Contrary to what was previously believed, the bacterium responsible for the Black Death probably caused small outbreaks of lung disease for many years before it evolved its better-known bubonic form, according to a new genetic study. Also, only one added gene was needed to turn the Yersinia pestis bacterium into a killer, and only one tiny mutation in that gene was needed to give it two ways of spreading — by cough or by flea bite, said Wyndham W. Lathem, a microbiologist at Northwestern University Feinberg School of Medicine who oversaw a team inserting genes into ancestral versions of Y. pestis in mice. During last year’s Ebola outbreak in West Africa, some feared that the disease, which spread through blood, vomit and feces, could become airborne. Plague bacteria are very different from Ebola virus, Dr. Lathem said, “but this shows that new modes of transmission can occur through very small changes, so you need to keep an eye out.” The study was published last week by Nature Communications. Y. pestis evolved from an ancestor, Yersinia pseudotuberculosis, that still circulates in European rodents but causes only mild intestinal illness in humans. Y. pestis emerged only 5,000 to 20,000 years ago, and developing twin modes of transmission helped it explode into the sixth-century Plague of Justinian, the 14th-century Black Death and epidemics in China well into the early 20th century. The important new gene, Dr. Lathem said, helped the bacteria make an enzyme that broke up the fibrous blood clots that the body’s defenses formed around them — in much the same way that enzyme injections break up blood clots in stroke victims. Source
