virus in the UK and France, outbreaks occurred again in 2016 and 2017.
The original source of this virus is still unclear but there are reports of SBV cross-reactive antibodies to other Simbu serogroup viruses found in African cattle, prior to and after the initial European outbreak. A report from Jordan in 2013 indicated detection of antibodies against Aino virus, another Simbu serogroup virus, in ruminants on farms where similar clinical symptoms associated with SBV infections were observed.
The virus was found in aborted cattle and sheep fetuses in Turkey, a year after the initial outbreak in Europe. Blood samples collected before 2011 were also found to be positive for SBV antibodies, using ELISA testing, though it’s possible that these tests were detecting cross-reactive antibodies induced by other Simbu serogroup viruses.
There have been multiple reports of fetal malformation in ruminants from the Mediterranean region, suggesting a possible circulation of Simbu serogroup viruses in this region.
SBV infection induces a solid protective immunity that persists for at least 4 or 6 years in sheep and cattle, respectively.
One of the main concerns of public-health authorities was to determine if there was any potential health risk to humans from the emerging virus. The Dutch National Institute for Public Health and the Environment produced a document called “Risk Profile Human Schmallenberg virus,” later endorsed by the European Center for Disease Prevention and Control.
The analysis indicated that other teratogenic (fetal deformity-causing)viruses of the Simbu serogroup, namely Akabane, Aino and Shamonda, which are genetically most related to SBV, are only found in livestock.
Some viruses within the Simbu serogroup (Oropouche virus and Iquitos virus) are known to be zoonotic and cause human outbreaks, however. Genetic re-assortment among members of the same serogroup within the Orthobunyavirus genus occurs in nature and has led to the emergence of new viruses, occasionally with increased pathogenicity. This may increase the zoonotic potential of reasserted viruses.
So far, there are no reports of unusual human illness from the regions in Europe where SBV has been identified, however. The veterinary health services indicate that farmers from affected farms have been specifically asked for symptoms of illness and have reported none.
Signs
Abortion, congenital malformations including contracted limbs and hydrocephalus, transient fever and diarrhea
Cause
Orthobunyavirus is a genus of the Bunyaviridae, which is prevalent in Africa, Asia, Australia and Oceania, but these viruses occur almost worldwide. They are vector-borne; the main transmitters are gnats (various species of Culicoides), but mosquitoes have also been known to spread these infections as well.
There are five serogroups: Bwamba, California, Simbu, Bunyamwera and Wyeomyia. Several members of the Simbu group, primarily the Akabane, Aino and Shamonda virus, and one of the Bunyamwera serogroup, the Cache valley virus, have been known for many decades as teratogenic (causing birth defects) in animals, predominantly cattle, sheep and goats.
In most cases, no clinical disease is observed in the infected animal itself, but if susceptible females are infected while pregnant, the infection may result in abortions, fetal resorption or congenital malformations such as arthrogryposis (deformed joints with contracted and malformed limbs) and hydranencephaly (part of the brain missing, with extra fluid in the brain cavity).
Vertical transmission of SBV from infected dam to fetus occurs during the first and early-second trimester of gestation and results in abortion, stillbirth and birth of malformed newborns. Although experimentally-infected animals shed the virus in feces, oral and nasal fluids, direct transmission of SBV from infected ruminants to naïve animals by contact or oro-nasal/feco-oral routes has not been reported.
Oral inoculation of cattle and nasal inoculation of sheep failed to produce viremia in the animals. Interestingly, SBV was detected in semen from infected bulls, but transmission of SBV from infected bulls to dams either through natural mating or AI has not been extensively studied. In one study, viral RNA was isolated from blood samples of cattle experimentally injected with SBV-RNA-positive semen.
The presence of SBV RNA in amniotic fluid and fetal tissues was suggested as one possibility in which the virus may persist over winter.
Prevention
Control of insect vectors such as gnats and mosquitoes is probably the main strategy but can be difficult.
There are inactivated-virus vaccines available in the UK and France, which can be used in sheep and cattle. Three vaccines are commercially available in Europe.
Vaccination of replacement stock and control of insect populations are the two most important methods for the prevention of SBV outbreaks. Vaccination helps reduce SBV infection in ruminants. Farmers in some countries, however, are unwilling to vaccinate their animals, claiming vector surveillance to be a more effective prevention strategy.
The re-emergence of SBV in Germany and the Netherlands in late 2014, and more recently in Belgium, France and the UK, however, is an indication that SBV is able to infect and spread in cattle and sheep flocks in the face of declining immunity.
Treatment
There is no specific treatment.