How Does Yersinia Pestis Attack and Spread?

Y.pestis is a rod-shaped facultative anaerobe that was discovered in 1894 by Alexandre Yersin, a French-born Swiss bacteriologist who was studying a plague epidemic in China. Throughout human history it has brought about the deaths of hundreds of millions of people, for example "the Black Death" that wreaked havoc in Europe in the 14th century. The bacteria is estimated to have killed between 30-60% of Europe's population at the time.

Yersina pestis cannot yet be consigned to the history books as it is still a major cause of plague in many countries around the world.

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Y. pestis is so successful because it is able to evade and suppress host cell immune response. Many of its virulence factors are anti-phagocytic such as the F1 antigen and the VW antigens. The plague-causing bacteria can resist phagocytosis by injecting proteins called YOPS (Yersinia Outer Proteins) into macrophages and other immune cells. These injected proteins form pores through which other YOPS travel to get to the cell cytoplasm and limit phagocytosis.

The bacteria are able to spread rapidly through the bloodstream and infect organs such as the liver, kidneys, and spleen. The lymphatic system is hardest hit with the bacteria congregating in lymph nodes. They avoid the immune response and multiply; the nodes swell, become hot and tender and bleed excessively. This gives rise to the black buboes responsible for the name "Bubonic Plague." As the infection spreads a patient develops a severe case of bacterial pneumonia and death is usually the result of endotoxic shock.

Without treatment the fatality rate is high - more than 90%. With treatment this drops to between 5 and 20%. Rapid treatment with antibiotics such as streptomycin and tetracycline is the most common procedure. They are usually administered within 24 hours, sometimes intravenously.

In 2001 scientists worked out the complete genetic structure of Y.pestis which will help researchers to come up with new ways of tackling illnesses caused by the bacteria. A team from the Sanger Centre, Cambridge, UK studied samples taken from a Colorado vet who died in 1992 after his plague-ridden cat sneezed on him. Part of their research consisted of figuring out how the bacterium turned into such a killer, as it evolved from a much more benign bug called Y.pseudotuberculosis.

Scanning electron microscope picture of Yersinia pestis in the foregut of a flea vector. Released into the public domain by US Federal Government