This diagram illustrates some of the transmission cycles of plague caused by Yersinia pestis. This image is useful in showing students how plague is transmitted to humans. Knowing how plague is transmitted is essential in the development of prevention plans and in tracking the sources of infection by Y. pestis.

Today nearly all plague infections are zoonotic with humans being accidental hosts. There are two different transmission cycles of Y. pestis infection: zoonotic and human to human. The first type, zoonotic (pertaining to animals) plague, involves transmission due to the bite of infected fleas or contact with infected animals. Zoonotic plague is further divided into urban and sylvatic (rural) plague. The second type involves the pneumonic transmission of infection occurring between humans.

The sylvatic plague cycle (wild mammals, usually rodents) involves the passing of plague from mammal to mammal by fleas (Xenopsylla cheopis) infected with Y. pestis. Mammal to mammal passage of Y. pestis can occur by direct contact but is less common. Many of these mammals are relatively resistant to the lethal effects of Y. pestis infection. Squirrels, rabbits, and field rats can all serve as long-term reservoirs for the plague bacterium (enzoonotic plague). Other mammals are highly susceptible to the lethal effects of Y. pestis resulting in rapid spread of plague among the animals with large numbers dying in the community (epizoonotic plague; e.g., prairie dogs). If humans enter these areas they acquire the infection via flea bites or direct contact with infected animals.

The urban plague cycle also involves the passing of plague from mammal to flea to mammal. Mammal to mammal passage of Y. pestis can occur by direct contact but is less common. These mammals, frequently rats, are usually highly susceptible to the lethal effects of Y. pestis. As a result, large numbers of these animals die (epizoonotic plague). The infected fleas lacking their more common rodent hosts then bite and infect humans. Direct contact with infected animals can also result in human infection.

The flea draws viable Y. pestis organisms into its intestinal tract. These organisms multiply in the flea and block the flea's proventriculus. Some Y. pestis in the flea are then regurgitated when the flea gets its next blood meal thus transferring the infection to a new host. While growing in the flea, Y. pestis loses its antiphagocytic capsular layer.

Human infections following flea bites or by direct contact with infected animals usually result in bubonic plague. Most of the unencapsulated organisms are phagocytosed (ingested) and killed by the polymorphonuclear leukocytes (PMN’s or neutrophils) in the human host. A few bacilli are taken up by tissue macrophages. The macrophages are unable to kill Y. pestis and provide a protected environment for the organisms to synthesize their capsular and other virulence factors. The Y. pestis are taken to the draining lymph nodes by the macrophages.

The encapsulated intracellular organisms then kill the macrophage and are released into the extracellular environment, where they resist phagocytosis by the PMN’s. The Y. pestis multiply rapidly and cause a hemorrhagic inflammatory response making the lymph nodes hot, swollen, tender, and hemorrhagic. This gives rise to the characteristic black buboes responsible for the name of this disease: bubonic plague.

In a relatively short period of time the bacteria get out of the swollen lymph nodes and into the bloodstream. They infect the liver, spleen, and lungs. Bacteremia (bloodstream infection; septicemic plague) occurs rapidly if not treated and mortality rates can be as high as 75%.

A severe bacterial pneumonia can develop: pneumonic plague. Patients expel large numbers of viable organisms during coughing fits. Other humans inhale these viable organisms and develop pneumonia. The spread of Y. pestis via droplets from human to human is also known as the demic plague cycle. Spread from person to person can be very rapid and has in the past caused epidemics with mortality rates over 90% if untreated.

References.

1. Murray, P. R., et al. 2002. Medical microbiology, 4th ed., p. 276-278. Mosby, St. Louis, Mo.
2. Hoeprich, P. D., et al. 1994. Infectious diseases: a treatise of infectious processes, 5th ed., p. 1302-1311. J. B. Lippincott Company, Philadelphia, Pa.