Viewpoint: Farm virus spreads to deer
Evidence of extensive Schmallenberg virus (SBV) infection of wild deer populations has far-reaching significance - not least for the future control of this devastating pathogen.
SBV emerged in northern Europe in the summer of 2011.
It was first observed in cattle, where its arrival was heralded by a series of relatively innocuous symptoms that included reduced milk production and diarrhoea.
But the ensuing lambing and calving season revealed a more sinister side to this virus.
Infection of pregnant sheep or cows resulted in miscarriage or in still-born or seriously deformed offspring.
Schmallenberg continued its march across northern Europe with UK cases reported in the early part of 2012.
Genetic studies showed it was a member of the bunyavirus family, which includes Akabane virus - already known to wreak similar havoc in sheep and cattle.Learning from the past
So can the natural history of this related virus tell us anything - is Akabane a suitable soothsayer to predict the future impact of SBV?
Yes… and no.
Akabane is mainly found in tropical and sub-tropical countries in Africa, the Middle East, south-east Asia and in Australia.
It is transmitted by the same type of insect that spreads SBV - biting midges or Culicoides.
Akabane infects a wide-range of animals and the consequences of infection are pre-determined by underlying levels of virus infection.
It is perhaps counter-intuitive, but animals living in regions with a long-standing history of frequent Akabane infection - so called endemic regions - are protected from its worst ravages. And the reason is simple.
Being exposed to high levels of virus ensures that the animal becomes infected in early life.
This early infection is harmless and gives rise to long-lasting protection - or immunity - and infection in later life, during pregnancy for example, does not occur.
So will SBV become endemic in Europe? Should farmers simply batten down the hatches until the viral tempest has passed?
To determine levels of virus infection you can look directly for the virus or for the tell-tale markers of past exposure - virus-specific antibodies. It is these antibodies that also protect against subsequent infection.
One study of SBV in Belgium cattle herds showed that following the initial wave of SBV in 2011 the number of animals that harboured virus antibodies was high - an indication that the virus was becoming endemic.
So, if SBV is charting an endemic course, should we simply sit back and let the inevitable happen or should we intervene?
To answer this we need to ruminate on the issues that will shape the long-term outcome.Inclement times
Climate undoubtedly exerts influence; perhaps more so in the temperate northern European home of SBV than in the sub-tropical and tropical ranges where Akabane prevails.
High levels of transmission are needed to ensure early-life exposure and to protect against the more adverse consequences of adult infection.
Transmission rates are intricately linked to the virus-laden midge populations - and these are sensitive to climate change.
Adverse weather can reduce midge numbers and leave significant numbers of young animals uninfected, making them vulnerable to infection during pregnancy.
Conversely, midge-friendly weather patterns can temporarily expand their range, enabling them to carry their deadly cargo to herds that had previously been safe from SBV. This could pose a particular threat to farms in southern Europe for example.
Research published in the International Journal of Health Geographics suggests that the initial spread of SBV in the summer of 2011 was facilitated by drought conditions in the northwest of Europe.
So, small fluctuations in European climates may wreak massive changes in the occurrence of SBV disease.Modern ways
And farming methods also come into play.
In Akabane-endemic countries livestock farming is generally less intensive and livestock breeding and midge seasons more diverse; meaning animals are more likely to become infected before they reach breeding age.
In SBV-affected areas mating periods are more rigid and overlap with the midge biting season. For new breeding stock, their first exposure to the virus will often coincide with pregnancy.
If reliance on natural infection to provide early protection from SBV is difficult does veterinary intervention have a role?
Preventing SBV infection through vaccination is feasible.
A vaccine containing killed virus is under development and a similar vaccine is already used to protect against Akabane infection.
Whether or not vaccination is cost-effective or really necessary is a key question that the farming fraternity will have to grapple with.
Ultimately the price of vaccination has to be weighed against the costs associated with SBV. In areas where infection is rife and underlying protection high, sporadic lamb and calf losses might be a preferable, if somewhat unpalatable, price to pay.
It is also too early to gauge whether a vaccine, or indeed natural protection, will be successful in the long-term.
A study published in the Journal of General Virology showed that viruses recovered from SBV outbreaks showed extensive amounts of genetic mutation.
Crucially these mutations occurred in the genes that code for the virus proteins targeted by protective antibodies.
It is unclear what significance, if any, these new findings have, but escape from antibody protection would mean a mutated virus would be free to infect once more.Too big a reservoir
Eradicating infectious disease is always preferable to management and control. So could elimination of infected livestock or mass vaccination programmes bear fruit?
The simple answer is no.
SBV infection of wild deer populations has already been described - and this may be the merest tip of the iceberg.
Akabane virus can infect and replicate in the midges that carries it and preliminary studies suggest that SBV can do the same. Wholesale elimination of midges would be impossible.
Some UK farmers are reporting major livestock losses.
It is too early to determine if the birth of animals with abnormalities will gather pace or if the insidious grip of SBV has diminished.
But one thing is for sure: Schmallenberg virus is here to stay.