Mad cow disease and its human equivalent : risks of infection via the Australian food chains.

Abstract

73 Mad cow disease and its human equivalent -- risks of infection via the Australian food chains J.V. Nolan Animal Science, University of New England, Ar midale NSW 2351 jnolan@metz.une.edu.au Summary Epidemiologist studies have shown that the `Mad Cow' (BSE) epidemic in Britain was almost certainly caused by the practice of feeding cattle with meat and bone meal (MBM) rendered down from the carcasses of infected animals, particularly sheep and cattle. The practice created a feedback loop that magnified the transmission of BSE, creating an epidemic. It is now believed that meat or meat products from BSE_infected cattle may contain prions that can infect humans causing a fatal neuro_degenerative disease (variant Creutzfeldt_ Jacob disease, vCJD). vCJD has now claimed more than 100 victims in Europe. Predictions of the eventual human toll from this disease in British residents are uncertain at this stage but may run to 250,000 and many tourists may also have been infected. BSE has now spread to European countries and almost certainly beyond, so people elsewhere in the world are therefore also at risk of becoming victims of vCJD. In hindsight, it is evident that there were numerous failings in the management of the detrimental effects of BSE on animal health and food safety in Britain. A knowledge of these failings can assist us to develop contingency plans to prevent similar events occurring in Australia. Keywords: BSE, mad cow, CJD, rendering, meat meal, prion Spongiform Encephalopathy, BSE) in Europe. The practice of feeding rendered down ruminant offal from infected animals in the form of meat and bone meal (MBM) back to animals of the same species was central to the development of the BSE epidemic in Europe with its subsequent tragic human consequences. The unfolding of the `Mad Cow' disease saga in Britain has many other fascinating twists and we in Australia have much to learn from our counterparts in the UK and Europe. The story exposes wider issues relating to how scientists interacted with politicians and other policy makers, and how all `experts' interacted with the public at large. Overseas the epidemic will continue to involve farmers, scientists, medical and veterinary professions and consumers--in fact all members of the public. In Australia, there are lessons to be learnt from the epidemic in relation to feed processing, cattle disease surveillance, medical implications and other matters. TSEs There is a family of neuro_degenerative diseases of humans and other mammals, similar to BSE, that cause irreversible brain damage and are invariably fatal, the Transmissible Spongiform Encephalopathies or TSEs. At autopsy the brain has a characteristic sponge_ like appearance. The sheep disease, scrapie, is a TSE. The disease has been recognized for nearly 200 years but does not appear to be easily transferred to humans or other animals. In humans, Creutzfeldt_Jacob disease (CJD) was described in the 1920s by the workers after which the disease is named. It is a dementia that appears sporadically in people in all countries, affecting one person in a million, typically at about age 60. There are about 20 deaths each year in Australia from this so_ called `sporadic_CJD'. In 1957, the disease kuru in the Fore Highlanders in Papua New Guinea was found, by Vincent Zigas of the Australian Public Health Service and D. Carleton Introduction Globally, each year 68 million metric tonnes (Mt) of pure protein are provided in feed prepared for farm animals, mainly pigs and poultry, that become meat for human consumption. Of the protein used, 86% is from plants, mainly soybean, and the remaining 14% is made up of animal proteins from by_products of meat production (5.5 Mt produced mainly in North America, Europe and Australia) and 3.9 Mt from fish that are caught and not used for human consumption (WHO 1999). The rendering industry plays an important role in the recycling of animal proteins (and fats) that has been implicated in the `Mad Cow' epidemics (Bovine Recent Advances in Animal Nutrition in Australia, Volume 13 (2001) 74 Nolan, J.V. Gajdusk of the U.S. National Institutes of Health, to be a similar spongiform encephalopathy. These workers found this disease, now known to be a human TSE, was spread between the highland people by a form of ritual cannibalism in which they honoured their dead relatives by eating their brains. Incidence of the disease has declined rapidly since cannibalism ceased in 1959, but clinical cases of the disease have continued to appear, the latest in September 2000. Long `incubation' periods (measured in years or decades) are characteristic of all TSEs that, until the 1980s, were thought to be caused by so_called `slow viruses' (e.g. Gajdusek 1977). Bovine Spongiform Encephalopathy is another TSE that was only discovered in 1986 in cattle in Britain. The infective agent, generally accepted to be a `proteinaceous infective particle' or `prion' for short, is thought to be spread mainly by animals ingesting protein meals made using rendered down offal from infected animals (cf. cannibalism and kuru), and to a minor extent by transmission from cow to calf. BSE has an ability to