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!@#$%! · 09.18.2006, 02:24 PM

Infection/transportation

Plague is primarily a disease of rodents, particularly marmots (in which the most virulent strains of plague are primarily found), but also black rats, prairie dogs, chipmunks, squirrels and other similar large rodents. Human infection most often occurs when a person is bitten by a rat flea (Xenopsylla cheopis) that has fed on an infected rodent. The bacteria multiply inside the flea, sticking together to form a plug that blocks its stomach and causes it to become very hungry. The flea then voraciously bites a host and continues to feed, even though it is unable to satisfy its hunger. During the feeding process, blood cannot flow into the blocked stomach, and consequently the flea vomits blood tainted with the bacteria back into the bite wound. The Bubonic plague bacteria then infects a new host, and the flea eventually dies from starvation. Any serious outbreak of plague is usually started by other disease outbreaks, or some other crash in the rodent population. During these outbreaks, infected fleas that have lost their normal hosts seek other sources of blood.
In 1894, two bacteriologists, the French Alexandre Yersin and the Japanese Shibasaburo Kitasato, independently isolated the responsible bacterium in Hong Kong during the Third Pandemic. Though both investigators reported their findings, a series of confusing and contradictory statements by Kitasato eventually led to the acceptance of Yersin as the primary discoverer of the organism. Yersin named it Pasteurella pestis in honour of the Pasteur Institute, where he worked, but in 1967 it was moved to a new genus, renamed Yersinia pestis in honour of Yersin. Yersin also noted that rats were affected by plague not only during plague epidemics but also often preceding such epidemics in humans, and that plague was regarded by many locals as a disease of the rats: villagers in China and India asserted that, when large numbers of rats were found dead, plague outbreaks in people soon followed.
In 1898, the French scientist Paul-Louis Simond (who had also come to China to battle the Third Pandemic) established the rat-flea vector that drives the disease. He had noted that persons who became ill did not have to be in close contact with each other to acquire the disease. In Yunnan, China, inhabitants would flee from their homes as soon as they saw dead rats, and on the island of Formosa (Taiwan), residents considered handling dead rats a risk for developing plague. These observations led him to suspect that the flea might be an intermediary factor in the transmission of plague, since people acquired plague only if they were in contact with recently dead rats, but not affected if they touched rats that had been dead for more than 24 hours. In a now classic experiment, Simond demonstrated how a healthy rat died of plague after infected fleas had jumped to it from a plague-dead rat.

09.18.2006, 02:24 PM	#47
!@#$%! invito al cielo Join Date: Mar 2006 Location: mars attacks Posts: 42,731	Infection/transportation Plague is primarily a disease of rodents, particularly marmots (in which the most virulent strains of plague are primarily found), but also black rats, prairie dogs, chipmunks, squirrels and other similar large rodents. Human infection most often occurs when a person is bitten by a rat flea (Xenopsylla cheopis) that has fed on an infected rodent. The bacteria multiply inside the flea, sticking together to form a plug that blocks its stomach and causes it to become very hungry. The flea then voraciously bites a host and continues to feed, even though it is unable to satisfy its hunger. During the feeding process, blood cannot flow into the blocked stomach, and consequently the flea vomits blood tainted with the bacteria back into the bite wound. The Bubonic plague bacteria then infects a new host, and the flea eventually dies from starvation. Any serious outbreak of plague is usually started by other disease outbreaks, or some other crash in the rodent population. During these outbreaks, infected fleas that have lost their normal hosts seek other sources of blood. In 1894, two bacteriologists, the French Alexandre Yersin and the Japanese Shibasaburo Kitasato, independently isolated the responsible bacterium in Hong Kong during the Third Pandemic. Though both investigators reported their findings, a series of confusing and contradictory statements by Kitasato eventually led to the acceptance of Yersin as the primary discoverer of the organism. Yersin named it Pasteurella pestis in honour of the Pasteur Institute, where he worked, but in 1967 it was moved to a new genus, renamed Yersinia pestis in honour of Yersin. Yersin also noted that rats were affected by plague not only during plague epidemics but also often preceding such epidemics in humans, and that plague was regarded by many locals as a disease of the rats: villagers in China and India asserted that, when large numbers of rats were found dead, plague outbreaks in people soon followed. In 1898, the French scientist Paul-Louis Simond (who had also come to China to battle the Third Pandemic) established the rat-flea vector that drives the disease. He had noted that persons who became ill did not have to be in close contact with each other to acquire the disease. In Yunnan, China, inhabitants would flee from their homes as soon as they saw dead rats, and on the island of Formosa (Taiwan), residents considered handling dead rats a risk for developing plague. These observations led him to suspect that the flea might be an intermediary factor in the transmission of plague, since people acquired plague only if they were in contact with recently dead rats, but not affected if they touched rats that had been dead for more than 24 hours. In a now classic experiment, Simond demonstrated how a healthy rat died of plague after infected fleas had jumped to it from a plague-dead rat.
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