Jennifer Vanderkelen, Alejandra Yep, Chris Kitts
Main Conclusions (Experiment 1-Hypothesis: Induction of efflux pumps by hormone) • The growth rates of wild-type and K12 E. coli strains are significantly inhibited by the presence of ciprofloxacin. The addition of 100ug/ml hormone slightly reduced the growth in the presence of antibiotic which suggests that hormone does not induce or activate efflux pumps. • The 0.0015ug/ml ciprofloxacin concentration used in this experiment was too low for CFT073, a uropathogenic strain, but 0.003ug/ml did cause some growth inhibition. Growth with and without hormone was essentially the same suggesting that the higher efflux activity of CFT073 could rid the cells of growth inhibiting hormone. • The loss of efflux activity in the CFT073ΔtolC mutant made it much more sensitive to ciprofloxacin than it’s CFT073 parent. The presence of hormone very slightly increased growth of this mutant suggesting that sequestration of antibiotic and hormone perhaps induced activity of a tolC-independent efflux pump. Main Conclusions (Experiment 2-Hypothesis: Selection for higher efflux pumps by hormonal contraceptive users) • There was no significant difference between the minimum inhibitory concentrations to ciprofloxacin between E.coli isolated from hormonal contraceptives users and E. coli isolated from non-users. It was founded that the protocol for Experiment 1 had a few complications that needed to be addressed. It is unknown as to whether or not the glucuronidated hormone is active once brought into solution or if it is even being uptaken by E. coli isolates. This may explain negative results. Future work entails further elucidating this by conducting a growth curve assay of specific E. coli strains which will be driven to become dependent on this glucuronidated hormone as an energy source. Additionally, future work entails repeating Experiment 1 as a whole.
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