Among the Enterobacteriaceae, Yersinia pestis is unique in both its choice of host habitat (blood, lymphoid system, reticuloendothelial system) and primary mode of transmission (flea vectors). Y. pestis has two main habitats—in the stomach of proventriculus of various flea species at ambient temperature or in the blood or tissues of a rodent host at body temperature (Perry 19997 in Prentice and Rahalison 2007). Y. pestis has been recorded to naturally infect over 203 rodent species and 14 lagomorph species. However only a small proportion are actually significant hosts, with rodents being far more important host taxa than lagomorphs (Gage and Kosoy 2005).

Curson et al. (1989) report that bubonic plague exhibits marked seasonality, closely related to seasonal changes in flea and rat populations. It tends to be a disease of late summer and early autumn, although it is possible that the artificially maintained indoor temperatures of many houses in the winter may allow fleas to survive. It is also possible that Y. pestis can be transmitted to humans via lice and other insects.
Fleas require fairly specific climatic conditions and do best in moderately warm (15-20 degrees Celsius) and moist climates (90-95% humidity). In species of fleas such as Xenopsylla cheopis , Y. pestis reproduces most rapidly at warm temperatures of up to 27 degrees Celsius. Above this temperature, changes occur in blood coagulation, resulting in digestion of the blocking plug and the rapid elimination of Y. pestis. Y. pestis produces two antiphagocytic components (that impede or prevent the function of defensive white blood cells), called F1 capsule antigen and the V antigen. Both are required for the disease to be harmful and are only produced when the host's body temperature is not lower than 37 degrees Celsius (Fix 1997).

Yersinia pestis 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 of Y. pestis infection 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.

Yersinia pestis has the potential to be used as a weapon in bioterrorism. The United States Centers for Disease Control classified Y. pestis a Category A Select Agent due to its potential to pose a severe threat to public health and safety. Concerns stem from the fact that during the Cold War, both American and Soviet scientists devised means to effectively aerosolize Y. pestis, thereby removing the need for the flea vector (Inglesby 2000 in Smiley 2008). Although antibiotics are effective against plague, antibiotic resistant strains are known to exist. \"Covertly aerosolized, antibioticresistant Y. pestis would be a formidable weapon of terror\" (Smiley 2008).

Among the Enterobacteriaceae, Yersinia pestis is unique in both its choice of host habitat (blood, lymphoid system, reticuloendothelial system) and primary mode of transmission (flea vectors). Y. pestis has two main habitats—in the stomach of proventriculus of various flea species at ambient temperature or in the blood or tissues of a rodent host at body temperature (Perry 19997 in Prentice and Rahalison 2007). Y. pestis has been recorded to naturally infect over 203 rodent species and 14 lagomorph species. However only a small proportion are actually significant hosts, with rodents being far more important host taxa than lagomorphs (Gage and Kosoy 2005).

According to Campbell et al. (1999), bacteria reproduce asexually using binary fission. Binary fission is a type of cellular division in which each dividing daughter cell receives a copy of the single parent chromosome. Growth of bacteria can be extremely fast if the resources needed are not limited and the colonies do not poison themselves with the accumulation of their own wastes (Campbell et al. 1999). The generation time (the time it takes for the colony to double in size) is 1.25 hours (Chu 2001).

Campbell et al. (1999) write that in order to grow in nature or in the laboratory, a bacterium must have an energy source, a source of carbon and other required nutrients, and a permissive range of physical conditions such as oxygen concentration, temperature, and pH. Y. pestis is a chemoheterotroph, meaning that it must consume organic molecules for energy and carbon.

The bacteria live in fleas, which are carried by rats, rabbits, humans and other mammals. These animals can be transported around the world with human cargo. Humans can carry the fleas and the disease unknowingly during the 1 to 6 day incubation period.

Yersinia pestis is the causal agent of plague in humans and other mammals, although the overwhelming proportion of attention and research has focused on its impacts on humans. Y. pestis is recognized as causing three major disease pandemics in the 1st, 14th-17th and 19th centuries, resulting in around 200 million deaths. The second pandemic known as the Black Death caused the deaths of over 30% of the population of Europe. While Y. pestis no longer causes problems of such magnitude, it is still a public health concern in Africa, Asia and South America (Titball and Williamson 2001). There are at least 2000 cases of plague reported annually. In the United States it is a rare disease of humans, with only 112 cases reported between 1988-2002, although fatality rates remain high (MNWR 2002 in Eisen et al. 2007-B).

Biologists are increasingly realizing that wild mammal species are highly susceptible to Y. pestis. In North America more than half of rodent species of conservation concern occur within the range of Y. pestis. The impacts of plague on these populations are not well understood, but certain features increase the vulnerability of rodent species to plague. These include low natural resistance, high population densities, coloniality and sociality, abundant flea vectors, and lack of ability to cope with high demographic or environmental stochasticity.

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