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Mad Cow Disease: A Manmade Pandemic Set to Put AIDS in the Shade

Mad Cow Disease: A Manmade Pandemic Set to Put AIDS in the Shade

Summer, 2001 The Touchstone (Texas A & M University) Vol. XI, 
No. 3 by Lynette J. Dumble
Background

Since the 1996 admission (1) that British cattle suffering from Bovine Spongiform Encephalopathy [BSE or mad cow disease] had introduced the agent of an invariably fatal brain illness [a variant of Creutzfeldt-Jakob disease referred to as vCJD] into the human food chain, BSE has subsequently spread across Europe to cattle in Austria, Belgium, Denmark, France, Germany, Italy, Ireland, Liechtenstein, Luxembourg, the Netherlands, Poland, Portugal, Spain, Switzerland, and as of June 2001 to the Czech Republic. To date, almost 200,000 cattle are known to have contracted BSE. Most were in Britain, where the number exceeds 180,000. Another five million cattle aged less than 30 months and without physical signs of BSE have been slaughtered in pre-emptive measures to safeguard public health.

Since the initial ten cases of vCJD were linked to BSE-infected beef in 1996, another 90 human lives were lost to the disease by February 2001, the vast majority being permanent or temporary residents of Britain. Estimates of the anticipated number of human deaths as a result of BSE vary considerably, but at the completion of the Lord Phillips Inquiry, the Blair Administration warned that the figure could reach 250,000 (2). Almost double the previous estimate of 136,000 vCJD deaths, the November 2000 announcement gave notice that UK authorities were working with the "worst case scenario" of one in every 250 people in Britain contracting the disease. In the words of microbiologist Dr. Stephen Dealler, "At the moment the number of cases of CJD we are seeing are doubling every year. If they double for a long time then the numbers are in millions, if they double for just a few years then the numbers are in thousands. At the moment it is very difficult to know." Scrapie, the sheep equivalent of brain illnesses like BSE in cattle and CJD in humans, has been around for more than two centuries. Human spongiform encephalopathy, or CJD, is, however, a disease of the twentieth century, reported independently by two German physicians, Creutzfeldt and Jakob, for the first time in the 1920s. BSE is also a disease of the twentieth century, unheard of until 1985.

The agent of spongiform encephalopathies incubates in animals and humans for a prolonged period of time before outward signs of the infection become obvious; in cattle, on average, after 5 years, and in human cases of CJD resulting from human pituitary growth and infertility hormone injections or contaminated surgical materials, after as few as two to as many as 40 years. Once symptoms appear, the agent of BSE/CJD has already turned the brain into the sponge-like mass which first led this group of diseases to be classified as spongiform slow virus disorders. BSE-symptomatic cattle are left confused and trembling, deprived of their own feet to stand on--a furnace their tragic fate. CJD-symptomatic humans also suffer gait problems, and over periods of time, varying from weeks to months to years, are progressively robbed of all dignity, and every means of communication, losing the ability to hear, see, speak, and comprehend either written or spoken native language. Unlike sporadic CJD which has a natural incidence of less than one per million, and generally claims victims who are in their sixties or seventies, BSE-related CJD was initially anticipated to be a disease which claimed the lives of much younger victims, teenagers and those in their twenties and thirties. Like numerous other postulates which cloud the BSE catastrophe, this theory fell apart in late 1999 with the vCJD death of a 74 year old man, raising suspicion that the CJD-like symptoms of Alzheimer's disease which account for misdiagnosis in ten per cent of sporadic CJD sufferers, might also account for vCJD escaping recognition in the elderly. The implications of BSE-infected cattle extend far outside the beef which frequents the table of today's predominantly meat-eating society. Rather, a vast array of cattle-derived products, including milk, cream, cheese, health supplements, and gelatin-based confectionery are everyday encounters.

