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Parasites & Vectors 2011
Effects of temperature on the transmission of Yersinia Pestis by the flea, Xenopsylla Cheopis, in the late phase periodKeywords: Yersinia pestis, Xenopsylla cheopis, biofilm, flea-borne transmission, temperature Abstract: Although no statistically significant differences in per flea transmission efficiencies were detected between 23 and 30°C, efficiencies were highest for fleas maintained at 23°C and they began to decline at 27 and 30°C by day 21 p.i. These declines coincided with declining median bacterial loads in fleas at 27 and 30°C. Survival and feeding rates of fleas also varied by temperature to suggest fleas at 27 and 30°C would be less likely to sustain transmission than fleas maintained at 23°C. Fleas held at 10°C transmitted Y. pestis infections, although flea survival was significantly reduced compared to that of uninfected fleas at this temperature. Median bacterial loads were significantly higher at 10°C than at the other temperatures.Our results suggest that temperature does not significantly effect the per flea efficiency of Y. pestis transmission by X. cheopis, but that temperature is likely to influence the dynamics of Y. pestis flea-borne transmission, perhaps by affecting persistence of the bacteria in the flea gut or by influencing flea survival. Whether Y. pestis biofilm production is important for transmission at different temperatures remains unresolved, although our results support the hypothesis that blockage is not necessary for efficient transmission.It is well documented that temperature is an important regulator of the transmission dynamics of vector-borne pathogens. This relationship is largely related to the effects that temperature has on the survival, growth, development, and reproduction of pathogens and their vectors [1,2]. Temperature also has the ability to alter the behavior and activity of vectors, resulting in changes in contact rates between vectors, pathogens, and the hosts that may be involved in pathogen life cycles [3]. Changes in temperatures, therefore, have the potential to shift or expand vector-host-pathogen geographic ranges, modify the seasonality or phenology of infections, and lead to changes in pathogen generation times and tran
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