Article written for Mary Critchley and Jane Barribal. Dr Ruth Watkins 11th August 2007
Arguments for why DEFRA should have vaccinated as soon as they had the information that the virus at the first farm in Normandy near Pirbright was the historic strain, O1 BFS 67.This would have entailed a delay of 2 days while the vaccine is prepared for delivery from storage in highly concentrated form, and vaccination teams are readied.
We may have been lucky with a point source of contamination at the first farm with waterborne spread to the second, so that the outbreak is very limited in spread. We must wait out the incubation period and also hope that infection in deer has either not occurred or that they are too dispersed to sustain infection and as hefted sheep were left in 1967 on their common pastures in extensive grazings to let any FMD infection 'burn-out'. Whilst hoping for the best, a point source, we should have taken precaution against the worst, a plume.
- The working hypothesis must be that the virus causing this outbreak derives from Pirbright because it is a historic strain.
- They have the vaccine that is the perfect match for this virus originally derived from the 1967 epidemic of FMD in the UK it being the vaccine strain that 'escaped' from Pirbright.
- They had an area near Pirbright which would have been appropriate to identify as a vaccination zone.
- They could have had the "rose" of the prevailing wind for the dates that they have defined in July when the exposure of the first infected farm was deemed likely to have occurred in case of airborne spread.
- They should know that it would take some time to establish what had happened namely if it was a viral 'plume' of aerosolised virus, or other exposure such as a contact; the latter a point source of contamination rather than contamination spread over a wider area by a plume.
- They should also know that it may not be possible to demonstrate the route of escape from Pirbright. Investigation of possible sabotage or bioterrorist activity would also be very time consuming. Vaccination cannot wait upon these results.
- The biological characteristics of the O1 virus must be known to them, and they should have considered spread by the very many possible routes including water and wildlife such as deer- these could create a problem in control.
- They should be able to explain to us how the excellent killed FMD vaccine works and lay to rest the fears of the unions such as the myth of perpetuating infection by vaccination or the belief that it is necessary to cull uninfected animals just because they have been vaccinated. Also the manner in which vaccinated and infected animals are distinguished on serology testing. The science backing the policy should be clearly articulated.
- The legislation which they, DEFRA, are responsible for both at EU level and within the UK should not give vaccination a penalty over culling, and indeed does not anymore by the EU.
- The supermarkets should state publicly and categorically that vaccinated meat is safe to eat and therefore they will not label vaccinated meat as such nor make any price differential to the producer or consumer.
We are also very lucky that decades of scientific research has provided us with excellent vaccine to all the major serotypes of FMD virus. We are also fortunate that we have these scientific and vaccine establishments in the UK, and we should be ready to take advantage of the benefits they can give us.
(Whilst we agonise over our FMD outbreak and allow the same arguments for and against vaccine to rage unresolved in the farming community as in 2001, Bluetongue Virus serotype 8 infection, BTV-8, has broken out again this year in Northern Europe - and in Holland alone there have been 125 farms with infected animals in the last 2 weeks.The FMD vaccine is much better than this in that it protects against infection with wild virus of the vaccine serotype. Also if FMD infection does occur post vaccination against the same serotype such animals have never been implicated in the spread of FMD in the many decades of use of vaccination to control and eliminate FMD outbreaks worldwide. Animals infected with FMD and either never vaccinated or infected prior to vaccination have been implicated in spread through carriage and shedding of infectious virus, particularly cattle and buffalo.
It first appeared in Holland in July 2006 and came from South Africa by means unknown but most likely in an imported infected ruminant or midges - these can be blown much longer distances than aerosolised FMD virus.
There is no vaccine against disease caused by BTV-8 in ruminants (it does not infect humans but is spread by biting midges so it has spread in Northern Europe inexorably despite control of domestic animal movements) but Merial and Intervet are to undertake development of a killed vaccine.
Whilst such a vaccine may not protect against infection with BTV-8 and therefore not eliminate BTV-8, on the basis of similar vaccines used against other serotypes of BTV, it may protect against disease.
