(A20.0) Bubonic plague is an infectious disease that is believed to have caused several epidemics or pandemics throughout history. The disease is caused by the bacterium Yersinia pestis. Bubonic plague is the most common form of plague, and is characterized by swollen, tender, inflamed lymph glands (called buboes).
(A20.7) Septicemic plague occurs when plague bacteria multiply in the blood.
(A20.2) Pneumonic plague occurs when the lungs are infected.

Infection/transportation

Bubonic plague is primarily a disease of rodents, particularly marmots (in which the most virulent strains of plague are primarily found), but also black rats, prairie dogs, chipmunks, squirrels and other similar large rodents. Human infection most often occurs when a person is bitten by a rat flea (Xenopsylla cheopsis) that has fed on an infected rodent. The bacillus multiplies in the stomach of the flea, blocking it. When the flea next bites a mammal, blood consumed by the flea is regurgitated along with the bacillus into the bloodstream of the bitten animal. Any serious outbreak of plague is started by other disease outbreaks in the rodent population. During these outbreaks, infected fleas that have lost their normal hosts seek other sources of blood.

In 1894, bacteriologists Alexandre Yersin and Shibasaburo Kitasato independently isolated the responsible bacterium and Yersin further determined that rodents were the likely common mode of transmission. The disease is caused by the bacterium Yersinia pestis.

Symptoms and treatment

The disease becomes evident 2–7 days after infection. Initial symptoms are chills, fever, headaches, and the formation of buboes. The buboes are formed by the infection of the lymph nodes, which swell and become prominent. If unchecked, the bacteria infects the bloodstream (septicemic plague), and can progress to the lungs (pneumonic plague).

In septicemic plague there is bleeding into the skin and other organs, which creates black patches on the skin. Untreated septicemic plague is universally fatal, but early treatment with antibiotics (usually streptomycin or gentamicin) is effective, reducing the mortality rate to around 15% (USA 1980s). People who die from this form of plague often die on the same day symptoms first appear.

With pneumonic plague infecting lungs comes the possibility of person-to-person transmission through respiratory droplets. The incubation period for pneumonic plague is usually between two and four days, but can be as little as a few hours. The initial symptoms of headache, weakness, and coughing with hemoptysis are indistinguishable from other respiratory illnesses. Without diagnosis and treatment, the infection can be fatal in one to six days; mortality in untreated cases may be as high as 95%. The disease can be effectively treated with antibiotics.

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Bubonic blockage - genetics of bubonic-plague causing bacteria Yersinia pestis - Break Throughs
From Discover, 11/1/96

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 fleas digestive tract is very in hospitable for bacteria," says Joe Hinnebusch, a microbiologist at the National Institutes of Healths Rocky Mountain Laboratories in Montana. "Fleas are frequent blood feeders and they excrete often, so its 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 hermin 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.

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