NR AQBF
AU Hansen,M.
TI rbGH Approval Could Hasten Spread of BSE
IA http://eagle.westnet.gr/~aesclep/scrapie.htm
PT Artikel
VT
The following material was prepared by Michael Hansen, PhD., from testimony that the Consumer Policy Institute (an affiliate of Consumer's Union) submitted March 31, 1993 to the Veterinary Medicine Advisory Committee of FDA on the subject of potential animal and human health effects of rbGH (recombinant bovine growth hormone) use.
A potential adverse animal and human health hazard that has not yet been considered by the FDA concerns the change in diet associated with rbGH use. Cows receiving rbGH require more energy-dense food than control cows. One major source of energy-dense food are the protein and energy supplements that come from rendering animals. (Indeed, as a CVM official states in a 1991 memo: "There is a growing trend in the use of meat and bone meal for calf rations... Most is used as a protein source for high production dairy cattle and for feed lot cattle." (Osborne, 1991: 4)). Use of rbGH will increase the amount of rendered protein fed to dairy cows. We are concerned that some of the rendered animals may be contaminated with bovine spongiform encephalopathy (BSE), or a BSE-like disease, and that rbGH will accelerate the spread of this disease.
A group of degenerative diseases affecting the central nervous system - particularly the brain, called transmissible spongiform encephalopathies, occurs in both human and animals. These diseases have been shown to be transmissible, in part, by eating the meat of infected animals. The group of diseases gets its technical name from the fact that the brains of infected animals develop holes filled with tangled protein fibrils. These diseases have disturbing attributes: long incubation period, invariably fatal, as yet unknown infective agents that are unusually resistant to most forms of sterilization (formaldehyde, 70% alcohol, heat, etc.), and produce no host immune response. A sheep form of the disease, called scrapie, has been known for hundreds of years.
A new form of this disease, known technically as bovine spongiform encephalopathy (BSE) and popularly as "mad cow disease" (because the animals act nervous and aggressive and jump around just before dying), appeared in England in 1985. To date, over 80,000 cows have been diagnosed with the disease in England, with more than 880 new cases a week.
Epidemiological work has shown that the cattle most likely acquired the disease by eating scrapie-infested animal protein feed supplements (primarily meat and bone meal), that the lag time between infection and development of clinical symptoms is between 2-8 years, and that the original infection in Britain probably happened around 2-8 years before the appearance of the first case. Two of the major risk factors that are thought to have contributed to the emergence of the disease are the use of meat and bone meal for up to 4% of the diet of young dairy cows and a change in the rendering process in the early 1980's. In the 1980's, rendering facilities in Britain moved away from the old system of using solvents (such as carbon tetrachloride, hexane, etc.) to extract fat from animal carcasses, followed by heating the mixture to very high temperatures to remove the solvent, and replaced it with a processing step that involves much lower temperatures and no solvents. It has been postulated that the combination of solvents and the high heat killed the infectious agent prior to the start of the early 1980's.
A blue-ribbon panel chaired by Sir Richard Southweed (a famous zoologist and ecologist) released a report in February 1989 (MAFF, 1989) that tried to allay fears by stating that there was no evidence that BSE could infect people, in large part because cows were deemed to be a "dead-end host" for the infection, i.e., they couldn't transmit it to other organisms.
Data reported after the publication of the Southwood report, however, show that cows are not a dead-end host. Mice (Fraser et al., 1988) and pigs (Dawson et al., 1990) experimentally inoculated with BSE developed a spongiform encephalopathy. In 1990, a number of domestic cats (Wyatt et al,. 1990) and zoo animals such as eland (Gibson, 1990), puma, and cheetah (Walton, 1992) developed spongiform encephalopathies, thought to be due to contaminated feed. In 1992, it was reported that BSE had been successfully transferred to marmosets, sheep, and goats (Walton, 1992).
Scientists and government officials tried to stem public panic by saying that there is no evidence that BSE can affect humans. However, as a precautionary measure, feeding of sheep and cow brains and organs to cows and humans was prohibited in England in July 1988, and other European countries where BSE has been confirmed (France, Switzerland, and Ireland). In England, all cows with the disease must be destroyed by incineration, and milk from infected animals is not permitted to be used for human consumption. (The rendering process does not destroy the infective agent.)
Ominously, in a Reuters news report from March 12, 1993, there is a story of an old dairy farmer in England who recently died from Creutzfeldt-Jakob disease (CJD), the human form of spongiform encephalopathy; the farmer had a herd of BSE-infected cattle that had to be destroyed in 1989 and had been drinking milk from the herd for at least seven years. Dr. Fred Shank, Director of FDA's Center for Food Safety and Applied Nutrition, sent a letter on Nov. 9, 1992 to manufacturers of a dietary supplement asking them to look into their sources of sheep and cow neural and glandular material. FDA had received a complaint from a woman who had come down with CJD, and who had taken a dietary supplement that contained bovine tissue (Food Chemical News, 1992).