Equally, the public health implications of BSE extend much further than the consumption of BSE-infected materials. Laboratory experiments since the late 1970s have shown that compared with the blood route, the oral pathway is a relatively inefficient means of transmitting these types of diseases from one animal to another (3). Extrapolating from that data, vCJD may ultimately claim fewer men than women since tradition in every world region places more women than men in the kitchen to risk knife injuries with BSE-infected meat. Additionally, BSE-infected beef consumers are possibly living incubators of vCJD. Like asymptomatic carriers of blood-borne infections such as hepatitis and syphilis, asymptomatic carriers of the vCJD agent have the potential to cross infect others via blood transfusion, organ transplants, and surgical instruments. Overall, in the context of an infected food chain, and the likelihood of a contaminated health system, BSE looms as a pandemic that may put HIV/AIDS in the shade (4).

Roots of BSE

The mystery illness now known as BSE first appeared in a British dairy cow in 1985. Within the space of three years, the annual number of BSE-infected cattle rose to 731. By 1989, 400 new cases appeared each week, and by 1992, 100 new cases appeared daily. By the 1990s, animal species other than cattle, but fed on cattle-containing rendered or raw meat and bones, began to die of BSE and CJD-like brain illnesses, including African antelopes, and domestic and captive wild cats.

An "infected fodder" theory maintains that the BSE epidemic emerged from a post-World War II British strategy adopted to increase the milk yield of dairy herds. In brief, cows were fed on protein-enriched pellets extracted from the animal carcasses held in abattoir and boning plants, and from animal leftovers discarded by butchers, restaurants, and knackeries. The carcasses of scrapie-infected sheep, and between the years of 1985 and 1988, those of BSE-infected cattle, found their way into the protein-enriched animal feed which initially turned cattle into carnivores, and, ultimately into cannibals.

Overall, Britain's rendering plants were part of a huge industry which supplied animal feed to livestock and pet owners, and to zoos for a number of animal species held in captivity. In the early days, the carcasses were boiled at atmospheric or higher pressure to produce a liquid protein layer under a layer of fat [tallow] which was then dried and marketed as protein-enriched animal fodder. Subsequently, in the late 1970s, the rendering process was deregulated. Cost cutting measures followed, including the omission of fat removing solvents and lowered "cooking" temperatures. Simultaneously, rendering procedures in other countries underwent similar changes, but by the mid 1980s only British cattle were afflicted with BSE, a phenomenon attributed to the large proportion of scrapie-infected sheep within Britain's rendered animal carcasses. The report from the government-convened Lord Phillips Inquiry (5) into BSE in Britain claimed that infected fodder the size of a peppercorn could transmit BSE to cattle.

In 1996, Mark Purdey, an organic farmer from Somerset in England, suggested that organophosphate pesticides might be responsible for BSE (6). Three years before the first case of BSE was reported in Kent, British authorities ordered the compulsory spraying of cattle with the organophosphate pesticide phosmet in order to combat a plague of Warble fly. Manufactured by Zeneca, a subdivision of the British chemical giant ICI, phosmet is a neurological toxin originally developed by the Nazis. Related to the infamous birth-defect drug Thalidomide, phosmet was used exclusively in Britain between 1982 and 1990.

Purdey's largely neglected theory argued that the exposure of the bovine embryo to high doses of lipophilic formulations of organophosphates triggers the deformation of cattle prion protein, thereby facilitating the onset of BSE. In addition to investigating clusters of BSE in cattle, Purdey extended his research to clusters of sporadic human CJD, and to the similar chronic wasting disease in deer and elk in the Unites States. His data indicated that high levels of manganese, the metal sprayed in high doses on cattle via organophosphate pest deterrents, was a common factor, and he suggested that, in addition to activating a prion mutation in cattle, excess manganese might also accelerate traditional forms of CJD to explain vCJD victims being several decades more youthful than sporadic victims.

