The Society for General Microbiology has released a nice, easy-to-read briefing on Schmallenberg virus which can be found here (pdf). Plus they have also made available the Schmallenberg lecture I mentioned in this post
Watching the research that surrounds the emergence of a novel virus is fascinating. I’m always amazed at how quickly scientists basically dissect the disease and the organism to find out what is going on.
Today’s post is going to look at Schmallenberg virus – a novel virus affecting livestock that was first identified only in November 2011.
The story actually begins before November 2011. It’s thought that the virus first started affecting livestock in Europe in summer 2011: cattle in Germany and the Netherlands started to show a few non-specific signs of disease (fever, diarrhoea, a drop in milk production). The animals generally got better again after a few days and herds were generally only affected for a few weeks. Samples were collected and tests were run to find out what was going on but the tests ruled out known viruses and it remained a mystery…
… until November. It was then that the virus was isolated by scientists who named it after the town, Schmallenberg, that the first positive sample came from. (I’m not sure how happy residents of Schmallenberg will be to have a virus named after their town!)
Since its first identification scientists have learnt a lot: SBV is very closely related to a subgroup of viruses in the Orthobunyavirus group. Other viruses in this subgroup are commonly transmitted from mammal to mammal by insects like midges and mosquitoes so it has been suggested that SBV may also be transmitted this way. This would fit in with the fact that the initial cases were seen in August and September – prime insect months.
The reason we (at least in the UK) started to hear of new cases at the beginning of 2012 is probably not because animals are still getting infected (in winter there are usually no midges or mosquitos around). We are seeing the long term consequences of animals infected by the virus when they were in their early pregnancy. Farmers are seeing an increase in the numbers of miscarriages and stillbirths of deformed young, especially in sheep, although cattle and goats have also been affected by the virus.
Since scientists first isolated SBV it has been grown in the lab and a very small number of cattle have been experimentally infected with it, resulting in a similar picture of non-specific symptoms as was seen in cattle in the summer of 2011. There is still a lot of work to be done in this area – we don’t yet know if animals can pass the virus directly to each other and we don’t know what is going to happen in 2012. Exposed animals may prove to have some immunity but what about those animals who were unexposed but are close to exposed ones?
SBV is currently not thought to be zoonotic: the European Centre for Disease Prevention and control states that it is “unlikely that this virus will cause disease in humans, but it cannot be excluded at this stage“. It actually must be quite hard to prove that a virus doesn’t cause disease in humans. You can do cell culture work and see if the virus affects particular cell lines, but barring injecting a large number of people with the virus, you basically have to say well x number of people have been exposed and no one has caught any disease (and you would have greater confidence the larger x is). (Well that’s how I understand it anyway – please correct me below if I am wrong.)
Countries across Europe are trying to get a handle on the disease and plan for the months when midges and mosquitoes will be around in 2012. In the UK, as of 30th March 2012 it had been detected 235 farms, mostly sheep farms. However the number of cattle herds affected may increase as those cattle infected in their pregnancy in late summer are now starting to calve. SBV is not currently a notifiable disease (although Defra does ask farmers to notify their vets if they suspect it) but I don’t know if this will change as the months go on.
I think it’s amazing how much scientists have learnt in the space of about 9 months since vets first saw the signs of infected cattle and I’ll be keeping a close eye out for the next set of results to be published.
Places to go for more info:
Scenarios for the future spread of Schmallenberg virus (Veterinary Record, 2012 170 245-246 doi: 10.1136/vr.e1598 – BEHIND A PAYWALL)
Lamb picture made available by Evelyn Simak under a Creative Commons Attribution-Share Alike 2.0 licence
Cow picture made available by CRV Arnhem under a CC-BY 3.0 licence
Before I start I should mention that this post will not be about the political aspects of the cull decision. Nor will it be about the scientific data that is being used to support and oppose the government’s plans. I am not an expert in these areas and so do not feel competent enough to blog about the issues. However, please feel free to discuss these things in the comments (please keep it polite and attack the argument rather than the person you disagree with).
