BIOLOGY OF THE BLACK PLAGUE

The cause of the plague was finally discovered by the medical community in the 1890s. As a result of the then new germ theory of disease, researchers found that the bubonic plague was in fact caused by a massive infection by the bacterium Yersinia Pestis. Only with this discovery, it became possible to synthesize antibiotic medicines that could counteract the bacteria.

The bacillus, Y. Pestis, is normally found living as a parasite within the bodies of rats. There, the bacteria can multiply, infecting the bloodstream, organs and other systems of the rodent hosts. Fleas living on these rats ingest infected blood when they feed, thus themselves becoming infected by the bacteria. Normally, the fleas live only on the rats, but the plague takes its toll on rats just as on humans so that soon the rat hosts themselves die off. The fleas must find substitute hosts and, largely because of the general proximity of rats and humans, the fleas soon begin to migrate to human hosts. Infection takes place when the fleas begin to feed on human blood and spit bacteria into the human host.

This type of infection leads to the type of plague called "bubonic". The bacteria begin to multiply within the infected person's bloodstream, the linings of blood vessels, and lung tissues. As a result, an infected person will often get discoloration of their skin caused by the hemorrhaging of capillaries. As a result, their skin may have a mottled appearance that looks like widespread bruising. The bacteria also begin to attack the lymph system. The infection of the lymph nodes in fact gives this form of the plague its name. The lymph nodes attempt to manufacture an appropriate antibody to fight off the infection, and as a result often swell to the size of a walnut or even an apple. The resultant swellings, located in the arm pits, neck, or groin, were called "buboes" by late medieval Europeans. It was commonly this particular symptom that allowed contemporary doctors to detect the presence of this disease. The bubonic form of this disease often proved fatal, but there are records of people recovering their full health after becoming gravely ill.

There are two other forms of this disease, pneumonic and septicemic. The former involves an infection of the lung tissue that causes a fluid build up that eventually causes death. Evidence suggests that a person can contract this form of the disease by inhaling droplets of fluid ejected by an infected person. The pneumonic form appears to have a death rate that approaches one hundred percent. The latter form of this disease, septicaemic, involves such a quick and massive form of infection that death occurs before any of the main symptoms have time to appear. This relatively rare form of the plague may account for contemporary records indicating that a person simply died during plague outbreaks for no apparent reason.

Both types of this disease affected European society in 1347-8 and in later outbreaks. Unfortunately, it is still often difficult to tell which form of the disease was present in some locations and during some plague epidemics. Indeed, evidence suggests that some outbreaks of "plague" were actually epidemics of dysentery, for example, and that several other diseases were conveniently labeled as plague in later epidemics. One clue for detecting the form of disease depends on the time of year in which a particular epidemic hit. Because of temperature and moisture conditions that allow flea populations to thrive, bubonic plague tends to flourish during the summer months while pneumonic plague does so during the winter. The relationship between the form of the plague, the climate, and the geographic location of outbreak is complex however, and definitive biological knowledge of this historical event is difficult to establish.


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Source: George Ouwedndijk and Bill Rednour

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