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Description
The world-wide panic occasioned by outbreaks of BSE was (and is) incommensurate with the number of human fatalities incurred. This apparent over-reaction can in part be accounted for by BSEs simultaneous disruption of cherished "boundaries" between those categories (civilization and savagery; cannibalism and carnivory; human and animal) upon which our human self-definition depends.
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Although the title of this paper invokes a disease of sheep as well as cattle, my primary concern is with the outbreak of another illness whose history in animal (and human) populations is more cryptic and more recent: so-called "mad cow" disease, or BSE (Bovine Spongiform Encephalopathy). Both the 2001 foot and mouth scourge in Britain and "mad cow" disease were (and are) widely represented in the media as disasters or catastrophes, in the case of foot and mouth for the sheep industry, and BSE for Britain's beef producers. The detection of a single cow with BSE on a Washington (US) farm in 2004 had major financial repercussions for Canada's farmers when the United States banned imports of Canadian cattle and meat products allegedly to protect its herds (and humans) from BSE and new variant Creutzfeldt-Jacob disease. (1) The animals (especially sheep) caught up in the foot and mouth outbreak in Britain were slaughtered and then burnt in huge pyres, a holocaust similar to that following the mass killing of over a million cattle in Britain in 1987. The sheep were destroyed for three reasons. The primary reason was to stop the spread of the disease. Second, although the animals suffer greatly from the symptoms, the majority recover; but affected animals become unsaleable due to loss of condition, and costs incurred in treatment and in waiting for their recovery outweigh, for the farmers, the alternative of replacing stocks. Third, the sheep were slaughtered because public perception had confused "foot and mouth" with the very different "mad cow" disease.
Because of the hypothesized connection between protein feed (derived from both sheep and cows) and the outbreak of Bovine Spongiform Encephalopathy (BSE) in cattle (and its equivalent, "new variant Creutzfeldt-Jacob Disease" [vCJD or nvCJD] in humans), consumers in Britain and elsewhere had become overly wary of the possible dangers of eating meat. Members of the public surveyed "felt" there was "some connection," however vaguely understood, between both animal illnesses: Human carnivores could no longer be sure their meat was "safe" (Fiddes). Public confidence had also been eroded in 2000 over the re-cycled chicken meat scandal, where chicken legs and breasts past their "use-by" dates had been pressure-hosed, treated with preservatives and painted with glycerin to be re-dated and re-placed in supermarket freezers. While the latter did not involve animal disease, and two out of three of these meat scares were the results of capitalist greed rather than any apparently "natural" animal contagion, the public were frightened and dismayed at the possibility of contracting a fatal disease from the flesh of animals traditionally a part of their diet.
Although this discussion focuses on BSE and its human counterpart, nvCJD, its broader subject is the way in which the so-called "mad cow" outbreak, from the 1980s to the present, posed (and poses) a threat less to our brains (in the disease's lethal spongification of the cerebellar region), than to our identity as "civilized" humans (rather than "savages" or "animals") and to our anthropocentric being-in-the-world. Through BSE/nvCJD's apparent transgressions of two closely guarded "boundaries"--that between humans and other animal species, and that between the "savage" and the "civilized" as articulated through what Peter Hulme has termed the "cannibal complex" (31)--nvCJD generated world-wide panic far in excess of the number of deaths it actually caused in human populations. Fewer than two hundred human deaths have so far been attributed to nvCJD, and though there were predictions of millions to follow (the protein prion that causes the disease is a slow acting one) no such pandemic has materialized nor seems likely to do so.
Since nvCJD has complex connections with other Transmissible Spongiform Encephalopathies (TSEs), it is necessary to include a brief preliminary sketch of the relationship between the various forms of Creutzfeldt-Jacob Disease itself. One of the most widely disseminated non-medical accounts of CJD is Jennifer Cooke's 1998 Cannibals, Cows and the CJD Catastrophe. (2) As Cooke explains, medical researchers Creutzfeldt and Jacob, between 1913 and 1921, isolated a particular form of dementia in some human patients whose pre-mortem symptoms included ataxia (staggering). Post-mortem examination of the brain revealed extensive destruction of the cerebellum. The cases investigated by Creutzfeldt and Jacob were of what is now known as "Sporadic CJD" and they occurred--without apparent cause--mostly in elderly patients. Occasionally (though not necessarily), such sporadic cases came to be linked to another very similar CJD, "Familial CJD." Symptoms and post-mortem appearance of the brain in both were the same, but in the latter the causal agent of the disease appeared to be, at least in part, heritable. Such an apparent genetic predisposition sometimes seemed to connect Familial CJD with yet another grouping, "Cluster CJD." The precise catalyst(s) for such cluster occurrences, in, for instance, a particular region of Czechoslovakia and amongst some Sephardic Jewish populations, has/have never been determined. While there may be a genetic proclivity, another agent--suggestions range from metal contamination to pine-needle tea or the eating of sheeps' eyeballs--is involved in the disease's manifestation (Cooke 210-19).
But Sporadic, Familial, and Cluster CJDs differ from both nvCJD and BSE in their order of symptom expression. While in the former group dementia generally precedes ataxia, in nvCJD and BSE, ataxia (staggering) is usually one of the first symptoms. All, however, are fatal. Though there has been some speculation--beyond genetics--that both Sporodic and Cluster CJD may be related to the ingestion of animate or inanimate material, there is no longer any doubt that, whether or not a heritable predisposition is also involved, nvCJD and BSE are caused by an infective agent (originally thought to be a slow virus, but now recognized as a protein prion) that is passed from one animal (whether "cow" or "man") to another through a passage of cellular material by ingestion, injection, or transplant. Jennifer Cooke's book is concerned primarily with nvCJD accidentally caused in recipients of human pituitary-derived hormone taken as a course of injections to induce fertility, increase growth in small-statured children, and more recently by athletes to improve performance. The infective prion in all forms of CJD (including nvCJD) is concentrated in the brain and spinal cord, though it can be... |
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