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The lifestyle of vector-borne pathogens such as Yersinia pestis requires the bacteria to adapt to two very different hosts. We are interested in learning about the contributions made by each member of the bacteria-vector-host triad. Specifically, we are identifying genes that allow the bacteria to survive in fleas without killing them prior to transmission. We are also studying the molecular basis of vector competence among fleas, including how the flea responds to infection and how this might influence transmission.

We have three main projects in the lab:

1. Identifying the normal flora of different flea species
Symbiotic bacteria or normal flora can influence the ability of arthropods to transmit pathogens. They might also be useful in creating paratransgenic insects that are unable to transmit disease. They are also a potential source of new antibiotic resistance or virulence genes for pathogenic bacteria. Very little is known about the normal flora of fleas. We are creating 16S rDNA clone libraries to identify bacteria that live in different flea species.

2. Examining gene expression patterns in flea vectors
We are interested to see if fleas alter gene expression in response to bacteria in their midguts, and if these responses affect the ability of Y. pestis to establish a transmissible infection. In particular, immune effectors of the insect such as antibacterial peptides, lectins, or reactive oxygen/nitrogen compounds likely limit the growth of the bacteria. Differences in the type, amount, or location of these responses could influence whether a particular flea is able to transmit plague. We are using suppression subtractive hybridization to create a library of clones representing the genes specifically active in infected fleas. We are developing RNA interference techniques in the fleas to knock down genes identified in these screens to test their impact on transmission.

3. Y. pestis adaption to the flea digestive tract and its effect on transmission
Relatively few bacteria are able to colonize the midguts of blood-feeding arthropods, in part due to the physiological and immunological stresses in this environment. We are examining the role of transcriptional regulators in Y. pestis survival in the flea. We are also studying whether phenotypes that the bacteria display in the flea help them resist the initial innate immune response when they are deposited in the skin after flea feeding.

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