Abstract
The ability to cause plague in mammals represents only half of the life history of Yersinia pestis. It is also able to colonize and produce a transmissible infection in the digestive tract of the flea, its insect host. Parallel to studies of the molecular mechanisms by which Y. pestis is able to overcome the immune response of its mammalian hosts, disseminate, and produce septicemia, studies of Y. pestis-flea interactions have led to the identification and characterization of important factors that lead to transmission by flea bite. Y. pestis adapts to the unique conditions in the flea gut by altering its metabolic physiology in ways that promote biofilm development, a common strategy by which bacteria cope with a nutrient-limited environment. Biofilm localization to the flea foregut disrupts normal fluid dynamics of blood feeding, resulting in regurgitative transmission. Many of the important genes, regulatory pathways, and molecules required for this process have been identified and are reviewed here.