jump the `species barrier ' and to cause neuro_degenerative disease in humans and other mammals. In humans, a new variant of CJD was diagnosed in a young man who died in 1995. It is referred to as variant CJD (vCJD) to distinguish it from the long_recognised sporadic CJD. The factors that contributed to amplification of BSE and its putative transmission to humans are shown in Figure 1. `Mad Cow' disease When BSE or `Mad Cow disease' was first acknowledged by the British Ministry of Agriculture, Food and Fisheries (MAFF) in 1986 (see Figure 1), there was probably little reason for most scientists to suspect it might cross the species barrier and affect humans. (Scrapie had been recognized in sheep for 200 years, and was thought never to have infected humans.) However, it was recognized by Dr. John Wildesmith, Head of the Central Veterinary Research Laboratory at Weybridge, that BSE might be spreading within cattle herds via the practice of feeding MBM made from BSE_contaminated carcass remnants from slaughtered animals. Retrospective analyses by Donnelly et al. (1997a) later suggested that BSE had been spreading via MBM in Britain well before 1986 and that a BSE epidemic in British cattle was already developing in the early 1980s. It would have been assisted by widespread MBM feeding, especially to dairy cattle. Subsequent computer models suggest that, without MBM in cattle feed, the epidemiological reproduction number (see Deikmann and Heesterbeek 2000) would have been less than one, and a BSE epidemic would not have developed (de Koeijer et al. 1998). In 1988, the British government outlawed the practice of feeding MBM made from ruminant offal to cattle, thereby in theory removing the principal reason for the multiplication of BSE among cattle. At that time Calf Infected mea t `Spongy' brain Prion BSE multiplication loop -- Meat-meal Variant-CJD Figure 1 Factors enabling multiplication of BSE, the transmission of BSE to humans by ingestion of BSE_infected meat, and the development after an `incubation period' of perhaps decades of clinical signs of vCJD. Mad cow disease and its human equivalent -- risks of infection via the Australian food chains 75 there were 41 rendering plants producing 0.35 Mt MBM and 0.23 Mt tallow (Southwood 1989). However, ignorant of the fact that the rate of infection at that time was thousands of cases a week, the government allowed a `period of grace' of 5 weeks for renderers to clear existing stocks. In addition, because BSE_infected cattle silently harbour the infective agent for many years before clinical signs become evident, and because the feed ban was flouted or misunderstood and cross_ contamination between ruminant and non_ruminant feeds continued in feed mills, the numbers of new diagnoses of BSE continued increasing until 1993, a year in which there were nearly 40,000 confirmed cases. There have now been about 178,000 of ficially confirmed cases of BSE in Britain, and new cases are still appearing in 2001. All BSE confirmations have been made by post_mortem examination of brain tissue: there are still no totally reliable tests for BSE in living animals. Back calculations suggest that at least 1 million cattle (six times the number of confirmed cases) have probably been infected with BSE to date (Figure 2). Many of these cattle were slaughtered to provide meat, and thus many thousands of British people and many tourists would have eaten BSE_infected beef during the height of this epidemic. These people may still be silently `incubating' BSE infections (perhaps acquired up to 20 years ago) and may in the future develop vCJD. Fortunately, a ban preventing the inclusion of brain and nervous system (thought to be highly infective tissues) in meat products destined for human consumption was imposed in 1989. This ban probably reduced the risk of human infection but would not have eliminated it. Moreover, quality assurance procedures were not in place and the ban was not universally observed. Since 1993, the cattle_BSE epidemic has been subsiding. This year only about 30 new BSE cases per week are being diagnosed by post_mortem brain testing in Britain, and authorities expect that BSE incidence will continue to decline over the next few years. From the time BSE was first recognized, warnings were made of the potential threat of transmission of the BSE agent to humans (e.g. Holt and Phillips 1988). Subsequently, in the years when the BSE epidemic was prominent (1990_1995), British politicians and public officials, to allay public concerns, claimed on many occasions that `British beef is safe to eat'. Minister for Agriculture, Gummer 's assertion to this effect has became one of the most celebrated examples after he posed for the media in 1990 with his four_year old daughter Cordelia, as both ate hambur gers to demonstrate the safety of British beef! However, many other public officials, including the Chief Medical and Veterinary Officers and later the Secretary of State and the Prime Minister, made similarly soothing statements, and we know now how misplaced those public assurances were. 177,85 7 1,812 4 16 648 32 70 (1 ) 379 318 16 0 0 0 0 45 564 Figure 2 The numbers of cattle putatively infected with BSE in Britain between 1982 and 2001 (after Donnelly et al. 1997a