The Northeast Branch of the American Society for Microbiology was pleased to host the Region I Branch Meeting this year, which was sponsored in conjunction with the Connecticut Valley, Eastern New York, and New York City Branches. We would like to acknowledge the generous support of the American Society for Microbiology to this 42nd Annual Meeting, which was held at the Harvard Conference Center in Boston, MA on November 1-2, 2007. We would also like to thank all our sponsors and exhibitors for their generosity and support. Thanks also to all our conveners and speakers - there were many exciting programs, only some of which could be summarized in this Newsletter.

Northeast Branch President Jeffrey Klinger, PhD opened the meeting Thursday morning and ASM President Clifford Houston, PhD welcomed the attendees! Keynote speaker Stuart B. Levy, MD described a different approach to managing infectious diseases in his presentation Alternatives to Antibiotics: Targeting Virulence Not Growth. He stressed that the current approach is to use antibiotics to “kill” the bacteria, resulting in the death of both “good” and “bad” bacteria. In reality, it is not the bacteria that are directly harming the patient, rather the toxin(s) produced by the infecting bacteria. His laboratory has participated in research leading to the discovery of previously synthesized organic molecules that appear to inactivate the microbial genes responsible for the synthesis of toxins. Once the toxin(s) production is “turned off” the bacteria can then live and reproduce without harming the patient. Since bacteria normally present in the host -“good” bacteria- are not eliminated by the use of antibiotics, the invading bacteria are forced to compete with normal or resident bacteria. The result is that the human’s invaded site is not their normal habitat and the invading bacteria are eventually “washed out” of the host.

Evidence was presented that in mice, there appears to be some resistance to subsequent infections. It was hypothesized that the extended presence of the bacterium with its toxin gene turned off, may have led to the development of partial resistance, perhaps as a result of immunization.