Symptomatic cases of BSE in British cattle now total more than 146,000. As BSE is one of a group of transmissible and fatal spongiform encephalopathies (TSEs) affecting both animals and humans this has raised concern regarding possible risks to human health. The infective agent in TSEs, thought to be a prion has not been clearly described. There are no early diagnostic tests, incubation periods are prolonged (possibly up to 30 years in humans) and the pathological process which leads to a rapidly progressive and fatal encephalopathy has yet to be explained.
It is not yet known if the BSE agent can cross the human species barrier to infect humans. It has now been transmitted to 18 species and to 16 of these (possibly 17 if pigs are included) by mouth.
Given the importance of beef in the human diet, it is essential that control measures to protect health are rigorous, comprehensive and objective. In this respect there are four factors which are important in assessing risks. These are the likely magnitude of the species barrier between cattle and humans, the dose (single or cumulative) that are needed to transmit the disease, the method of exposure (oral or subcutaneous) and the likely period before symptomatic disease appears.
To assist knowledge and understanding in these areas we recommend the wider involvement of public health professionals in the existing nationally co-ordinated multi-agency research programme. We also recommend further studies into the oral transmissibility of the BSE agent to primates, an acceleration of the search for diagnostic tools and treatments for established prion infection and enhanced surveillance of neurological disease in humans.
It is now clear that probably a large percentage of the population will have been exposed to BSE in the UK.
Humans will have eaten 1,800,000 infected cattle by 2001 and
will have eaten tissues that have been shown to be infective in
other species, but inadequately tested in cattle.
Humans have already taken risks in eating bovine products that
have now been banned. The recurrent banning of foods or
procedures by MAFF will not help the people that have been
exposed before the ban. It is possible that further action such
as this by MAFF will seriously damage the public's respect for
The article's most important part is to show that the World Health Organisation's publicised opinions on how to decide whether or not the exposure of a human to a specific amount of an infective agent could not have been carried out as inadequate information was available with which to decide the action. As a result of this it was important that Government action should assume a tolerable level for human exposure to BSE to be very low indeed, possibly 10,000 times less then the amount felt acceptable by MAFF. Concerning the article in the British Food Journal 1995, volume 97, 3-18.
The most important aspect of the article seems to be the WHO directives as to how to decide what levels of an agent should be considered non-toxic to humans. Clearly a wide error margin is given by the WHO but still this would suggest the risk that is being taken with BSE as being unacceptable in public health terms.
British Food Journal 1995, volume 97, p3-18
The article explains that, as a fatal disease, with no method of treatment, inadequate methods of diagnosis and no method of prevention in any animal afer infection has taken place, this subject should be studied closely. Infectivity is presumed, if like in other TSEs, to be present in many tissues and to not be destroyed by cooking. One of the major problems is in trying to calculate the number of infected animals that are being eaten and at what point in their incubation period this takes place. It seems that there is adequate data now available from MAFF for this to found. The major findings of the article are:
Cases of BSE are becoming severely under-reported. For instance only 40% of clinical cases of BSE reached UK Government statistics in 1993.
BSE may continue in the UK for many years, with cases born each year, showing symptoms 3 to 8 years later.
BSE may not be derived from the disease of sheep, scrapie and if it is, we cannot rely on it to carry the same properties as that disease. The UK Government used the idea that BSE was scrapie originally to suggest that BSE would not infect humans although this was invalid at the time.
1,800,000 cattle incubating BSE will have been eaten before 2001 even if no cases are born after 1991. This figure assumes that all cattle with BSE were always reported by farmers to veterinary officers, that the VOs always accepted them, and that histological diagnosis was always correct (up to 1991). It is therefore likely to be an underestimate of the true BSE incidence. Many of the younger cattle incubating BSE would have been exported to Europe.
The epidemiology of BSE in the UK is that of an infection passed down from the mother to the offspring but where the mother would show symptoms later in life. It may be that BSE cases that we see are derived from infections in their mother and it was the mother that ate infected food. If this is true then the total number of infeced cattle eaten in the UK will be around 8,000,000 by 2001.
UK Government advisors have suggested that there is little risk from eating liver, kidneys, nerves and muscle from infected cattle. The article shows that this cannot be true if these tissues contain the same amount of infectivity as is found in other species with a similar disease.
The acceptable levels (UK Government) of infectivity to found in food may be 10,000 times the amount that could be seen as acceptable under WHO directives used for other potentially fatal diseases.
UK Governernment Advisory Committee on Dangerous Pathogens reported in October 1994 showing that cattle that may be infected should be treated as if they are infective. They say that some tissues should not be even touched (e.g. liver) that the UK Government continues to tell its population as being acceptable to eat.
The risk to humans in Europe from BSE is unacceptably high but cannot be stated precisely at this time. The article states again that the cumulative amounts of BSE in our diet in the UK is expected to be between 10,000 times and 100,000 times the amounts of scrapie that we would be eating.
No directions are given as to whether bovine tissue in the UK should be considered toxic.
It is suggested that scrapie is the source of all TSEs in animals and man but that, by passing from one species to another the agent is either selected or changed in such a way as to alter the range or type of disease that it might produce in a further animal species.
For instance it is suggested that scrapie does indeed cause the endemic types of CJD that seem to be present in some parts of the world (e.g. Slovakia) and partly associated with PrP gene aberrations. However, when scrapie is transmitted to cattle, it then becomes more infective to humans and is involved in the production of sporadic CJD in many parts of the world.
The cases of GSS that are not fully penetrant may be because the genes are correct but the agent (scrapie) is still required. In cases of fully penetrant GSS perhaps the agent also remains with the infected person.
The argument is fairly reasonable in that it will be very difficult to find groups that have not been exposed to meat at all, even though they think they have not. It will also take a long time to be able to carry out statistical research to say if beef is involved in sporadic CJD or not (because the controls will also eat a lot of beef and the difference between the groups will be small). Diringer recommends research as the way to find out what is going on but the current PrP research avalanche may only be of some use if animal inoculation studies are carried out similarly.