How the Bubonic Plague Bacterium Co-Opted Fleas

Scanning electron micrograph of Yersinia pestis, which causes bubonic plague, on proventricular spines of a Xenopsylla cheopis flea / National Institute of Allergy and Infectious Diseases (NIAID)
Janet Fang 03 Dec 2014, 19:03

The Bubonic Plague caused 50 million deaths in the 14th century, and even today, its buboes and flu-like symptoms can be severe. Last year, over a hundred people died from plague infections. The bacterium that causes this infectious disease is transmitted by fleas (living on rats, mostly). However, its close evolutionary cousin is toxic to fleas, and people infected with this pathogen suffer mild symptoms in comparison. So, what turned it into a killer bacterium spread through flea bites? Researchers have now identified the evolutionary path that led to the plague bacterium’s unique ability to spread through fleas: It was the loss of an enzyme involved in the breakdown of urea. The findings were published in Proceedings of the National Academy of Sciences this week. 

The flea-borne plague bacterium, Yersinia pestis, blooms into a biofilm in a muscular valve in the gut of fleas. These thick colonies block the passage between the esophagus and the rest of the gut, impeding the fleas’ intake of blood meals from humans. That way, infected fleas must feed repeatedly, and each successive feeding attempt helps transmit the bacterium to more hosts. Its close relative Y. pseudotuberculosis, on the other hand, is toxic to fleas. This food- and water-borne pathogen is transmitted through the fecal-oral route (that is, when you ingest fecal particles through contaminated food or water). Fleas who ingest Y. pseudotuberculosis suffer diarrhea and immobility, and nearly half of them will die. The two bacterial species diverged recently, less than 6,400 years ago. 

Here’s a Xenopsylla cheopis flea infected with Y. pestis, shown as a dark mass. The foregut of this flea is blocked by a biofilm, a prerequisite for efficient transmission.

To understand the emergence and evolution of the plague bacterium, Iman Chouikha and B. Joseph Hinnebusch from Rocky Mountain Laboratories explored how Y. pestis adopted this flea-borne transmission method. They narrowed the list of molecular suspects down to the urease enzyme, which hydrolyzes urea and is responsible for the oral toxicity of Y. pseudotuberculosis to fleas. The corresponding gene that codes for urease in Y. pestis strains is mutated, cancelling the enzyme’s activity.

When they deleted the gene from Y. pseudotuberculosis, that rendered the bacterium non-toxic to fleas. And accordingly, restoring a functional ureD gene to Y. pestis made the plague bacterium toxic to fleas. And dead fleas bite no humans.

Because urease-induced mortality can wipe out more than a third of infected fleas, selection must have strongly favored the mutant gene during the evolution of the plague bacterium. Without the mutation that broke ureD, National Geographic reports, the plague bacterium would never have reached Black Death proportions.

Images: National Institutes of Health 

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