pentagon to superbugs: resistance is futile

Wired | Common antibiotics work by attaching to a specific molecule (like an enzyme) inside bacterial cells. With some minor adaptive changes, bacteria can alter their cell structure to prevent antibiotic binding, thereby becoming resistant to the drugs. Some infections even develop “persister cells,” which stop growing when the antibiotics are administered, and then turn back on once a round of meds is completed.

But Tew and his team have developed antibiotics that work from the outside to quickly destroy bacterial cells. The drugs work by poking holes in bacterial membranes, killing the cells instantly. Within a few hours, the antibiotics are able to kill off entire colonies of bacterial pathogens. And resistance is futile: Because the meds don’t enter the actual cell, it’s impossible for the bacteria to fight back through structural adaptation.

The method has already proven effective in clinical trials for treating staph infections, and the Pentagon is betting it’ll be effective in combating Iraqibacter too. In 2009 alone, they doled out nearly $8 million to UMass and PolyMedix, to “study its antibiotic compounds for other biodefense applications and bacterial infections.”

Right now, the group is starting animal studies of Iraqibacter antibiotics, though Tew anticipates that human application is several years off. The scientists are also involved in preliminary research on using the membrane-puncture method to address other strains of bacteria.

But a means of mitigating antibiotic-resistant bacteria can’t come a moment too soon. Just last month, federal health officials warned that if resistance keeps growing, Americans could soon be living in “a post antibiotic era.”