antibiotic resistance

A major study in hospital ICUs shows that bathing patients daily with an antimicrobial soap and applying antibiotic ointment in the nose reduced by 44 percent the bloodstream infections caused by dangerous pathogens, including the drug-resistant bacteria MRSA (pictured).

Soil bacteria and bacteria that cause human diseases have recently swapped at least seven antibiotic-resistance genes, researchers at Washington University School of Medicine report on Aug. 31 in Science.

Disease-causing bacteria’s efforts to resist antibiotics may get help from their distant bacterial relatives that live in the soil, new research by Kevin Forsberg, a graduate student at Washington University School of Medicine suggests. The researchers found identical genes for antibiotic resistance in soil bacteria and in pathogens from clinics around the world.

Bacteria often attack with toxins designed to hijack or even kill host cells. To avoid self-destruction, bacteria have ways of protecting themselves from their own toxins. Now, researchers have described one of these protective mechanisms, potentially paving the way for new classes of antibiotics that cause the bacteria’s toxins to turn on themselves.

The schematic in the center shows how a drug molecule (in the circle) prevents UTIs by stopping pili formation.A different approach to treating urinary tract infections (UTIs) could defeat the bacteria that cause the infections without directly killing them, a strategy that could help slow the growth of antibiotic-resistant infections. Instead of trying to wipe out bacteria, researchers at the School of Medicine have been working to create pharmaceuticals that essentially “defang” the bacteria by preventing them from assembling pili, microscopic hairs that enable the bacteria to invade host cells and defend themselves against the host’s immune system.

The schematic in the center shows how a drug molecule (in the circle) prevents UTIs by stopping pili formation.A different approach to treating urinary tract infections (UTIs) could defeat the bacteria that cause the infections without directly killing them, a strategy that could help slow the growth of antibiotic-resistant infections. Instead of trying to wipe out bacteria, researchers at Washington University School of Medicine in St. Louis have been working to create pharmaceuticals that essentially “defang” the bacteria by preventing them from assembling pili, microscopic hairs that enable the bacteria to invade host cells and defend themselves against the host’s immune system.

Antibiotics are not the answer to curing the common cold.The sniffles. A runny nose. A cough. That’s right — the cold season is upon us. But before you head off to your doctor demanding antibiotics to lessen your symptoms, be aware that those drugs don’t always work and can have serious side effects, say two physicians at Washington University in St. Louis.

Antibiotics are not the answer to curing the common cold.The sniffles. A runny nose. A cough. That’s right — the cold season is upon us. But before you head off to your doctor demanding antibiotics to lessen your symptoms, be aware that those drugs don’t always work and can have serious side effects, say two physicians at Washington University in St. Louis. “People need to remember that antibiotics are used for bacterial infections. A common cold is a virus. Antibiotics simply won’t work on viral infections,” says David C. Mellinger, M.D., associate director and chief physician at the university’s Student Health Service. “Antibiotics are drugs prescribed to kill bacteria, not viruses.”

E. Coli (yellow) attaches to a host cell using sticky fibersNew insights into the bacteria responsible for urinary tract infections appear to open up an opportunity for disabling a wide range of infectious bacteria. Researchers at the School of Medicine recently revealed how a protein known as PapD helps E. coli assemble sticky fibers called pili that allow the bacterium to latch onto and infect host cells. Scientists are using what they’ve learned to begin designing pilicides, new treatments that stop pili formation and disrupt the infection process.

E. Coli (yellow) attaches to a host cell using sticky fibersNew insights into the bacteria responsible for urinary tract infections appear to open up an opportunity for disabling a wide range of infectious bacteria. Researchers at the School of Medicine recently revealed how a protein known as PapD helps E. coli assemble sticky fibers called pili that allow the bacterium to latch onto and infect host cells. Scientists are using what they’ve learned to begin designing pilicides, new treatments that stop pili formation and disrupt the infection process.