Yersinia pestis causes the plague, a devastating infection that has resulted in pandemics both in the past and recently. It continues to be a concern with sporadic natural surges throughout the world and as a form of bioterrorism.
Y. pestis is a facultative, anaerobic, gram-negative bacteria shaped like a coccobacillus and with a safety pin appearance.11 (Figure 22-1). Y. pestis has caused three pandemics, in 6th century AD (541–760) causing 100 million deaths, the Black Death in 1347–1353 with 50 million deaths, and the Oriental plague starting in 1894 causing 12 million deaths.2–6 It has also been used as a biological weapon.9,10
The main reservoir of Y. pestis are rodents in different geographical foci around the world. Predators such as birds can also spread the vectors over long distances.14 Cats, dogs, bandicoots, and shrews can also act as reservoirs. Humans are only incidental hosts and not the primary host in nature.4 Fleas from rodents, such as Xenopsylla ceopis and sylvanic or forest cycle fleas, are vectors and bite humans.
In the USA most cases occur in the southwest; New Mexico, Arizona, Colorado, Utah, Nevada, Idaho, Wyoming, Montana, and California in rural areas and semi-rural areas. It occurs in any season but mostly in late spring to early fall. The last major USA outbreak was in Los Angeles in 1924–1925.7 Outbreaks occurred in the mid-1960s, 1970s, and 1980s. From 2010 to 2015, 3,248 cases were reported to the World Health Organization (WHO) of which there were 584 deaths. Active foci of plague are currently mainly in Madagascar, Congo, southern China, Myanmar, Vietnam, Indonesia, and Peru. Plague has been found in all continents currently with the exception of Australia and Antarctica.8
Climate is known to play an important role in Y. pestis infections. Temperature, rainfall, and humidity can factor into the timing of outbreaks. Humidity levels between 60 and 80% were associated with plague outbreaks.16
Y. pestis infects a host without causing severe immune response. After the infection has spread in the bubonic or pneumonic form, the bacteria multiply inside the cells and then suddenly the host goes into the septicemic form of plague.
The type III secretion system (T3SS), which is an important virulence factor, is not yet expressed by the bacteria at 26°C, which is the temperature in fleas. There is a lack of a pre-inflammatory phase of infection as a result. Once the Y. pestis is taken up to the lymph nodes where the temperature is higher, the bacteria proliferate. Various genes in Y. pestis are switched ...