The Opposing Thumb

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Becoming the Plague

Readers may be surprised to learn that the Bubonic Plague, aka The Black Death, is still around. Up to 2000 cases a year are reported to the World Health Organization. Most cases currently occur in Africa (32 people died in a 2013 outbreak in Madagascar), but Los Angeles suffered a Plague outbreak as late as 1924. Untreated, the plague has a fatality rate of over 50%. In the 5-year period from 1347 to 1351, it fanned out from the Caspian Sea to kill between a third and half of Europe’s population. The Plague is spread by fleas that feed on infected rodents, and can transmit the disease to humans by biting.

Bubonic plague gets it name from the swollen lymph nodes it causes, particularly in the armpits and groin- boubon being the Greek for groin. The disease is caused by the Gram-negative bacteria Yersinia pestis, a recently evolved relative of the older and less virulent Yersinia pseudotuberculosis. Sequencing of ancient DNA extracted from corpses in medieval plague pits in London and throughout Europe confirms that the pathogen, first identified in 1894, was indeed responsible for the plague of the Middle Ages (and the attendant positive effects). Yi-Cheng Sun and colleagues in the journal Cell Host&Microbe  retrace the evolutionary path that may have led to Y pestis‘ extraordinary lethality. They propose that the fatal transition involved changes to only 4 genes. One is a gain of function mutation to a gene coding for an enzyme that breaks down some forms of fat, which probably allowed for efficient colonization of the regions of flea gut closest to its mouth (whereas Y pseudotuberculosis lives further down, in the hindgut). The other three changes are loss of function mutations, the net result of which seems to be enhanced biofilm formation. Biofilms are colllective structures formed by bacteria that stick together on a surface and secrete polymers to form a sticky matrix between them. The three genes with lost function normally repress the creation of this structure in the less virulent Yersinia species. These sticky clumps of bacteria obstruct the flea gut, and lead to angry, starving fleas that feed much more agressively. The combined effect of the 4 mutated genes is a high rate of transmission that, when combined with poor sanitary conditions and increases in urban rat populations, can produce a catastrophic epidemic like the Black Death.

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