In Europe, the argichemical division of Switzerland's Sandoz leaked tons of organophosphate pesticide into the Rhine in 1986, killing all aquatic life in the river between Basel and the North Sea. It took seven years to revive the river, but it can be argued that Sandoz's spill played a role in the BSE which subsequently afflicted cattle in Switzerland, France and Germany in the late 1990s.

According to Purdey (7), funding for BSE-organophosphate research might never eventuate: "No one's prepared to admit it because it would involve massive compensation. By keeping the causal agent as something mystified, no one's to blame." He could be right. The transnational companies behind the pesticide trade exert considerable political influence, with the giant Syngenta Ag now heading the worldwide distribution of organophosphate pesticides.

Syngenta's rise to become the world number one in agrichemical supplies, number two in seed treatment, and number three in seed supplies has been nothing short of astronomical, and can be traced back to the 1996 merger between the agrichemical divisions of two Basel-based companies, Sandoz and Ciba (8). April 1999 saw the agrichemical divisions of the Swedish Astra AB and the British Zeneca Group PLC merge and give birth to AstraZeneca, but by December 1999 both AstraZeneca, and the Basel-based duo by then known as Novartis, had also merged to form Syngenta. The Novartis-AstraZeneca empire had combined 1998 sales close to US $8 billion, but with its new Syngenta identity has effectively removed the organophosphate faces of Zeneca and Sandoz from public view.

From Cattle to Humans

As the BSE epidemic escalated, so too did concerns about human safety (9). BSE was presumed to have originated from scrapie, a human nonpathogen, but mouse-adapted strains of scrapie were known to adopt an altered host range after passage through hamsters to become transmissible thereafter to rodents (10). Similarly, human strains of kuru or CJD did not transmit to ferrets or goats until passaged through primates or cats (11), as too, a bovine strain of BSE was converted in the laboratory from nontransmissible to transmissible to hamsters by passage through mice (12). Nonetheless, measures to eradicate BSE and prevent potentially infected meat from entering the human food chain were slow to commence. It took until July of 1988 for Britain to ban the feeding of rendered fodder to cattle, but, for the best part of the next eight years, authorities insisted that it was absolutely safe to eat British beef. Few will forget the then-Minister for Agriculture, John Gummer, stuffing hamburger into his five year-old daughter's mouth to demonstrate his confidence! But, from the time BSE-like illnesses began to emerge in zoo ungulates, together with domestic and wild cats, it became impossible to ignore the possibility that BSE might also cross the species barrier to humans from the consumption of bovine products, or from the occupational contact of farmers, and dairy and slaughterhouse workers with cattle.

In May 1990, a CJD surveillance unit was established, a move extended 3 years later to Europe, to detect possible changes in British and European CJD epidemiology. In 1995, the Surveillance Unit in Edinburgh was notified of CJD in three victims aged 16, 19, and 29 years. The British cases may not have been the first BSE-related deaths in humans, since five years earlier, three cases of CJD in young patients had been reported in Poland (13). The neuropathology of all three British cases revealed extensive amyloid plaques, a feature which occurs in only five to ten per cent of sporadic cases of CJD. By December 1995, the neuropathology of a 29 year old and a 30 year old CJD victim, like the three unusually youthful 1995 cases, revealed an identical picture.

In early 1996, CJD claimed two more youthful victims, both with amyloid plaque neuropathology. A distinctive clinical syndrome had emerged to assist in diagnosing vCJD: young age at onset, early psychiatric symptoms, prominent ataxia, absence of periodic electroencephalographic activity, and a comparatively prolonged illness. Two further vCJD cases were confirmed by the end of February 1996, and a report (14) on ten cases concluded that the novel form CJD was most likely the result of BSE-infected meat. The link between vCJD and BSE was subsequently proven by laboratory studies (15) demonstrating the identical characteristics of the prions isolated from BSE-infected cattle and human cases of vCJD. In between, on March 20,1996, the British Prime Minister John Major publicly admitted that BSE had jumped the species barrier to infect humans, and Britain finally put an end to exporting animal rendered fodder.