with addition of MAFF data after 1996) and the timing of some significant events relating to the histor y of BSE. 76 Nolan, J.V. Spread of BSE to other countries The BSE trail now extends beyond Britain and probably world _ wide. Unfortunately, although feeding of MBM to ruminants was no longer permitted in Britain, after 1998 large tonnages of meal were still exported. MBM was exported to more than 70 countries (the risk of, and consequences of, BSE transfer overseas being considered to rest with the recipient country). Recipients of the meals made from offal from potentially infected British cattle included European countries, Japan, Thailand and Indonesia ( Sunday Times , London, 4 February 2001). In March 1996 the European Commission (EC) introduced a ban on the export from the UK of bovine animals, semen and embryos, beef or beef products and mammalian MBM but, unfortunately, total bans on exports of meals from other EC countries were not implemented until January 2000. In response to the 1996 export ban, a concerned British Government implemented two control programs: culling of animals over 30 months of age (OTMS), and a selective cull of herds with a history of high incidence of BSE. About 1.4 million cattle were slaughtered under the OTMS in 1996_97, and 19,271 cattle were selectively culled. However, the records of these culling programs were deficient. Donnelly and co_workers have attempted to study the impact of both programs, but found this was difficult because records were not kept on the ages of animals slaughtered under OTMS and there was limited information on the animals selectively culled from high_risk herds. Between 1988 and 1996, while the BSE epidemic was at its highest, Britain exported 3.2 million `BSE_free' cattle to 36 countries throughout the world. EC countries also exported millions of cattle worldwide. In contrast to the declining BSE incidence in Britain, in some other EC countries, numbers of confirmed BSE cases are increasing (Figure 2; CompuServe, 2001). Donnelly's modelling group (Donnelly 2000) has estimated that, since 1987, at least 1200 French cattle have been infected by BSE_infected cattle from Britain and similar infections have probably occurred in many other countries. Some countries in Europe have only recently discovered BSE in their cattle: in the future others such Romania and the Czech Republic will almost certainly find they have the disease. BSE has been detected in Canada, Oman and the Falkland Islands in cattle imported from Europe. It is likely that BSE is now present but undetected in other parts of the world. Outside Britain, another BSE epidemic is probably looming and it may therefore be many more years before BSE is brought under control globally. The BSE infective agent -- the prion Most infections of animals and people are caused by bacteria or viruses that replicate and thereby spread disease. The infective agent of TSEs is now thought, by most scientists, to contain no nucleic acid and to be a relatively small proteinaceous particle or `prion'--a name coined by Dr Stanley Prusiner and co_workers (see Prusiner 1982). Prusiner was awarded a Nobel prize in 1997 for his contribution to an understanding of the role of prions. In the early 1980s, to suggest as Prusiner did, that a protein particle alone could be infectious was a scientific heresy. It was thought that no organism on the planet could replicate without the participation of nucleic acid. It is perhaps for this reason that a minority of experts still believe that the prion may not act alone in causing TSEs. It is fascinating to note that the now widely accepted theory of how protein particles could replicate and be infective had been described in 1967 by a mathematician (Griffith 1967) and quickly dismissed. Griffith argued that the same genetically determined protein particle would have to be able to exist in two different forms in cells--in its normal cellular structure (healthy cells), or in another disease causing conformation. It is now thought that a naturally occurring glycoprotein molecule that is rich in alpha_ helical regions switches to a thermodynamically more stable beta_rich isoform (Baskakov 2001) that is highly insoluble and protease resistant (Horwich and Weissman 1997). All higher animals have a highly conserved gene that controls the formation of a 35 kD protein that is found in the membranes and contents of normal nerve and immune system cells. The normal protein is synthesized in three topologic forms at the endoplasmic reticulum (ER) (Hegde et al. 1999). The predominant isoform is fully translocated into the ER lumen, while the other two forms are single_spanning membrane proteins. A similar form occurs in all mammals and is thought to play a role in the metabolism of nucleic acids (Gabus et al. 2001) and copper at synapses (Kretzschmar et al. 2000). Copper alters the biochemical properties of this protein by directly binding to its N_terminal region and may play a role in its conversion to a protease_resistant isoform (Quaglio et al. 2001). Prion protein (PrP) appears to be necessary for normal synaptic function: nevertheless, mice homozygous for disrupted PrP genes appear developmentally and behaviourally normal (Collinge et al. (1994). In animals developing