132 GLOBAL CLIMATE CHANGE AND EXTREME WEATHER EVENTS
politics (Twigg, 1984; Ziegler, 1969). Although some have questioned whether the Black Death (as well as the first pandemics) was caused by Y. pestis (Cohn, 2002; Scott and Duncan, 2001), it seems settled today (Stenseth et al., 2008). It is generally accepted that the epidemiology of the Black Death plague, as reflected in historical records, does not always match the "classical" rat-flea-human plague cycle, but the reported medical symptoms were very similar during each historical pandemic. It should be appreciated, however, that "classical" plague epidemiology is only one of several possibilities to explain the Black Death and may not even be the most typical of the different plague ecology systems (Drancourt et al., 2006). The discovery of Y. pestis genetic material in those who died from the Black Death and are buried in medieval graves (Raoult and Aboudharam, 2000) further supports the view that Y. pestis was the causative agent of the Black Death.
The (Full) Plague Eco-Epidemiological System
Soon after Yersin's discovery of the plague bacillus (Yersin, 1894), it became clear that urban outbreaks were linked to transmission among commensal rats and their fleas. In this classic urban plague scenario, infected rats (transported, for example, by ships) arrive in a new city and transmit the infection to local house rats and their fleas, which then serve as sources of human infection. Occasionally, humans develop a pneumonic form of plague, which is then directly transmitted from human to human through respiratory droplets.
The epidemiology of plague, however, is much more complicated than this urban plague scenario suggests, involving several other pathways of transmission. This complicated epidemiology necessitates reconsidering plague ecology within its full ecological web (Figure 2-13).
Maintenance of plague foci depends on a whole suite of rodent hosts and their associated fleas. Under favorable conditions, the plague bacillus might survive in the environment, essentially in rodent burrows (Baltazard et al., 1963). When an infected flea happens to feed on a commensal rodent, the cycle continues in the latter. As commensal rodents die, their fleas are forced to move to alternate hosts (e.g., humans). If humans develop pneumonic plague, the infection may transmit from person to person through exposures to respiratory droplets spread by coughing. Humans may also become infected through handling infected animals (or meat), including rodents, camels, or cats. Cats may also develop pneumonic plague, passing their infection to their owners through coughing. Finally, there is evidence that the human flea, Pulex irritans, can be involved in human-to-human transmission (Blanc, 1956; Laudisoit et al., 2007). Mammalian predators, birds of prey, and other birds that use rodent burrows for nesting may move over larger areas than the rodents themselves, spreading the infection over longer distances. Infected commensal rats or humans may also travel over long distances.
Because of its widespread occurrence in wildlife rodent reservoir species one must recognize that plague cannot be eradicated. There is a critical need,
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