Although U.S. officials have said that there are no cases of BSE in this country and that the disease is unlikely to occur here, there are some disturbing developments here. As a national average, 14% of all dead cattle are rendered and end up as protein supplements (Marsh 1992).
In 1985, an outbreak of transmissible encephalopathy (called TME for transmissible mink encephalopathy) was discovered in a mink ranch in Setsonville, Wisconsin (Marsh, 1992). The minks' diet consisted of 95% "downer cow" (cows that die prematurely for unknown reasons) and 5% horse meat. The minks received no sheep meat so scrapie can be ruled out as the infectious agent. It appears that cows were the source of the infectious agent. In an experiment, cows inoculated with TME died of a spongiform encephalopathy (Marsh et al., 1991).
An experiment done in Mission, Texas, found that cattle inoculated with tissue from scrapie-infected sheep also develop a spongiform encephalopathy. However, the symptoms of this spongiform encephalopathy differ slightly from BSE in England. First, rather than exhibiting "mad cow" symptoms, these animal simply keel over and die. This symptomatology (apparently healthy looking cows simply dropping dead) is known as "downer cow disease" and is thought due to a number of causes. Second, the brain lesions seen in the Texas experiment are more variable than those seen in England, yet the animals definitely have spongiform encephalopathy. Both the behavioral and morphological traits associated with spongiform encephalopathy in the U.S. would make it much harder to detect. Thus, it appears that a different strain of BSE than the one in England, or a BSE-like disease, could be in some unknown portion of the 100,000 cows that die annually from "downer cow disease" in the United States (Marsh, 1992).
The government has set up a BSE surveillance plan and has looked at some 459 cases of cows that died; none of them were confirmed BSE cases (Walton, 1992). This is not completely reassuring, however, because the surveillance program has a potential flaw; the only two risk categories of cows sampled are rabies-suspect cattle that are rabies negative, and cattle over two years of age that have been given protein supplements for a good part of their diet and have developed signs of neurological disease. Given Marsh's work and the work in Texas, it is possible that the USDA is looking at the wrong population of cows; they need to be sampling "downer cows." Since rendering does not appear to destroy the transmissible agent, and given the fact that authorities are only on the lookout for cows exhibiting "mad cow"-like behavior, the agent causing the spongiform encephalopathy may be spreading through the use of rendered ruminant protein.
In conclusion, at a minimum, we believe the feeding of cows to cows should be discontinued not expanded. We urge the Committee to recommend that rbGH not be approved on the grounds that it may promote dissemination of BSE, or a BSE-like disease, because cows given rbGH require high-protein feed. We urge Monsanto, on moral grounds, not to sell this product for the same reason. If the moral argument isn't persuasive, perhaps an economic argument would be. Monsanto should consider the possibility that they could be held liable if use of their product increases the risk of a cow contracting BSE. We note that in England, indemnification costs, paid to farmers, are running at 1 million pounds a week (Brown, 1993).
REFERENCES
Brown, D. 1993. "Farm Death Linked to Mad Cow Disease." The Weekly Telegraph, London UK, Issue 88, March 21, 1993.
Dawson, M., Wells, G.A.H., Parker, B.N.J. and A.C. Scott. 1990. "Primary parenteral transmission of bovine spongiform encephalopathy to the pig". Veterinary Record, pg. 338.
Food Chemical News, 1992. "Supplement manufacturers alerted to BSE concerns by FDA". Nov. 16, 1992.
Fraser, H., McConnell, I., Wells, G.A., and M. Dawson. 1988. "Transmission of bovine spongiform encephalopathy to mice." Veterinary Record, 123(18):472.
Gibson, P.H. 1990. "Spongiform encephalopathy in an eland." Veterinary Record, 189:
MAFF (Ministry of Agriculture, Fisheries and Forestry). 1989. "Report of the Working Party on Bovine Spongiform Encephalopathy (the Southweood Report)." MAFF, England, 3 February, 1989.
Marsh, R.F. 1992, "Transmissible mink encephalopathy, scrapie and dower cow disease: potential linkss." Paper presented at the Third International Workshop on Bovine Spongiform Encephalopathy, Bethesda, Maryland, December 9-10.
Bessen, R.A., Lehmann, S. and G.R. Hartsough. 1991. "Epidemiological and experimental studies on a new incident of transmissible mink encephalopathy." Journal of Genetics and Virology, 72: 589-594.
Osborne, C. 1991. Memo entitled "Bovine Spongiform Encephalopathy: CVM Options for Control and Prevention," dated July 3, 1991. 7pp
Walton, T.E. 1992. Report/memo on the scapie/bovine spongiform encephalopathy (S/BSE) Consultants Group Meeting, June 22, 1992, Ames, Iowa. 4pp.
Wyatt, J.M., Pearson, G.R., Smerdon, T., Gruffydd-Jones, T.J., and G.A.H. Wells. 1990. Veterinary Record, 109:513.
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