Bubonic plague, we’ve long known, is transmitted by fleas infected with the bacteria Yersinia pestis. The bacteria form large masses in the fleas’ digestive tracts and eventually starve them to death; but before they die, during their increasingly persistent and frustrated attempts to feed, the fleas regurgitate infected blood into their victims. All that is clear. What has puzzled researchers, however, is just how Y. pestis manages to survive inside fleas in the first place. The flea’s digestive tract is very inhospitable for bacteria, says Joe Hinnebusch, a microbiologist at the National Institutes of Health’s Rocky Mountain Laboratories in Montana. Fleas are frequent blood feeders and they excrete often, so it’s hard for bacteria to stick around.
Hinnebusch hasn’t found a way to control the spread of the plague (the disease is readily treatable with antibiotics if diagnosed early enough), but he may have discovered how Y. pestis manages to thrive where other bacteria cannot. He started with the suspicion that the solution must somehow involve the bacteria’s interaction with blood. Eventually that led him to focus on a stretch of dna in the bacteria called the hemin storage, or hms, locus, which contains genes that code for proteins that bind hemin, an iron-carrying molecule found in blood. Hinnebusch knew from earlier studies that these genes don’t function at the relatively high temperatures found in mammalian bodies. They become active only at lower temperatures-- about 78 degrees--suggesting that their job in the plague scenario is performed in the cold-blooded flea and not the hot human.
Hinnebusch found that Y. pestis bacteria missing the hms genes could indeed infect fleas, but they did not block their digestive tracts-- the mutants lived peacefully in the midgut, allowing the fleas to feed normally. The fleas also excreted normally, though, and many of the mutants got flushed out in the process.
Bacteria with hms genes, however, not only colonize the midgut but clump together in a mass in the passageway leading from the esophagus to the midgut. The hms proteins somehow make a bacterium’s cell surface hydrophobic, or water fearing, says Hinnebusch, so the bacteria clump to avoid contact with blood. The bacteria clog the works, drive the flea into a feeding frenzy, and kill it--but not before they’ve moved on.
Hinnebusch hasn’t found a way to control the spread of the plague (the disease is readily treatable with antibiotics if diagnosed early enough), but he may have discovered how Y. pestis manages to thrive where other bacteria cannot. He started with the suspicion that the solution must somehow involve the bacteria’s interaction with blood. Eventually that led him to focus on a stretch of dna in the bacteria called the hemin storage, or hms, locus, which contains genes that code for proteins that bind hemin, an iron-carrying molecule found in blood. Hinnebusch knew from earlier studies that these genes don’t function at the relatively high temperatures found in mammalian bodies. They become active only at lower temperatures-- about 78 degrees--suggesting that their job in the plague scenario is performed in the cold-blooded flea and not the hot human.
Hinnebusch found that Y. pestis bacteria missing the hms genes could indeed infect fleas, but they did not block their digestive tracts-- the mutants lived peacefully in the midgut, allowing the fleas to feed normally. The fleas also excreted normally, though, and many of the mutants got flushed out in the process.
Bacteria with hms genes, however, not only colonize the midgut but clump together in a mass in the passageway leading from the esophagus to the midgut. The hms proteins somehow make a bacterium’s cell surface hydrophobic, or water fearing, says Hinnebusch, so the bacteria clump to avoid contact with blood. The bacteria clog the works, drive the flea into a feeding frenzy, and kill it--but not before they’ve moved on.
