TheBubonic Plaguecaused 50 million deaths in the 14th hundred , and even today , its buboes and flu - like symptoms can be severe . Last year , over a hundred people exit from plague infections . The bacterium that causes this infectious disease is channelize by fleas ( dwell on squealer , mostly ) . However , its close evolutionary cousin is toxic to fleas , and people infected with this pathogen suffer mild symptoms in comparing . So , what turned it into a killer bacteria spread through flea raciness ? Researchers have now describe the evolutionary track that lead to the pest bacteria ’s singular ability to diffuse through flea : It was the personnel casualty of an enzyme involve in the breakdown of urea . Thefindingswere bring out inProceedings of the National Academy of Sciencesthis calendar week .
The flea - borne plague bacterium , Yersinia pestilence , blooms into a biofilm in a muscular valve in the catgut of fleas . These thick colonies block the passing between the esophagus and the rest of the gut , impeding the flea ’ intake of blood line meal from humans . That path , infected fleas must fertilise repeatedly , and each successive feeding attempt help oneself transmit the bacterium to more hosts . Its close relativeY. pseudotuberculosis , on the other hand , is toxic to flea . This food- and water - stomach pathogen is impart through the fecal - oral route ( that is , when you ingest fecal particle through pollute food or H2O ) . Fleas who ingestY. pseudotuberculosissuffer diarrhea and immobility , and nearly one-half of them will die . The two bacterial metal money diverged recently , less than 6,400 years ago .
Here ’s aXenopsylla cheopisflea infected withY. pestis , shown as a dark multitude . The foregut of this flea is blocked by a biofilm , a prerequisite for efficient transmitting .
To understand the emergence and phylogeny of the plague bacteria , Iman Chouikha andB. Joseph Hinnebusch from Rocky Mountain Laboratoriesexplored howY. pestisadopted this flea - bear transmission method . They pin down the list of molecular suspects down to the urease enzyme , which hydrolyzes urea and is responsible for the oral toxicity ofY. pseudotuberculosisto fleas . The corresponding gene that encrypt for urease inY. pestisstrains is mutated , cancelling the enzyme ’s activity .
When they blue-pencil the gene fromY. pseudotuberculosis , that rendered the bacteria non - toxic to fleas . And consequently , restoring a functional ureD cistron toY. pestismade the pestilence bacterium toxic to fleas . And dead fleas bite no world .
Because urease - induced mortality can wipe out more than a third of septic flea , selection must have powerfully favour the mutant gene during the phylogenesis of the plague bacteria . Without the mutation that broke ureD , National Geographic report , the plague bacterium would never have reached Black Death proportions .
Images : National Institutes of Health
