The Medical Journal - A baker's dozen of skeletons laid out in two rows in a long-lost London burial ground may help reveal some genetic secrets of the bacterium that causes bubonic plague.
Discovered in early March during excavations for a new subway line, archaeologists say the 13 sets of bones may represent a few of as many as 50,000 victims of the Black Death laid to rest in the emergency cemetery during an epidemic that first swept across Europe 660 years ago.
The way the bodies were laid out, the depth of the burials (about 8 feet) and pottery dating to about 1350 all point to the skeletons as likely plague victims. British scientists are hoping the bones may hold DNA from the plague bacteria that they might use to better analyze the cause of a disease estimated to have killed 75 million to 100 million people worldwide in just a few years. Scholars say it took Europe 150 years to recover from the population loss.
Their interest in the bones is far from academic. Plague is established in rodent populations -- and the fleas they carry -- in much of the world. That includes the western half of the United States, where the disease was introduced in the 1890s during the last great pandemic.
There are seldom more than 20 plague cases reported each year to the federal Centers for Disease Control and Prevention, and only a few thousand worldwide. Although it is readily treated with antibiotics, the disease remains a potent threat largely because it spreads so readily and has been so deadly.
The infection is a triple threat. In its most common form, bacteria infect the lymph system, causing the signature swelling and eruption of boil-like buboes around the neck, armpit and groin. But the bacteria can also strike in the blood or lungs.
Bacteria typically spread through a rodent or flea bite, but can enter open skin from contaminated clothing or blankets. And they can also be passed from person to person through coughing or sneezing.
William H. McNeill, the noted disease historian, observed in his book "Plagues and Peoples" that until the advent of antibiotics in the 1940s, "it is sobering to realize that in spite of all that modern hospital care could accomplish, the average mortality remained between 60 and 70 percent in those affected" by plague.
But there is great worry that the fast-spreading disease may become less controllable and re-emerge. The bacteria may be evolving to resist at least some antibiotics, particularly in developing countries.
Public-health and homeland-security officials, fearing that terrorists might try to use plague as a weapon, have placed it in the same class as anthrax, smallpox and Ebola.
Government-funded researchers have mapped plague genes and are working on vaccine that can be cultured and delivered rapidly. There is also ongoing research into new antibiotics to fight the disease.
Scientists only identified the bacterial culprit, Yersinia pestis, during the last major outbreak in the 1890s, which mainly affected Asia and India. Before that, the chief defenses were isolation and quarantine of travelers and ship's crews from areas known to be experiencing outbreaks.
One recent paper -- in the journal Infection, Genetics and Evolution -- analyzed the Great Plague of Marseille. It killed more than 100,000 people in southern France between 1720 and 1723, but was limited by quarantines and other measures.
Modern researchers had been stumped at how another bacteria -- Yersinia pseudotuberculosis, seemingly identical to the plague germ -- could be so mild. At worst, it causes mild stomach upset, and often no symptoms.
Researchers at Northwestern University compared the two subspecies using some new genetic-sequencing tools two years ago, and found the difference seems to have risen from small RNAs, molecules that control many cellular processes but not protein production. They reported their findings in the Proceedings of the National Academy of Sciences in September 2011.
It appears that the plague virus shed six small RNAs between 1,500 and 20,000 years ago, possibly the key for turning it from a mild disease to a rapidly spreading killer, first in Asia, then across the globe.
(Contact Scripps health and science writer Lee Bowman at BowmanL@shns.com .)