Laboratory evidence indicates that, rather than being present within beef muscle, the agent of BSE finds its way into the human food chain via beef products which are contaminated by nervous system tissue. This can occur by way of the cranial stunning instruments used to immobilize cattle before they are slaughtered; or from paraspinal ganglia within cuts of meat like T-bone steak; or from residual spinal cord and paraspinal ganglia within mechanically recovered meat pastes which, in the pre-BSE era, were added to steak pies, sausages, and various types of canned beef.

Until December 2000, with the exception of three cases in France, all vCJD victims had lived in or visited the UK. None was vegetarian. British beef could well be the source of vCJD in the French cases too since approximately ten per cent of France's beef for human consumption is imported from the UK, as too is a significant proportion of beef consumed across mainland Europe. Given the vast number of nationals and tourists exposed to Britain's BSE-suspect meat, and the possibility that vast numbers are silently incubating the disease, the potential for human-to-human transmission via blood and organ donation, and surgical instruments, looms as a major public health threat.

In the late 1970s, Laura and the late Eli Manuelidis, and their colleagues from Yale University in the United States illustrated that injections of human blood taken from CJD victims had the capacity to transmit CJD across the species barrier to laboratory animals (16). The implications of the Yale experiment evaded authorities for the better part of the 1990s, though Canadian (17) and New Zealand (18) authorities spent millions of dollars in 1995 and 1996 respectively to withdraw pooled plasma containing a donation from a CJD victim.

The years-long incubation time preceding CJD symptoms increases the difficulty to link a blood transfusion recipient's CJD with a donor source. It is even possible that secondary CJD in a transfusion recipient may appear months or even years in advance of the primary CJD in a blood donor, as happened in the case of CJD in a liver transplant recipient which was eventually traced back to a CJD-like illness in one of the blood donors (19). In the UK whole blood or blood products from donors who have later died of vCJD has already been administered to a considerable number of recipients. Britain now imports all plasma for transfusion purposes, and all blood from UK donors is filtered to remove the white blood cells which are the most likely carriers of vCJD infectivity. A number of other countries, including Australia, Canada, Germany, Japan, New Zealand, Switzerland, and the United States, now exclude blood donations from any who have resided in Britain for 6 months or more during 1980 to 1996. Similar policies are pending with respect to organ donation, and in Britain, regarding the reuse of surgical instruments, particularly those used in neurologic and ophthalmic procedures.

From Britain to Europe And Further

In 1989, one year after banning rendered cattle fodder, UK authorities reassured national and international audiences that the BSE epidemic was under control, but simultaneously summoned world experts to a meeting seeking advice. Unwittingly, the solutions put forward by the experts shaped the events which have effectively spread BSE across the globe. All were sworn to secrecy, notably regarding the risk attached to Britain's global trade in cattle and rendered animal fodder. One, Laura Manuelidis, physician and professor of neuroscience at Yale University, proposed that the epidemic could be brought to a close with the immediate cull of infected herds (20). Britain's attitude to the Manuelidis solution was, in her words, penny-wise, pound-foolish, and her idea was dismissed on the grounds that compensation for the owners of the herds was financially out of the question. From then onwards, the global spread of mad cow disease went into full swing. Britons were placed at further risk of vCJD when an estimated 700,000 BSE-infected cattle entered their food chain, chiefly because the animals' slaughter age, usually three years, was below the age at which they would show signs of BSE infection (21).

Next, the duplicity of the British Ministry of Agriculture, Fisheries and Food [MAFF] exposed mainland Europeans to an unknown quantity of BSE-contaminated veal among the two million calves transported to European saleyards between 1990 and 1995 (22). MAFF also sabotaged a 1990 Brussels ruling designed to prevent the spread of BSE outside Britain when it issued civil servants with secret orders to skip the computer vetting of calves which was intended to identify BSE-infected animals.