TSEs the normal cellular protein forms may suddenly flip from their normal structure into the protease_resistant disease provoking form, especially if triggered by the presence of a closely related abnormal protein (prion) acquired from another animal via infected food, or perhaps via contaminated surgical instruments, blood or donated tissues. A chain reaction ensues with formation of large amounts of the protease_resistant protein molecules that are associated with the death of nerve cells and the spongiform appearance of the brain at autopsy. Prions that are ingested in MBM by farm animals or in meat or meat products by humans may be absorbed across the gut wall at Peyer 's patches that are part of the mucosa _ associated lymphoid tissue (MALT). Mad cow disease and its human equivalent -- risks of infection via the Australian food chains 77 Lymphoid cells may engulf the particle by phagocytosis and then travel to other lymphoid tissues such as lymph nodes, and the spleen and tonsils where the prion can probably promote the change in confirmation of its normal cellular analogues. Mature B lymphocytes are apparently necessary for disease to establish following infection of animals via a peripheral route (Weissmann et al. 2001). After an extended silent period, cattle develop BSE and humans develop vCJD. The infectivity of prions after rendering Prions are not only protease_resistant, but also highly resistant to most treatments used to eliminate pathogenic viruses and bacteria: autoclaving, hospital detergents, alcohol, UV radiation, gamma irradiation, microwave radiation, hydrogen peroxide, chlorine dioxide. They are therefore particularly difficult to eliminate from the environment. BSE _ infected material was found to be still infective after being buried for 3 years and, which almost defies belief, hamster_adapted scrapie agent (263K) survived combustion at 600�C for 15 min (Brown et al. 2000). In short, prions in the environment may remain infective for a very long time! They are also resistant to natural digestive enzymes and to intracellular proteases, including those that remove their normal counterparts in healthy cells. In the infected animal cell, the prion form is associated with build_up of white plaques in brain tissue and somehow promotes death of brain cells, leaving the sponge _ like brain appearance that is characteristic of vCJD. It has been claimed that an infected piece of tissue `the size of a peppercorn' is sufficient to infect a cow and it has further been suggested, but not scientifically verified, that one infected cow could potentially infect hundreds of thousands of people. Taylor et al. (1995) used bovine brain samples infected with the BSE agent to spike materials (representing those rendered in commercial plants). The spiked material that was then processed into MBM and tallow in pilot scale facsimiles of 12 rendering processes then being used within the European Union, and three others. Suspensions of all the MBM samples and two of the tallow fractions were assayed in inbred mice for BSE infectivity. MBM from four of the 15 processes showed detectable BSE infectivity whereas the tallow samples had no detectable infectivity. Taylor (1996) found that the infectivity in macerates of mouse_brain infected with the ME7 strain of scrapie agent was not completely inactivated by exposure to dry heat at temperatures up to 180�C for 1 h but infectivity was reduced progressively as the temperature was increased. No infectivity was recovered after a 1 h exposure at 200�C. The resistance of the prion to destruction means that the minimum conditions normally used to render beef offal in Australia (120�C at 2 bar for 20 min) certainly could not be relied upon to remove BSE infectivity. Because the rendering conditions do not completely remove prion infectivity, huge quantities of potentially infective offal are still being produced in Europe and the question is: how can the MBM being fed to pigs, poultry and fish be processed to guarantee that it no longer poses a risk of infecting animals or people in the food chain? In Europe, since1996 all EC rendering plants producing mammalian proteins destined for farm_animal feeds are capable of meeting pressure_cooking standards (133�C at 3 bar for 20 min). There is, however, currently a ban in the EC on feeding the resulting meals to farm animals. This ban may be lifted in the future when current failings in the processing and distribution of MBM have been overcome. For the EC to lift the ban, certain principles would need to be guaranteed: � � � only animal by_products considered fit for human consumption should be rendered down to MBM there should be a complete separation of animal feed from wastes not fit for human consumption plants dedicated to animal feed production should be separate from those processing other animal waste. Until the present, cross_contamination between general animal and ruminant feeds in feed mills has been found to be widespread in many EC member states (EC 2001). Meanwhile, there are plans to incinerate 3 Mt of MBM unfit for use for animals that have been stockpiled, along with partially rendered carcasses that have been stored in various locations. (In the EC, 14 Mt of MBM are produced annually.) However, incineration