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    ABSTRACT: The discovery and development of antibacterial drugs in the twentieth century were major scientific and medical achievements that have had profound benefits for human society. However, in the twenty-first century the widespread global occurrence of bacteria resistant to the antibiotics and synthetic drugs discovered in the previous century threatens to reverse our ability to treat infectious diseases. Although some new drugs are in development they do not adequately cover growing medical needs. Furthermore, these drugs are mostly derivatives of older classes already in use and therefore prone to existing bacterial resistance mechanisms. Thus, new drug classes are urgently needed. Despite investment in antibacterial drug discovery, no new drug class has been discovered in the past 20 years. In this review, based upon my career as a research scientist in the field of antibacterial drug discovery, I consider some of the technical reasons for the recent failure and look to the future developments that may help to reverse the poor current success rate. Diversification of screening libraries to include new natural products will be important as well as ensuring that the promising drug hits arising from structure-based drug design can achieve effective concentrations at their target sites within the bacterial cell.
    Preview · Article · Nov 2012 · Journal of Antimicrobial Chemotherapy
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    ABSTRACT: The enterococcal plasmid pKQ10 has been reported to carry a poorly characterized tetracycline resistance determinant designated tet(U). However, in a series of studies intended to further characterize this determinant, we have been unable to substantiate the claim that tet(U) confers resistance to tetracyclines. In line with these results, bioinformatic analysis provides compelling evidence that “tet(U)” is in fact the misannotated 3′ end of a gene encoding a rolling-circle replication initiator (Rep) protein.
    Full-text · Article · Apr 2012 · Antimicrobial Agents and Chemotherapy
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    ABSTRACT: The genetic basis of tolerance to inhibitors of peptidoglycan biosynthesis in Staphylococcus aureus was investigated by generating tolerant mutants in vitro and characterizing them by comparative genome sequencing. Two independently selected tolerant mutants harbored nonsynonymous mutations in gdpP, a gene encoding a putative membrane-located signaling protein. Insertional inactivation of gdpP also conferred tolerance. Our findings further implicate altered signal transduction as a route to antibiotic tolerance in S. aureus.
    Preview · Article · Jan 2012 · Antimicrobial Agents and Chemotherapy
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