What I want to write about today is why it is actually important to reduce the levels of bovine TB in our cattle and wildlife. There is a good review article here (unfortunately behind a paywall) and it is from this that much of what will follow is taken.
Bovine tuberculosis (bTB) is caused by Mycobacterium bovis – a species closely related to Mycobacterium tuberculosis which is the most common cause of human TB. M. bovis can infect and potentially cause disease in most mammals, and is zoonotic (so can infect humans too).
Humans and Mycobacterium bovis
People can be infected by three main routes:
The World Health Organisation has this to say about bovine TB:
TB due to M. bovis often occupies sites other than the lungs (it is extra-pulmonary), but in many cases is clinically indistinguishable from M. tuberculosis infection. However, patients with M. bovis often do not respond to the drugs commonly used to treat TB, sometimes resulting in a fatal outcome.
In general there is a period of latency after exposure to the organism – in this period there are no clinical signs of disease. Some (but not the majority) of latent infections will then go on to develop active disease which if not treated can be fatal. This progression is more common if the person is immunosuppressed.
The picture in cattle is reasonably similar to that in humans. Animals most commonly get infected via aerosolised droplets but there is the potential for calves to be infected via milk. Some animals may never show signs of disease, in some the signs of disease may start off being quite vague (loss of appetite, weight loss) but cases can then develop into tuberculous lung disease.
Badgers and Mycobacterium bovis
Badgers, like cattle, are considered a “maintenance host” for bovine TB – the organism multiplies and infects the population from generation to generation and even if badgers never came into contact with any other possible Mycobacterium host the organism would still survive in the population.
Again, some badgers may never show any signs of clinical disease but some may suffer from “florid disease” (as the paper by Gallagher and Clifton-Hadley – see below – beautifully describes it) including tuberculous lung disease and tuberculous lesions in other body sites. That same paper proposes that it is those badgers with the most advanced disease that are the main reservoir of infection for other animals species such as cattle.
Other animals and Mycobacterium bovis
Some other species have also been proposed to act as maintenance hosts including deer and possibly goats. Some species are thought to act as “spill-over” hosts (in these species the infection is self-limiting and they can be considered a “dead-end” host unless they happen to infect a maintenance host). Currently considered as spill-over hosts are pigs, cats and dogs. These animals may also show signs of disease (although again it can take a long time for disease to develop).
Importance in the UK
Because of milk pasteurisation and the control methods currently implemented in cattle the human cases of M. bovis are extremely rare. This disease is much more of a problem in the developing world where these control mechanisms may not be in place.
However, this does not mean the the disease should be forgotten about.
The incidence of the infection in cattle seems to be increasing (see the HPA link below) so there’s more chance of people coming into contact with it, if not directly from cattle, then from some of the spill-over hosts like cats and dogs.
Another extremely important reason not to forget this disease is because the number of immunosuppressed people in the population is increasing (this includes people suffering from diseases like AIDs and also includes people on immunosuppressive drugs like chemotherapy) and as I mentioned before, this leads to greater chance of an infection becoming active and clinical symptoms developing.
It may be (this is my speculation here) that in the future the most common picture for human infection (although it will still be extremely rare) will be an immunosuppressed person getting infected via a spill-over host like a pet cat or dog.
As I’ve discussed, this disease is not only bad for us but it is also bad for cattle, for badgers, and for many other animals should they become infected. In the end, it is in all (and I’m including animals in this ‘all’) of our best interests to eradicate this disease from our country.
And this is generally accepted. However, what still remains to argue about is “How?”
Defra’s policy statement on bovine TB control from December 2011 (also PDF)
Health Protection Agency information on bovine TB
Animal Health information on bovine TB
GALLAGHER, J. (2000). Tuberculosis in badgers; a review of the disease and its significance for other animals Research in Veterinary Science, 69 (3), 203-217 DOI: 10.1053/rvsc.2000.0422
de la Rua-Domenech, R. (2006). Human Mycobacterium bovis infection in the United Kingdom: Incidence, risks, control measures and review of the zoonotic aspects of bovine tuberculosis Tuberculosis, 86 (2), 77-109 DOI: 10.1016/j.tube.2005.05.002