Epidemiology term paper

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�By the 1970s, the Fore sorcery beliefs remained intact, perhaps strengthened by a decade of inquisition and self-reflection. An etymology that placed responsibility for death in the hands of Fore sorcerers was an assertion of Fore authority over their own affairs during an era of waning autonomy, particularly in face of an alternate paradigm proposed by foreign kuru investigators and a colonial administration. As indicated, however, Fore paradigms were not unchanging. During the 1950s and 1960s the projective sorcery count had risen even as the zones of safety contracted. End causation, once the mark of capricious spirits, now accounted for major afflictions which were the work of malevolent enemies, possibly located within the parish. The identification of close-range sorcery fears contributed to and also registered the disintegration of former kin communities. The taxonomic shift whereby tokabu killers (not projective sorcerers) began to account for a larger burden of sudden illness and death provides evidence of an explanatory system increasingly distanced from a theory in which the Fore assert their own sense of control. Tokabu killers are the "unknowable." As killers for hire, they operate now at distances beyond the social epidemiology of political and personal contest. In contrast to the symptoms of projective sorcery which can be "read" (with some slippage) for their clinical and diagnostic social contents, tokabu is a grab-bag category rather than a uniquely perceived condition. The symptoms of the victims of tokabu are notably vague. Beyond control or therapeutic intervention, tokabu killers appear more demonic, more superhuman, than detectable, enemy sorcerers. If the identification of projective sorcery shows the Fore analyzing changing social, political, and epidemiological conditions with some authority, the designation of tokabu deaths tells a less confident story.�
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�Host resistance does not eliminate the agent, however. Because of the greater natural resistance, prevalence may actually increase. The virulence of the agent decreases, and infections become milder (sub clinical). The deaths that do occur are less sudden, so the length of time between onset of disease and death increases. This gives the micro organism a better chance to reproduce and, along with its progeny, to move to other hosts (via air, water, food, vector, touch, or blood exchange, depending on the agent's mode of transmission). In this way the micro organism continues to survive and infect hosts as the resistance of the host population increases (Burnet and White, 1972:82, 84, 163). Therefore, in the natural history model of infectious disease, a disease starts with a few deaths, evolves to an epidemic stage in which there are many deaths, and then moves to an endemic stage in which the death rate is much lower, though it may still be high ( Dubos and Dubos, 1987:187). The progress of the disease resembles a bell-shaped curve, following the principle of Farr's law. In the endemic stage (the right portion of the curve), much of the population beyond childhood has been infected and thus naturally immunized, and it is among children that morbidity and mortality are usually high. For this reason endemic infectious diseases are frequently referred to as childhood diseases. Then as effective vaccines are developed, the diseases become rare and, as with smallpox, may disappear.�
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�Influenza is spread from person to person by coughs and sneezes, but the virus doesn't begin its journey in a human host. Instead, wild aquatic birds such as ducks and shore birds perpetuate the influenza viruses that cause human pandemics. Although these birds carry the genes for influenza in their intestines, they usually don't become sick from the virus. And because they can migrate thousands of miles, the healthy birds can spread the virus across the globe even before the microbe makes contact with the human population.

As it happens, the form of the virus found in wild birds doesn't replicate well in human beings, and so it must first move to an intermediate host--usually domestic fowl or swine--that drinks water contaminated by the feces of aquatic birds. Horses, whales, seals and mink are also periodically infected with influenza. Although the intermediate hosts can sicken and die from the infection, swine can live long enough to serve as "mixing vessels" for the genes of avian, porcine and human forms of influenza. This occurs because swine have receptors for both avian viruses and human viruses.
Swine have probably played an important role in the history of the human disease. These animals appear to serve as living laboratories where the avian and mammalian influenza viruses can come together and share their genes (a reassortment of RNA segments) and create new strains of flu. When a strain of virus migrates into the human population, it changes into a disease-causing microbe that replicates in the respiratory tract. A sneeze or a cough spreads the virus in a contagious aerosol mist that is rich in virus particles. Most pandemics originate in China, where birds, pigs and people live in close proximity. Hong Kong's 1997 "bird flu" was an avian influenza virus that probably attained virulence through reassortment of genes from geese, quail and teal. Many bird species were housed together in the Hong Kong poultry markets, and this was an ideal environment for reassortment.�
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