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first global, dedicated agribusiness company", the Novartis—AstraZeneca empire notched up combined sales in 1998 of close to US$8 billion, and with its new Syngenta identity has effectively removed the organophosphate faces of Zeneca and Sandoz from public view. first global, dedicated agribusiness company", the to humans from the consumption of beef or dairy products or Novartis—AstraZeneca empire notched up combined sales in 1998 from the occupational contact of farmers and dairy and slaughter- of close to US$8 billion, and with its new Syngenta identity has house workers with cattle. effectively removed the organophosphate faces of Zeneca and Additionally, although BSE was presumed to have originated Sandoz from public view. from scrapie, and scrapie was not a human pathogen, mouse- adapted strains of scrapie were known to adopt an altered host - Animal Protein—Enriched Feed range after passage through hamsters, to become transmissible And now to the more popular "infected animal feed" theory, thereafter to rodents.* Similarly, human strains of kuru or CJD one which claims that BSE emerged from the post-World War II did not transmit to ferrets or goats until passaged through primates British strategy adopted to increase the milk yield of dairy herds. or cats,’ as, too, a bovine strain of BSE was converted in the In brief, cows were fed on protein-enriched pellets made from the laboratory from nontransmissible to transmissible to hamsters by meat and bones extracted from the animal carcasses that littered passage through mice." abattoir and boning plants and from the animal leftovers discarded By May 1990, the CJD Surveillance Unit was established, a by butchers, restaurants and knackeries. The carcasses of scrapie- move extended three years later to Europe, to detect possible infected sheep, and, between the years 1985 and 1988, those of changes in British and European CJD epidemiology. In 1995, the BSE-infected cattle, found their way into the protein-enriched ani- unit in Edinburgh was notified of CJD in three victims, aged 16, mal feed which initially turned cattle into carnivores and ulti- 19 and 29 years. The British cases may not have been the first mately into cannibals. BSE-related deaths in humans; five years earlier, three cases of During the rendering process, the carcasses were milled and CJD in young patients had been reported in Poland.'' The neu- then decomposed in large vats by boiling at atmospheric pressure —_ ropathology of all three British cases revealed amyloid plaques, a or higher pressure to produce a liquid protein layer under a layer _—‘ feature which occurs in only five to 10 per cent of sporadic cases of fat (tallow). Once the fat was separated, the protein solution of CJD. By December 1995, the CJD Surveillance Unit had been was dried into a meat and bone meal product. Overall, Britain's informed of 10 suspected cases of CJD in persons under 50 years rendering plants are part of a huge industry that supplied animal of age. Some turned out to have suffered sporadic or familial protein-enriched animal feed to livestock farmers, to pet owners, CJD, others a non-CJD illness, but one case was that of a 29-year- and to zoos for a number of animal old and the other a 30-year-old. species held in captivity. Neuropathology subsequently con- The rendering process was deregu- Pe . firmed that both had suffered CJD lated in the late 1970s when, as a Britain $ rendering plants and, like the three unusually youthful cost-saving measure, fat-removing are part ofa huge industry that 1995 cases, had extensive deposition solvents were dropped from the of amyloid plaques. decomposition menu and the "cook- supplied animal protein-enriched In the first months of 1996, two ing" temperature was lowered. animal feed to livestock farmers, further cases of CJD emerged in During the same era, rendering pro- youthful victims, and both with amy- cedures in other countries also under - to pet owners, and to Zoos for oid plaque neuropathology. By then, went similar changes. i i a distinctive clinical syndrome had Numerous other countries exposed a number of animal species egun to emerge to assist in diagnos- cattle to organophosphate pesticides, held In captivity. ing vCJD: young age at onset, early but only British cattle were afflicted with BSE by the mid-1980s—a phe- nomenon put down to the large pro- psychiatric symptoms, prominent ataxia, absence of periodic electroen- cephalographic activity, and a com- portion of scrapie-infected sheep within the mix of rendered ani- paratively prolonged illness. Two additional vCJD cases were mal carcasses in Britain. Nonetheless, it took until 20 March confirmed by the end of February 1996, and a report” on a total of 1996—the day on which the British Prime Minister John Major 10 cases concluded that an unrecognised variant of CJD, unique at publicly admitted that BSE apparently had jumped the species that time to residents of Britain aged less than 45 years, was prob- barrier from cows to humans—for Britain finally to ban the export ably due to exposure to BSE infection in cattle. of animal meat-and-bone-meal feed. The link between vCJD and BSE was subsequently proved by laboratory studies'* which demonstrated the identical characteris- FROM CATTLE TO HUMANS tics of the pathological agents isolated from BSE-infected cattle As the BSE epidemic escalated from the initial case in Daisy and human cases of vCJD. the dairy cow, so too did concerns about human safety.” By and Laboratory evidence has also indicated that, rather than being large, measures to eradicate BSE and prevent potentially infected present within beef muscle, the agent of BSE finds its way into tissues from reaching the human food chain were slow to com- the human food chain via beef products which are contaminated mence. It was not until July 1988 that Britain banned the practice —_ by nervous system tissue. This could have happened as a result of of feeding cattle with meal containing the ground-up remains of _ the cranium-stunning instruments which are used to immobilise cows, but, for the best part of the next eight years, authorities per- cattle before they are killed by exsanguination; or from the inclu- sisted with assurances that it was absolutely safe to eat British sion of paraspinal ganglia in cuts of meat, e.g., in T-bone steak; or beef. Few will forget the then Minister for Agriculture, John from the presence of residual spinal cord and paraspinal ganglia Gummer, stuffing a hamburger into his five-year-old daughter's tissue in the paste of mechanically recovered meat which, in the mouth to demonstrate his confidence! pre—mad cow disease era, was added to cooked meat products like But, from the time BSE-like illnesses began to emerge in zoo meat pies, beef sausages and a number of canned meat products. ungulates and domestic and wild cats, it became impossible to Up until December 2000, all vCJD victims, with the exception ignore the possibility that BSE might also cross the species barrier of three cases in France, had lived in or visited the UK, indicating to pet owners, and to zoos for , a number of animal species held in captivity. FROM CATTLE TO HUMANS As the BSE epidemic escalated from the initial case in Daisy the dairy cow, so too did concerns about human safety.” By and large, measures to eradicate BSE and prevent potentially infected tissues from reaching the human food chain were slow to com- mence. It was not until July 1988 that Britain banned the practice of feeding cattle with meal containing the ground-up remains of cows, but, for the best part of the next eight years, authorities per- sisted with assurances that it was absolutely safe to eat British beef. Few will forget the then Minister for Agriculture, John Gummer, stuffing a 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 and domestic and wild cats, it became impossible to ignore the possibility that BSE might also cross the species barrier APRIL — MAY 2001 NEXUS = 13 www.nexusmagazine.com