Lifecycle Stages

is maintained in nature through transmission between hematophagous [blood feeding] adult fleas and certain rodent hosts, with occasional involvement of some lagomorphs (Gage 1998; Pollitzer 1961)” (Gage and Kosoy 2005). Evidence ofinfection in a wide range of other mammal groups suggests that virtually all mammals are susceptible to this bacterium (Gage 1998; Gage 1999; Pollitzer 1961 in Gage and Kosoy 2005).

“Typically, plague is thought to exist indefinitely in so-called enzootic (maintenance) cycles that cause little obvious host mortality and involve transmission between partially resistant rodents (enzootic or maintenance hosts) and their fleas (Gage et al 1995; Poland and Barnes 1979; Poland et al. 1994). Occasionally, the disease spreads from enzootic hosts to more highly susceptible animals, termed epizootic or amplifying hosts, often causing rapidly spreading die-offs (epizootics)” (Gage and Kosoy 2005). Humans and other highly susceptible mammals also experience their greatest exposure risks during epizootics.”

However, there is some debate over whether epizootic and enzootic cycles actually exist. In North America plague causes die-offs of colonies of prairie dogs (Cynomys ludovicianus). “It has been argued that other small rodents are reservoirs for plague, spreading disease during epizootics and maintaining the pathogen in the absence of prairie dogs; yet there is little empirical support for distinct enzootic and epizootic cycles.” Stapp et al. (2008) investigated a number of small rodent species in northern Colorado, and found no evidence that any small rodent acts as a long-term, enzootic host for Y. pestis in prairie dog colonies.

The question of whether Y. pestis can survive outside its normal host or vector has been a controversial issue. A recent study by Ayyadurai et al. (2008) confirmed that Y. pestis remains viable and virulent after 40 weeks incubation in sterilized humidified sand. Survival in soil is clearly an important mechanism for plague persistence during inter-epizootic periods and plays an important role in the epidemiology of the plague (Ayyadurai et al. 2008).

The main vectors responsible for transmission of Y. pestis to humans are usually rodent fleas, Xenopsylla cheopis and Nosopsylla fasciatus, or in some cases the human flea, Pulex irritans (Curson et al. 1989). In North America the primary vector of Y. pestis to humans is Oropsylla Montana (Eisen et al. 2007-C). When a flea bites its host it ingests Y. pestis and becomes infected. Y. pestis may reproduce so rapidly that it blocks the flea's proventriculus, a small organ located between the esophageus and stomach. This block prevents any ingested blood from reaching the midgut, causing the flea to starve. Regurgitation of ingested blood and infectious material from the blockage are forced back into the wound, infecting the host. This combined with increased feeding attempts from starvation make blocked fleas dangerous vectors of Y. pestis (Eisen et al. 2007-D). Spread by blocked fleas has been the accepted paradigm for plague transmission for many years.

However Eisen et al. (2007-D) point out “that this mechanism, which requires a lengthy extrinsic incubation period before a short infectious window often followed by death of the flea, cannot sufficiently explain the rapid rate of spread that typifies plague epidemics and epizootics” and explain the importance of unblocked fleas in Y. pestis epizootics. Unblocked fleas are immediately infectious, transmit the bacterium for at least 4 days, and remain infectious for long periods as they do not suffer block-induced mortality.