Between the years of 1988 and 1992, the European market for Britain's animal protein-enriched fodder evaporated. To fill the gap, a new apartheid was adopted (23) with Prosper de Mulder, Britain's largest rendering company, exporting 80,000 tons of BSE-suspect fodder over the next four years to chiefly Third World countries, Indonesia, Israel, Japan, Kenya, Lebanon, Malta, Saudi Arabia, Singapore, South Korea, Sri Lanka, Taiwan and Thailand. Other European countries followed suit, with Belgium, the Netherlands, and France offloading their stockpiles of animal fodder imported from Britain into the Middle East and North Africa.

Britain did not act alone in globalizing BSE. In September, 1996, it was revealed that a memorandum from France's Gilbert Castille suggested back in 1990 that Britain "would be better to minimize BSE [panic] by practicing disinformation." Rather than ganging up on Britain, Brussels via Guy Legras, head of the European Commission's agricultural directorate, warned of the financial repercussions from a beef panic and hushed news of the BSE implications (24).

Britain's defense today is that her agricultural and public health authorities had debated the propriety of allowing the country's rendering industry to continue exporting meat-and-bone meal which was taboo at home. In the end, the decision was left to veterinary authorities in the importing countries, the argument being that those officials had been adequately informed of the risks!

In the thirst for greater and greater market profits through hybrid strains, between 1988 and 1996, Britain also exported 3.2 million live cattle to 36 countries, representing every world region. Claimed to be "BSE free," over the years these cattle have spread BSE not only to mainland Europe, but also to Canada, the Falkland Islands and Oman. Several other European countries also exported millions of live cattle worldwide, and in December 2000, Kuwait reported a BSE case in a three-year-old dairy cow imported from the European mainland.

Ultimately, the dumping of BSE-implicated produce, considered unfit for sale in Britain and Europe, is another shameful chapter of anti-Third World imperialism. The French Minister for Agriculture, Jean Glavany, recently pointed the finger at Britain saying that "morally, they should be judged for that one day. They even allowed themselves the luxury of banning the use of such feed [in Britain] while allowing it to be exported." But while mainland Europe takes the high moral ground on the globalization of BSE, a number of European countries continued to ship tons of their own BSE-suspect animal fodder to developing regions until January 2000 (25).

Already there are reports of vCJD-like illnesses in India, Hong Kong, Korea, Pakistan, South Africa, Thailand and the French Caribbean. One thing is certain, as the WHO and Professor Manuelidis have recently underlined, the social and environmental impact of BSE-infected herds and food chains in developing regions may be far more tragic than that presently bemoaned in Europe.

Authorities in Australia, like those in the United States, claim to have imported little or no live cattle, beef products, or livestock nutritional supplements, from the UK, and boast not to be at risk of BSE. History may well tell otherwise.

A wartime mentality of panic buying has taken over in the face of Britain's current meat shortage, but there are lessons aplenty stemming from the man-made BSE pandemic, not the least the price for placing profit ahead of animal integrity and public welfare.

By and large, it may prove irrelevant whether organophosphate pesticides, or scrapie/BSE-infected animal feed triggered the BSE pandemic in cattle because both have been spread to the four corners of the globe with gay abandon. Should organophosphates be the culprit, it remains a matter of time before BSE outbreaks resembling that in Britain occur worldwide. Should the protein-enriched animal feed be the culprit, Britain's rendering economy has practically made certain that no region will escape.

