June 2006 Archives

With the pace of drug resistance far outstripping that of antibiotic development, the medical news doesn’t get bigger than the discovery of an entirely new class of drugs effective against even the most multidrug-resistant strains of hospital-bred staph.


This past month, scientists at Merck’s Rahway, New Jersey, research labs announced their discovery of platensimycin, a chemical that kills Staphylococcus aureus via a new biological target—the bacterial enzyme FabF, crucial in the assembly of the fatty acids that make up a gram-positive bacterium's cell wall.

It’s been four decades since medicine gained a new class of antimicrobial drug, four decades in which standard drugs have driven the rise of once-rare bacterial genes for chopping up, pumping out or otherwise neutralizing them. These genes can now be found in abundance in the bacteria that inhabit not only our hospitals but also our bodies. For good reason, hope for treating drug-resistant infectious diseases has long resided in blind-siding the bugs with something entirely new, something against which no bacterial resistance mechanism has yet been found.

That’s what Merck scientist Jun Wang and colleagues say they have found in platensimycin, a small molecule produced by Streptomyces plantensis, a bacterium they isolated from a clod of South African dirt. S. platensis hails from the same family of soil bacteria that have already supplied us with the bulk of our antibiotic drugs, from streptomycin to daptomycin. [See recent entry, Shovelful of Resistance.]

The good news is that no antibiotic currently in use in either people or livestock has plantensimycin’s novel mode of action. The bad news is that many bacteria now possess the genetic blueprints for efflux pumps, a kind of generic resistance mechanism for expunging a bacterial cell of most anything noxious.

In fact, efflux pumps are just the sort of resistance mechanism switched on by two other antibiotics in the news this past month. Triclosan and triclocarban target another bacteria enzyme involved in fatty acid synthesis, and they can be found in thousands of consumer products including many kinds of soaps, deodorants, and toothpastes.

In the May issue of Environmental Science & Technology, scientists at Johns Hopkins’ Department of Environmental Health Sciences report that 75 percent of the triclocarban Americans rinse down their drains ends up intact in the sewer sludge applied to farm fields. The researchers estimate that this translates into some 200 tons of the antimicrobial and its cousin triclosan being applied to croplands each year. Last year, the same team found triclocarban contaminating every stream tested within miles of their Baltimore campus. The consequence of all this antibiotic in our water and on our croplands? Unknown.