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BSE Inquiry Report

An inquiry was established by the UK Government in January 1998 to review the history of the emergence and identification of BSE and new variant CJD in the United Kingdom. The Inquiry Committee was also asked to review action taken in response to this emergency up to 20 March 1996 and to reach conclusions on the adequacy of that response taking into account the state of knowledge at the time.

The Inquiry Committee under the chairmanship of Lord Phillips handed down its report in October 2000.The 4,000 page, 16 volume report is available in full on the web site: http://www.bseinquiry.gov.uk

The Committee emphasises in its findings that it has confined itself strictly to the lessons to be learned from the BSE experience up to 20 March 1996 and says, 'If some of these lessons have already been learned, others may bear repeating.'

In view of renewed public and media interest in Australia in BSE some important findings and conclusions of the Report are outlined below. Thirteen key conclusions are listed in the Report together with a large number of lessons to be learned.

Many of these lessons refer to how Governments, departmental officers and advisory committees should be prepared for and conduct themselves in a crisis such as the emergency of BSE. However the Committee concluded that in the years up to March 1996, most of those responsible for responding to the challenge posed by BSE emerge with credit. However, there were a number of shortcomings in the way things were done and recommendations are made to prevent these shortcomings from recurring.

The Committee notes that the Government was preoccupied with preventing an alarmist over-reaction to BSE because it believed the risk to human health was remote. It is now clear concludes the Committee that this campaign of reassurance was a mistake. The UK Government has (February 2001) issued an interim response to the report which agrees with most of the report's findings.

Conclusions with regard to the cause of BSE and the risk posed by BSE to humans include:
  • BSE developed into an epidemic as a consequence of an intensive farming practice – the recycling of animal protein in ruminant feed. This practice, unchallenged over decades, proved a recipe for disaster.
  • BSE probably originated from a novel source early in the 1970s, possibly a cow or other animal that developed disease as a consequence of a gene mutation. The origin of the disease will probably never be certainly known.
  • The theory that BSE resulted from changes in rendering methods has no validity. Rendering methods have never been capable of completely inactivating TSEs.
  • The theory that BSE is caused by the application to cattle of organophosphorus pesticides is not viable, although there is a possibility that these can increase the susceptibility of cattle to BSE.
  • The cases of BSE initially identified between 1986 and 1988 were not index or first generation cases. Nor were they the result of scrapie, a TSE usually associated with sheep. They were consequences of recycling of cattle infected with BSE itself. The BSE agent was spread in meat and bone meal.
  • The Government was anxious to act in the best interests of human and animal health. To this end it sought and followed the advice of independent scientific experts – sometimes when decisions could have been reached more swiftly and satisfactorily within government.
  • The Government introduced measures (from 1989) to guard against the risk that BSE might be a matter of life and death not merely for cattle but also for humans. However the possibility of a risk to humans was not communicated to the public and those whose job it was to implement and enforce the precautionary measures.
  • One of the most significant features of BSE and other TSEs is the fact that they are diseases with a very long incubation period. The question of whether BSE was transmissible to humans was unlikely to be answered with any certainty for many years.
  • Cases of a new variant of CJD (vCJD) were identified by the CJD Surveillance Unit and the conclusion that they were probably linked to BSE was reached as early as was reasonably possible. The link between BSE and vCJD is now clearly established though not the means of infection.

One perhaps unexpected finding of the inquiry is that BSE was not introduced into cattle from the remains of scrapie-infected sheep included in ruminant feed till July 1988. A second is that the BSE outbreak was not caused by a change in the way meat and bone meal was treated in rendering plants.

A recent review published jointly by experts from the USA and the UK disagrees with these two findings of the Phillips Inquiry. (Emerging Infectious Diseases 2001, 7.1 *full text here*)

The authors of this review note that even though rendering procedures in other countries underwent changes similar to those in the UK during the 1970s, BSE has apparently emerged solely within the UK This may or may not be true as the origin of cases in other countries has yet to be fully determined. However these workers believe that the most plausible explanation of this is that the proportion of sheep in the mix of rendered animal carcasses and the proportion of scrapie infections in such sheep were probably higher in the UK than elsewhere. It is postulated that these proportions were apparently sufficient to bring very low levels of the infectious agent in batches of rendered carcasses over the threshold of transmission.

For reasons they do not give, these reviewers do not accept that the rendering process as it was applied prior to the 1980s was also not capable of inactivating moderate levels of the BSE agent. This is despite compelling experimental evidence to the contrary. (Journal of Food Safety 1998 18 p.265)

BSE     Bovine Spongiform Encephalopathy, fatal neurological disease of adult cattle.
CJD     Creutzfeldt Jakob Disease, a human transmissible spongiform encephalopathy.
TSE     Transmissible spongiform encephalopathy, disease of the neurological system which can be transmitted to the hostspecies or other species.
vCJD     New variant CJD. Identified in 1996 as a previously unrecognised form of CJD.
Food Safety and Hygiene
Prepared by Keith Richardson and Beverley George
Food Science Australia
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