is not feasible in the short term because there are not enough suitable incinerators, and other methods of benign disposal are urgently needed. In this connection it is pleasing to note that an Australian company, Australian Dehydration Technologies Pty Ltd (ADT), managed by a graduate of the UNE, Mr. Phil Kemp, has patented a new process for rendering meat products. This is a biochemical process (alkaline hydrolysis) that is claimed to be more energy_efficient than conventional rendering and uses simple and inexpensive technology. The MBM produced is of high quality and has excellent keeping properties. At UNE, we have evaluated MBM made from kangaroo offal by the ADT process against conventional MBM in diets used to grow female broiler chickens from 5 and 20 days of age. MBM was included at a level of 12% in a standard formulation consisting of sorghum (48%), wheat (20%), soybean meal (20%) and 0.35% of both DL_methionine and L_lysine. The mean values for feed intake and growth rate per bird and feed conversion efficiency did not differ between diets and were 54.5 g/d, 38.2 g/d and 1.4 g/g respectively. The results indicate that the ADT_rendered MBM from kangaroo offal can replace conventional MBM without affecting chicken growth. 78 Nolan, J.V. Ironically, the alkali _ rendering technology might turn out to be an ideal way of removing BSE infectivity in animal carcasses. The alkali is likely to be able to chemically alter the prion, thereby removing its functionality and its ability to infect animals or people. Support for this concept is given by work of Ernst and Race (1993) who demonstrated that, when scrapie_infected hamster brain homogenates prions were treated with 0.1M sodium hydroxide for 2 h, followed by autoclaving at 120�C for 1 h, prions were inactivated. Taylor et al. (1999) found that there was no infectivity in samples spiked with the highly thermostable 301V strain of mouse_passaged BSE agent after boiling samples containing the agent in 1M sodium hydroxide for 1 min. The patented ADT rendering process is currently under investigation in Scotland to determine if it also eliminates the infectivity of meat products spiked with thermo_stable TSE agents (P. Kemp, pers. comm.). that clusters of prion_related diseases have occurred in regions with high levels of manganese in conjunction with low levels of copper. These clusters could also be related to the practice of feeding mineral supplements to cattle (Purdey 2000). His theory does not, however, explain why BSE has appeared only in British cattle if genuinely similar conditions have existed elsewhere. Human BSE -- a global epidemic? Since the first case of a new variant of Creutzfeldt_ Jacob disease (vCJD) was confirmed as the cause of death of a young man named Steven Churchill in Britain in 1995, there has been overwhelming, albeit circumstantial, evidence linking the fatal human disease to the incidence of BSE. Humans who develop this disease lose motor function, suffer memory loss and hallucinations, progressive brain damage, and eventually die. In contrast to the long_recognised `sporadic CJD' which usually occurs in older people, vCJD seems to infect younger people. Recent reports have confirmed that vCJD is distinct from sporadic and acquired CJD (Ironside 2000). vCJD has affected younger patients (average age 29 years, as opposed to 65 years), has a relatively longer duration of illness (median of 14 months as opposed to 4.5 months) and is strongly linked to exposure, probably through meat or meat products, to BSE (WHO 1999). The reasons why vCJD affects mainly younger people are not clear, although some experts argue that young people are more likely to eat reprocessed meat _ this meat being more likely to contain neural and lymphoid tissues (SBOs) that are considered to be more infective than other beef products. At the time of writing, 103 people have died of vCJD. They probably acquired the infection 10_20 years before their death (the putative `silent' period before vCJD symptoms appear), i.e. in the 1980s. Notably, all the deaths so far have been in people with a genetic condition that occurs in about 30 _ 40% of the population, i.e. homozygous for methionine at codon 129 in the prion_protein (PrP) gene. Codon 129 can also code for valine but there is no evidence that vCJD has occurred in Britons who are MV or VV at codon 129 in the PrP gene (Ironside 2000). This could mean either that these people are not susceptible to vCJD or, because polymorphisms in the prion gene are known to affect incubation times and TSE susceptibility in humans and mice (Collinge et al. 1991; Westaway et al. 1987), that BSE incubation periods in these latter groups may be longer than in methionine homozygotes. It is therefore almost impossible at present to predict the likely numbers of future cases of vCJD in Britain. The senario, however, is clearly a grim one; the question is `how grim'? Workers at Oxford University (Ghani et al. 1998) have used models based on conservative assumptions (e.g. that the disease affects only genetically susceptible people in younger age groups) to predict the likely future deaths from vCJD in Britain and their Where did BSE come from? The source of BSE is still unclear. In her comprehensively researched