With global warming we may expect the incursion of a number of exotic viruses into the domestic animals of Northern Europe, which if they are insect borne or infect a wildlife reservoir may not be eliminated. May we have diagnostics and vaccines ready to meet them. However fortunately we don't have to live with FMD and vaccination has historically been important in control and elimination of FMD infection from regions or countries. In places like Brazil or Saudi Arabia repeated incursion of FMD cannot be prevented it seems at present from poorer surrounding countries because infected animals are continually imported legally or illegally.
Why does FMD vaccine work so well?
FMD virus belongs to the family of viruses called Piconaviridae. They can be imagined as a box, the capsid, containing and protecting the delicate contents, a nucleic acid genome, an RNA molecule a mere 5000 nucleic acid bases long - as viruses they are simple and minute, much less complicated than bacteria. The function of the box or capsid is to introduce the virus into a cell whereupon it opens to release the genome so it can start to multiply. This gives rise to an infection.
After infection antibody is formed to all the virus proteins, those found in infected cells and those making up the virus itself, including the box , the capsid.
Vaccination is designed to evoke antibody to the outside surface of the box, the virus capsid.
Infection of an animal with FMD virus is distinguished from vaccination by the presence of antibodies to proteins other than those that comprise the virus, those that make up the box, the capsid. In infection antibody is made to all proteins the virus genome encodes. The virus encodes proteins that facilitate its multiplication, many new genome RNA molecules made by copying the infecting genome RNA. The RNA to RNA synthesis this process requires does not occur in any animal cell, so the infecting virus encodes the proteins necessary for this- they are not found in the FMD vaccine.
Viruses in the Picornaviridae family have well conserved neutralisation sites on the surface of their box , the capsid. The neutralisation sites are special antigenic sites that when bound by an antibody that fits perfectly or almost perfectly causes the box to remain closed and therefore the nucleic acid cannot be released even when the virus, or box, enters a cell. The nucleic acid is locked in and eventually the virus particle is harmlessly degraded by the cell. Cells cannot therefore be infected by neutralised virus.
Vaccination is designed to protect against infection by evoking antibodies against the neutralisation site.
These antibodies are present ready to meet a virus and if matched to the neutralisation site on the surface render the virus non-infectious as described above.
There are at least 7 different serotypes of FMD, that is virus types with different neutralisation sites. In order to evoke the protective neutralising antibody the vaccine used must be of the same serotype as the outbreak or epidemic virus. Hence the importance of typing an outbreak virus done most quickly now by sequencing the nucleic acid.
Each different serotype of FMD has been grown up by Merial and inactivated to form the appropriate vaccine to match each and all of the different possible serotypes of FMD. Live attenuated strains of FMD have not been developed for reasons I am not sure of, so the vaccine preparation involves the culture of very large quantities of the wild virus types, the pathogenic or disease causing virus, now historic such as the British Field Strain from the 1967 outbreak for example, before it is inactivated or 'killed' to make up the vaccine.
Though the current circulating strains of FMD, or other Picornaviridae such as polio which has 3 serotypes, do slowly evolve in that changes gradually accrue to the RNA genome the neutralisation site is as a rule highly conserved in this virus family. There must be constraints on its evolution such as any change to the neutralisation site renders the virus incompetent. This is why the laboratory strains of FMD are historic, their genome reflecting a circulating wild type virus of yester year. Historic strains of virus are used in preparation of FMD vaccines as they are in the preparation of polio vaccine.
This is in contrast to influenza virus for example where the vaccine must be updated at least annually to take account of the slow evolution of the neutralisation sites on the heamagglutinin or H molecule on the outside of the influenza virus (if a new H type comes along the vaccine must be reformulated entirely).
All virus families have different characteristics, and to some we may never be able to make protective neutralising antibody at all such as Hepatitis C virus. How lucky we are to have such a good vaccine against FMD - it is theoretically possible to eliminate FMD from the world by vaccination as has nearly been accomplished with poliovirus.
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