FRI-526 ¬¬¬¬Revealing the mechanistic determinants of host specificity: using the parasite Schistosoma mansoni and the snail Biomphalaria obstructa as a model system

Friday, October 12, 2012: 10:20 PM
Hall 4E/F (WSCC)
Megan A. Hudgell , Biology, Center for Evolutionary and Theoretical Immunology, University of New Mexico, Albuquerque, NM
Michelle A. Forys , Biology, Center for Evolutionary and Theoretical Immunology, University of New Mexico, Albuquerque, NM
Eric S. Loker, PhD , Biology, Center for Evolutionary and Theoretical Immunology, University of New Mexico, Albuquerque, NM
The majority of parasite species exhibit host specificity. In general, our understanding of this phenomenon is poor. We address this question using the digenean Schistosoma mansoni as our model parasite. The larval development of S. mansoni occurs in snails of the genus Biomphalaria. For example, the Neotropical snail B. glabrata supports S. mansoni development whereas the North and Central American species B. obstructa does not. A series of experiments is underway to explore B. obstructa’s lack of compatibility with S. mansoni. Snails were exposed to S. mansoni miracidia and sectioned to determine if there is an epidermal barrier that prevents penetration. Histological sections revealed that miracidia penetrated B. obstructa although no exposed snails shed S. mansoni cercariae. Second, we exposed B. obstructa to Echinostoma paraensei - a parasite known to interfere with hemocytes of B. glabrata – to see if pre-exposure to this parasite would enable development of S. mansoni in B. obstructa. Although we were successful in establishing E. paraensei infections in B. obstructa, this did not facilitate S. mansoni infection. Thus, unlike some B. glabrata strains, B. obstructa snails cannot be made more vulnerable by exposure to E. paraensei. Additional experiments are underway to determine if B. obstructa’s lack of compatibility to S. mansoni is specific to certain life stages of parasite development, or if resistance can be broken down by application of environmental stresses or by knock-down of specific immune genes.