Arthropod-borne transmission of bacterial pathogens is somewhat rare but has evolved in a phylogenetically diverse group that includes the rickettsiae, Borrelia spirochetes, and the gram-negative bacteria Francisella tularensis and Yersinia pestis, the plague bacillus. Y. pestis circulates among many species of wild rodents, its primary reservoir hosts, via flea bite. As it alternates between fleas and mammals, it is postulated that Y. pestis regulates gene expression appropriately to adapt to the two disparate host environments, and that different sets of genes are required to produce a transmissible infection in the flea and disease in the mammal. Many important Y. pestis virulence factors that are required for plague in mammals have been identified, and most of them are induced by a temperature shift from <26°C to 37°C, which mimics the transition from a flea to the warm-blooded host. To date, only three transmission factors (genes specifically required to produce a transmissible infection in the flea) have been characterized.
Bubonic plague cycles depend on the ability of Y. pestis to alternately infect two very different hosts – a mammal and a flea. Like any arthropod-borne pathogen, Y. pestis must sense host-specific environmental cues and regulate gene expression accordingly to produce a transmissible infection in the flea after being taken up in a blood meal, and again when it exits the flea and enters the mammal. Researchers examined the Y. pestis phenotype at the point of transmission by in vivo gene expression analyses, the first description of the transcriptome of an arthropod-borne bacterium in its vector. In addition to genes associated with physiological adaptation to the flea gut, several Y. pestis virulence factors required for resistance to innate immunity and dissemination in the mammal were induced in the flea, suggesting that the arthropod life stage primes Y. pestis for successful infection of the mammal.
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