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Scientists Find a Weak Spot In Some Superbugs’ Defenses

Researchers have found a new way to attack some of the bacteria behind treatment-resistant infections. An anonymous reader shares a report from Wired: In 2004, a 64-year-old woman in Indiana had a catheter put in to help with dialysis. Soon after the procedure, she came to a local hospital with low blood pressure and what turned out to be a dangerous antibiotic-resistant infection from a bacteria called Enterococcus faecalis. […] After the patient in Indiana returned to the hospital, doctors sampled her blood and tested various antibiotics to see what might cure her infection. The strain she was infected with was already resistant to the antibiotic vancomycin, which was traditionally considered the treatment of last resort. But the bacteria that were making her sick were susceptible to a powerful new drug, approved by the FDA just a year before, called daptomycin. With a prescription for daptomycin, the patient improved enough to go home.

But two weeks later, the woman was back in the hospital again, this time with a high fever. Nothing her medical team tried worked, and the woman died. A study out today in the Proceedings of the National Academy of Sciences, though, offers new hope — along with clues about how drug developers might fight back against this foe. VRE bacteria reproduce by pinching in at the center and dividing into two separate cells. Daptomycin fights VRE by binding to its cell membrane right at that center point, which disrupts its ability to divide, among other things. After the patient in Indiana died, doctors compared a sample of her blood with one they’d taken weeks earlier, when she first came to the hospital. They discovered that the daptomycin-resistant strain had a new mechanism that reorganized the cell. Daptomycin could no longer attach and halt the bacteria’s cell division. “[The researchers] were puzzled that the cells somehow knew when to organize their membranes to resist the daptomycin,” reports Wired. “[Researcher Ayesha Khan] noticed these drug-resistant strains had a lot of the protein LiaX both on the cell membranes and outside the cell, so she zeroed in on it. LiaX, the research team found, is an alarm system. The protein binds to daptomycin, sending a signal back telling the cell that it’s time to reorganize. This same mechanism also helps VRE ward off the human immune system, they found, which might contribute to its deadly nature.”

“We knew prior to this study that LiaX likely has a role in daptomycin resistance, and this work goes a long way toward explaining what that role is,” Kelli Palmer, a biologist who studies antibiotic resistance at the University of Texas at Dallas, said. “It is critical that we understand how daptomycin resistance works at a molecular level, so that we can design strategies to reverse it.”

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