An email from Sabine Zentis, the German expert on Bluetongue, with a commentary to Ruth Watkins about her original posting this morning. September 22 2007
Dear Ruth,just some quick notes on your thoughts about Bluetongue, you are right to be worried but BT can't be compared to other viral diseases like FMD, because the crucial factor in the chain of infection is the vector : the midge.
Email from Ruth Watkins Sept 22
I would like to share with you a worry I have about bluetongue.
Now in the second year of bluetongue infection in Europe and with the midge numbers favoured by the weather, this year the exposure of animals will probably be different because there will be a greater number of infected midges and a greater number of bites - so that infected animals this year might be exposed to an inoculating dose of virus that is on average a thousand fold say greater than last year.
My thoughts: last year the disease might have started from a single point, i.e. one infected animal and went undetected for a couple of weeks thus the overall virus load was much smaller compared to this year. Expression of clinical disease is dependent on the amount of virus and this explains the more severe cases in sheep this year.
I don't think overall mortality is higher, compared to last year but we have much more virus around - thus more animals become infected.
More animals in sheep flocks will be infected and greater number will have disease.
I believe last year they thought on, fairly limited sampling of whole flocks, that few sheep were infected in a flock whereas most cattle in a herd were infected.
Disease in cattle can go undetected whereras in sheep you will see infection very soon. Sampling of flocks has only been done on a small scale and there were rarely animals positive in absence of clinical signs. It was proposed to do surveillance in cattle herds using serology while in sheep clinical disease gives you a picture of the state of infection. Although disease in cattle often is not as obvious as in sheep it can be detected easily. One only has to know where to look for.
I don't know what Ab Osterhus and other virology experts are saying. Nor the midge experts.
One word about the midges : it has been shown that the vectors (different Culicoides midges with very different habitats) are indigenious to Western Europe. They are very well adapted to our climate and they can happily survive during the colder time of the year. It is known that they follow cattle inside the barns - so they might be breeding and living inside during winter.
They might keep the virus circulating at a low level but the virus itself needs higher temperatures to multiply in the vector. Sunshine (radiation) is another factor supporting spread (and severity of clinical signs) of Bluetongue.
I do wonder whether bluetongue could have been present late in 2005 - for instance in November and the one or two animals diseased unnoticed and undiagnosed.
Does this make any difference? BT is know to be a seasonal disease, peaking in late summer and autumn due to the numbers/activity of the vector. I live in the place where the first cases have been detected and we haven't seen this disease before. I had the first case in a cow on August 21st 2006 and although I had never seen cases of BT before it was pretty obvious that this was something completely different.
I don't think BT was present in 2005 because then we would have seen many more cases last year.
This is because the outbreak began this year at almost the same time as last year, in late July. I had expected that it would start in June perhaps. But it started explosively in the same areas as last year.
Again, the disease is seasonal and there is an interaction between vector/virus/temperature. This is well documented from other outbreak regions. So this was not unexpected, especially when taking into account the very mild winter.
Were there carrier animals left amongst the cattle herds? Can wild deer carry it? (viz outbreaks of epidemic haemorrhagic disease annually in deer in USA, particularly bad this year)
Of course there were "carrier" animals left. This could have been cattle, sheep, deer or wild sheep. There are several cases reported and confirmed in deer in Germany. The latest victims have been a Bison, a Yak and an Alpaca.
There are discussions about the overwintering mechanismn of the virus, . Some scientists believe it could survive in the larvae of culicoides. But there are many unknowns because :
a) the serotype 8 is not very well researched as it doesn't seem to be much of a problem in endemic regions
b) the European climate/vectors/vector habitats are very different to other outbreak regions so drawing conclusions from research into other serotypes/ regions is a dangerous thing.
It does occur to me that England should fall partly in the surveillance zone from France and Belgium.
It does of course change the focus of attitudes to vaccination even to FMD
I am glad to hear the German vets advocating FMD control by vaccination to live without penalties greater than stamping out by culling. When it comes to bluetongue diagnosis I hope we will be doing what our European colleagues do and that is RT-PCR as well as serology. None of this penside testing with a lateral flow device to the exclusion of RT-PCR as the first line test for FMD. As bluetongue animals are not being culled there is not pressure to use RT-PCR at the farm gate.
I don't want to go into the details but surveillance and lab diagnosis of Bluetongue in Germany is non existent. At the moment , in case of suspicion, the vets are advised to take only 1 bloodsample per holding and this is only tested for antibodies (ELISA) The labs can't deal with more samples as the numbers of infected animals are increasing every day and no funding is available. They do the ELISA because it is "much easier and cheaper" and the opinion is that detectable antibodies show up at a very stage of infection. To me this is utter nonsense; the antibodies might be a result of last years infection and the animal might well be suffering from another disease. There is no follow up and no screening, the authorities are just trying to enter the daily numbers into the database.
The main limitation of not doing farm gate real time PCR on screening farms within the protection zone for instance to detect spread is that they are waiting for the development of recognised clinical signs in cattle and the development of antibody in sheep before screening and will miss early infection on a farm or infection without any clinical signs viz farm no 5 where they had been three times and must have missed clinical disease if there was any.
It is characteristic of virus infections, with very few exceptions such as rabies, that infection may go unremarked or be without illness yet such infections are fully infectious to others and play a role in the chain of onward transmission.
I don't have any objection to their use of the penside lateral flow device but I do object to the exclusion of the use of the more sophisticated and sensitive technology of real time RT-PCR as a first line screening test.
One word of caution : everyone is focusing on the BTV 8 outbreak. This outbreak is quite unique in that you see so many cattle involved showing clinical signs. Other serotypes will involve cattle but without clinical disease. Looking for cattle as a first warning sign might distract from the fact that another serotype can get into the population that produces clinical disease only in sheep. As the diagnostic tests usually are serotype specific testing for BTV 8 might miss other serotypes. Doing surveillance of bulk milk for BTV as an early warning system is another stupidity; by the time you get a positive result the virus has spread already. This disease is much more difficult to understand than other diseases as so many factors beyond our influence are involved.
I attach a picture of lesions on the teats of one of my old cows (cow survived and is happy and healthy again). Do you think these signs would have gone undetected for a year ?
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