Endnotes

1. Webster, P., Laurence, J. New infection linked to mad cow disease. The Times [U.K.] March 21, 1996.
2. Hyland, Julie. British government warns variant CJD deaths may rise to 250,000. World Socialist Web Site, November 3, 2000. http//www.wsws.org/articles/2000/nov2000/bse-n03.shtml
3. Manuelidis, Laura [Personal communication, Yale University, November 26, 1993].
4. Dumble, Lynette. J. Approaching pandemic is Britain's shame. Sydney Morning Herald January 17, 2001.
5. The BSE inquiry Lord Phillips of Worth Matravers, Chairman. London The Stationery Office. October 26, 2000.
6. Purdey, M. The UK epidemic of BSE slow virus or chronic pesticide-initiated modification of the prion protein? Part 2 An epidemiological perspective. Medical Hypotheses. 1996 46; 445-454.
7. Piper, Elizabeth. INTERVIEW-Could the scientists be wrong on mad cow disease? Reuters February 1, 2001.
8. Dumble, Lynette J. Feeding the world via biotechnology A failed neo-Malthusian ploy? Proceedings of 8th International Women In Leadership Conference, Edith Cowan University, Western Australia, November 1999.
9. Editorial. BSE and scrapie agents for change. Lancet 1988 2; 607-8.
10. Kimberlin, R.H., Cole, S., Walker, C.A. Temporary and permanent modifications to a single strain of mouse scrapie on transmission to rats and hamsters. Journal General Virology 1987 68; 1875-81.
11. Gibbs, C.J., Gajdusek, D.C. and Amyx H. Strain variation in the viruses of Creutzfeldt-Jakob disease and kuru. In: Slow Transmissible Diseases of the Nervous System. Volume 2. Academic Press; 1979. p. 87-110.
12. Foster, J.D., Hope, J., McConnell, I. et al. Transmission of bovine spongiform encephalopathy to sheep, goats, and mice. Annals New York Academy of Sciences. 1994 724; 300-3.
13. Kulczycki, J., Jedrzejowska, H., Gajkowski, K. et al. Creutzfeldt-Jakob disease in young people. European Journal of Epidemiology 1991 5; 501-4.
14. Will, R.G., Ironside, J.W., Zeidler, M. et al. A new variant of Creutzfeldt-Jakob disease in the UK. Lancet 1996 347; 921-5.
15. Collinge, J., Sidle, K.C., Heads, J. et al. Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD. Nature 1996; 383 685-90.
16. Manuelidis, E.E., Gorgacz, E.J. and Manuelidis, Laura. Viremia in experimental Creutzfeldt-Jakob disease. Science 1978; 200 1069-1071.
17. Picard, Anne. Blood withdrawal to cost $15 million. Toronto Globe and Mail, September 5, 1995.
18. Slinger, Sonja. Suspect blood product withdrawn. The Daily News [New Zealand], May 11, 1996.
19. Creange, A., Gray, F., Cesaro, P. et al. Creutzfeldt-Jakob disease after liver transplantation. Annals Neurology 1995 38; 269-271.
20. Manuelidis, Laura. Penny Wise, Pound Foolish--A Retrospective. Science 2000: 290; 2257.
21. Radford, Tim. 700,000 BSE cattle 'fed to humans'. Guardian Weekly, September 8, 1996.
22. Hooper, John. Britain evaded BSE checks for Europe. Guardian Weekly, September 1, 1996.
23. Shiva, Vandana. The New Apartheid - Contaminated beef for the South. In: Stolen Harvest: The Hijacking of the Global Food Supply South End Press, Cambridge, MA 2000, and Zed Books, London 2001, page 65.
24. Bates, Stephen. EU hushed up BSE scandal for five years. Guardian Weekly, September 8, 1996.
25. Stecklow, Steve. U.K.'s exports may have expanded the boundaries of mad cow disease. Wall Street Journal, January 23, 2001.

[This article is a revised version of an article that appeared in Nexus New Times, Volume 8, No. 3, April-May 2001 on pages 11-14. Dr. Lynette J. Dumble is a medical and environmental scientist and the international coordinator of the Global Sisterhood Network. She is a former professor of surgery at the University of Texas in Houston, and senior research fellow in history and philosophy of science at the University of Melbourne. She can be contacted by email at ljdumble@connexus.net.au.]


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