The competitive advantage is short-lived after standing 18 h, freshly shed V. cholerae greatly out-competes bacteria grown in vitro, by as much as 700-fold. Laboratory experiments demonstrate that when inoculated into the intestines of mice via gavage feeding, freshly shed V. cholerae O1 Inaba El Tor through the human host appears to transiently increase the infectivity of V. cholerae ID 50 depends upon the length of time the pathogen has existed outside the host. In this context, recent experimental observations suggest that the V. cholerae relative to the ID 50 is key to understanding the intensity of cholera transmission. When challenged with a small fraction of the ID 50, transmission will develop less rapidly, be less intense, and the outbreak will develop less rapidly. When individuals in a population are challenged with a dose many times larger than the ID 50 (the infectious dose sufficient to produce frank disease in 50% of those exposed), the majority will be very likely to develop disease an “explosive” epidemic will result. cholerae are thought to be in the range of 10 2–10 3 cells. The existence of such a dose-response relation (though typically difficult to measure) implies that the ability to infect a host is a key determinant of disease. In volunteer studies, the frequency and severity of cholera has been correlated with inoculum. “Epidemic” strains colonize the small intestine and elaborate an enterotoxin (cholera toxin), which stimulates water and electrolyte secretion by intestinal endothelial cells and leads to massive fluid loss and profuse diarrhea. cholerae, epidemic disease has been linked almost exclusively with serogroups O1 and O139. Among more than 200 documented serogroups of V. Epidemic cholera is characteristically explosive in nature when introduced into populations lacking prior immunity to the organism, spread through the population is measured in weeks, and involves all age groups. It may also afford us insight into new prevention, intervention, and control strategies to limit or prevent cholera transmission. In epidemic situations, a fundamental question regarding the epidemiology of cholera is: what is the relative importance of human-to-human (i.e., fecal-oral) versus environment-to-human transmission (i.e., exposure to the environmental reservoir of Vibrio cholerae)? Answering this question may allow us to predict the onset, and potentially the intensity, of epidemics in endemic regions, as well as the speed and intensity of spread of cholera as it emerges in naïve regions. The risk factors for cholera are varied and stem from multiple transmission pathways, including direct person-to-person contact and indirect transmission through the environment (e.g., food and water contamination). A complex web of interactions between the human host, pathogen, and environment are associated with the seasonal epidemics of cholera seen in endemic regions. While advances in medicine and public health have vanquished many pandemic diseases, 52 nations reported 142,311 cholera cases and 4,564 deaths in 2002, though these statistics are thought to represent a small subset of actual cases and deaths globally due to poor surveillance and under-reporting.
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