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Lindenbaum. Week10. ANTC68.docx

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University of Toronto Scarborough
Erin Bryce

ANTC68 Week 10 - Lidenbaum 2001 o Past epidemics have left beneficial imprint on social institutions - cholera  public health approach stressing quarantine o First response to epidemic (miasma, contagion) is FLIGHT, diseases carriers = SCAPEGOATS + STIGMATIZED o Epidemics have elicited religious and ritual responses that promised effective action, social upheavals, war, famine, migration, and sometimes pilgrimage o AIDS (1988) forefront of epidemic discussion, until BSE and vCJD were seen o FOCUS of paper: Kuru in Papa New Guinea and bovine spongiform encephalopathy (BSE), BSE which is associated with variant Creutzfeldt-Jakob disease (vCJD – here it is discussed as BSE/vCJD as a single related epidemic) Kuru, BSE (and vCJD) o FIRST BSE case (Britain – 1986) o BSE – new neurological disease in cattle o BSE brain pathology similar to “scrapie” – fatal neurological sheep endemic disease o Scrapie has similar clinical and pathological features of Kuru (fatal neurological disorder of humans in Papa New Guinea) o Kuru and Scrapie – both transmissible by inoculation o Kuru – hereditary disorder determined by a single autosomal gene, dominant in FEMALES but recessive in males o No evidence that Kuru had selective survival advantage, even though it killed off such a high fatal incidence o Chimpanzees injected with brain material from deceased kuru patients had developed a clinical syndrome akin to kuru o Kuru (similar to scrapie) seemed like a viral disease of extraordinarily long incubation transmitted by cannibalism o The 3 diseases – Kuru, BSE, and vCJD were suggested by Prusiner (1982) that their infectivity could be due to prion protein o Prion protein – causes degenerative disorders in humans and animals because prion has altered conformation of a normal cellular protein - it is different from virus or viroids - prions are small protenacious infectious particles that resist inactivation by procedures that modify nucleic acids - UNIQUE because – inherited disorders and yet often transmissible experimentally to laboratory animals & can cause sporadic disease in which neither inheritance nor transmission between individuals is evident o MECHANISM : Prion diseases slowly attack brain tissue, leaving microscopic spongelike holes characterized by accumulations of abnormal forms of prion protein (which naturally occur in brain) & infectious prion accumulates without any clinical signs o PRION DISEASES: - Scrapie (in sheep & goats) - BSE – bovine spongiform encephalopathy – cattle, mink, death of domestic cats and exotic cats in zoos (lions) - CWD – chronic wasting disease – mule deer, elk - Gerstmann-Straussler-Scheinker syndrome (GSS) - Fatal familial insomnia - Creutzfeldt-Jakob disease (CJD) - Kuru – humans o SOCIAL CIRCUMSTANCES of BSE – result of unforeseen dangers with industrialized farming because current theory is that BSE originated from cows with a genetic mutation, & government evaluation/monitoring of beef industry - possible problems in farming practices – cow feed was made of manure that was deprived of copper and doses with manganese (causing prions in brain to be distorted) o Study of Kuru, BSE, vCJD – intersection of genetics, cell biology, and virology and includes human sciences/social circumstances in epidemic study Kuru and Human Affairs o Kuru epidemic follows this plot line (like any other epidemic) for PEOPLE LIVING IN FORE REGION ACT 1 – PROGRESSIVE REVELATION - began in Fore (late 1920s, early 1930s) with emergence of puzzling cases - thought to be a benign shaking disorder ―sowary disease‖, ―negi nagi‖ silly or foolish behavior ACT 2 – AGREEMENT BY DIFFERENT ACTORS ON EXPLANATORY FRAMEWORK - after seeing many victims die uniformly, it was concluded that living sorcerers were to blame and was assigned etiology - called ―kuru‖ – denoting shaking or fear (victim\s tremors) ACT 3 – SENSE OF CRISIS = INIDVIDUAL/COLLECTIVE POLITICAL/RITUAL ACTION - late 1950s and 1960s when epidemic reached its height and the Fore began to speak of a social and moral crisis - sexual bias of kuru mortality = 3:1 (male:female), many men wifeless and no mothers; now large scale investigations being made and ceremonies, society greatly believed it was in danger ACT 4 – GRADUAL SHIFT TOWARDS CLOSURE - 1990s – cases extremely rare and sense of crisis passed (currently ~4 cases/yr), attention in the Fore now focus on development and more pressing matters o Analysis of the kuru epidemic reveals Fore consensus concerning etiology, intervention and therapeutic response (epidemic assumptions and theories are tied to particular social forms) Differences in Kuru PLOT For NON-FORE Observers - - ACT 1: 1953 – government patrol officer noted girl shivering and jerking, and then continued with clinical description of the disease and spatial mapping - ACT 2: transmission of kuru infectious agent to laboratory primates - this evidence showed that no cases of kuru had occurred among people born after the cessation of cannibalism, and this fact strengthened the hypothesis that KURU was a disease transmitted by cannibalism and caused by infectious agent of extremely long incubation - ACT 3: Fore and Non-Fore same complexity – attended ceremonies and funerals and people were beginning to notice the high mortality - ACT 4: 1974- kuru, scrapie and classical Creutzfeldt-Jakob diseases were ―THE SINISTER TRIO‖ belonging to category of transmissible spongiform encephalopathies, nature of infectious agent unknown until 1980 when Prusiner figured out that prion diseases were transmissible o Connection between kuru and cannibalism
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