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Joshua Messinger Faculty Advisor: Dr. Dave Gondek Evaluation of Recombination across Chlamydia Species Known in the United States primarily as a sexually transmitted disease, Chlamydia is one of the most common bacterial infections worldwide and is the leading cause of preventable blindness in developing nations. Tanzania still very much fights trachoma (blindness due to Chlamydia trachomatis) and is hoping to eradicate this problem by 2020. While treatments have been widely available for this disease, a vaccine has not yet been discovered. This summer, I propose to do a research project in the biology lab of Dr. Dave Gondek. Dr. Gondek’s lab explores how the Chlamydia bacteria have come become a highly specialized intracellular (lives within your cells) pathogen capable of manipulating the host organism. Due to the fact that it must live within host cells in order to survive, its genome (genetic information) has become highly specialized to specific hosts and has thus has reduced the size of its genome immensely. Thus, it lacks the ability to activate a lot of its own proteins and therefore has adapted Type III secretion methods in order to manipulate the host cell. Through Type III secretion, the Chlamydia bacteria inject inactive, effector, proteins into the host cell which the host then activates. In effect, the host has been manipulated into activating the proteins that will inevitably lead to its own demise. Chlamydia is highly host specific and thus many strains of the bacteria exist that are capable of occupying unique hosts. For example, Chlamydia trachomatis occupies the human host, while Chlamydia muridarum occupies mice. Due to the fact that Chlamydia bacteria has made its genome smaller over time, it should not be able to cross into new species and should thus be restricted to occupying just that native host. Our experiments have shown that these strains of Chlamydia have been able to cross into new, non-native, hosts at least to some limited degree. This provides evidence that this bacterial species is capable, under the right conditions, of crossing into a new host therefore giving it the potential to become an emerging disease in new organisms over time. Humanity has encountered this before in the form of new versions of the flu ever year and how SARS suddenly became a prominent disease. By continually studying how pathogenic bacteria adapt to new hosts, humanity can become better equipped to cure new and emerging diseases when they enter the population. One particular strain of Chlamydia, Chlamydia muridarum (native to mice) has shown particular versatility in crossing into a new host in the laboratory setting. This provides evidence that there are additional genetic components that C. muridarum has that the other strains of Chlamydia do not have. To assess what these differences may be, the Gondek laboratory has begun examining what unique elements of C. muridarum may exist and what these genetic components allow this strain to do that other strains are unable to do. Having conducted this large screen of how these three strains of Chlamydia adapt to non-native hosts, many potentially novel characteristics about these organisms have been exposed that may lead to a better understanding of how new diseases emerge and how we can cure them upon encountering them. Figures and Results 1.00E+10 1.00E+09 1.00E+08 1.00E+07 1.00E+06 Trachomatis 1.00E+05 Caviae Muridarum 1.00E+04 1.00E+03 1.00E+02 1.00E+01 1.00E+00 McCoy Vero HeLa Cat Lung Guinea Pig Figure 1: Survey of Chlamydia Growth across 5 different species of hosts This figure shows the degree to which the Chlamydia bacteria survive in crossing into a new host. The x-axis represents different species of hosts. McCoy corresponds to mice, Vero to monkeys, HeLa to humans and lastly cat and guinea pig hosts were assessed. The y-axis demonstrates, on average across 4 experiments, how many infectious units per milliliter of sample were obtained after a 24 hour infection.