book, Cooke (1998) has summarized the various theories on the origins of BSE, often assisted by personal interviews with relevant people. One suggestion is that scrapie_infected sheep were rendered into MBM and the sheep_cattle species barrier was breached by changes in rendering conditions. The removal of solvent extraction and introduction of lower temperature `continuous flow' cooking in the late 1970s and early 80s may have increased the likelihood of this chance occurrence. An adjunct to this theory was the suggestion that a mutant strain of scrapie had jumped the species barrier. However, Dr. Alan Dickinson, Head of the Neuropathology Unit in Edinburgh (a scrapie expert interviewed by Cooke) has argued that it is unlikely that scrapie would have crossed a species barrier that had existed between sheep and cattle for more than a century. He suggested that the BSE agent might have been imported in a cow from another country. Recently, Professor Morris, Massey University has added a further possibility (AP 2001), that an African antelope brought the TSE into safari parks in southern Britain and BSE developed from there. Ford (1995) on the other hand suggested that BSE has long existed in Britain as a `sporadic' TSE specific to cattle. The feeding of MBM manufactured from cattle offal under less rigorous conditions simply amplified a `sporadic' cattle TSE. An associated theory for the origin of BSE has been promoted by UK farmer, Mark Purdey. He suggests that instability of the normal conformation of the normal cellular protein resembling the infective agent (a metallo_protein) may arise when the diet of the animal contains unusually high ratios of manganese relative to copper, leading to a greater likelihood that prions will be formed and the animal will develop a TSE. He claims Mad cow disease and its human equivalent -- risks of infection via the Australian food chains 79 estimates range from 20,000 to 136,000. A new set of predictions due for release shortly, is likely to suggest the deaths for vCJD could exceed 250,000. To date only a few confirmed cases of vCJD have occurred outside the UK. In European countries and elsewhere, the situation is even less clear than in Britain, but it is possible that many countries may unknowingly have imported infected cattle or infected MBM or meat products and may already have BSE infection in both cattle and human food chains. Against this background, the World Health Organisation (WHO 2000) has recently stated: the future potential public health threat of vCJD-- not only in the UK but in Europe and the rest of the world--is alarming, and currently unquantifiable. 1993 that beef was safe to eat, explained to the inquiry that his earlier reassurances that beef was safe to eat `did not mean there was no risk'. His comments, taken at face value, highlight how differently statements and assurances may be interpreted by members of the lay public. At the end of the BSE hearings in 1999, Lord Phillips, the Committee's chairman, said: `It is now for us to prepare a report which identifies what went right and what went wrong and draws attention to the lessons to be learned for the future.' The inquiry presented its report to the government in October 2000 (Phillips 2000). At that time, the BBC website provided the following summary of the Committee's main findings. BSE developed into an epidemic as a result of an intensive farming practice--the recycling of animal protein in ruminant feed. This proved a `recipe for disaster '. Government ministers played down the links between BSE_infected beef and variant Creutzfeldt_Jakob Disease. They also misled the public about [the extent of] the risks posed by mad cow disease. Up to March 1996, most of those responsible for responding to BSE did so with credit, though there were shortcomings. The government was too preoccupied with preventing a panic reaction to BSE and therefore the way in which the risk was communicated to the public was flawed. Although a ban existed in 1989 to prevent specified bovine offal--brain, spinal cord and other tissue-- entering the human food chain, there was a failure to enforce it properly. A failure to ensure proper communication between government departments meant the Department of Health was not kept informed of the increasing weight of evidence proving a link between BSE and vCJD. Ministers and civil servants failed to develop any contingency plans to cope with a situation where vCJD was found to be caused by BSE_infected beef despite the fact that years had passed since the first evidence of a link had been uncovered. The government relied too much on experts from the spongiform encephalopathy advisory committee (SEAC) to formulate policy and spent too long consulting with experts before implementing advice. A `lack of rigour ' was applied when considering how to turn policy into practice, partly because until early 1996 many believed there was no threat to human life. The Ministry of Agriculture did not favour agriculture producers over consumers. Phillips Report An official inquiry into events leading to the human disease consequences of the BSE epidemic was set up at the end of 1997 by the Blair Government `to establish and review the history of the emer gence and identificatio