dangerous liaison. vancomycin resistance probably jumped out of E. faecalis to S. aureus via a plasmid (black loop) carrying a transposon (red) that infested the local plasmid (blue) .
The long dreaded superbug surface on a Friday summer in 02. The new strain of the resistance Staphylococcus aureus , cultured from a patient with diabetes at Detroit, had developed to vancomycin, one of the few antibiotics left to reliably kills staph. Now a study shows how the microbe became a threat.
S. aureus lives on the skin and in the nose of healthy people, causing nothing worse than pimples and boils. But in hospitalized patients, it causes tens of thousands of infections each year, including serious infections and surgical wound sometimes fatal, infections of the bloodstream, and pneumonia. The microbe has learned to evade antibiotic after another, and in the late 1980s, vancomycin was the drug of last resort.
When the Detroit vancomycin-resistant S. aureus (VRSA) strain appeared the detective work began. Doctors two strains almost identical patient. The only difference seems to be vancomycin resistance or sensitivity. Doctors also grown Enterococcus faecalis of ulcers resistant to vancomycin foot of the patient. circular loops of DNA called plasmids of VRSA and E. faecalis strains, but not sensitive S. aureus strain had a gene called vanA as wards of vancomycin. This suggests that the drug resistance gene had jumped species, says Weigel.
To see how he made the jump, microbiologists Linda and Fred Weigel Tenover of CDC and colleagues examined the plasmids for a mobile genetic element called a transposon, a DNA extract that can jump from a plasmid and worm its way into another. Indeed, the two strains resistant to vancomycin welcomed with a plasmid containing a transposon vanA .
The results suggest that E. faecalis in the woman's ulcer crept up S. aureus and passed along its resistance plasmid, the researchers report in the November issue 28 Science . Enzymes in S. aureus seem to have destroyed abroad E. faecalis plasmid, but before that happened, the transposon jumped like a rat escape from a sinking ship, and infiltrated the S. aureus plasmid resident to create a new hybrid. This created a new S villain. aureus strain that can spread easily in hospitals, withstand almost all drugs to kill him, and share his weapons with S. aureus cousins who remain vulnerable to vancomycin. "What we have is really isolated the triple threat," says Tenover.
Two antibiotics, linezolid (Zyvox) and quinupristin / dalfopristin (Synercid), always stop VRSA, said microbiologist Donald Low University . Toronto But it is important that pharmaceutical companies intensify efforts to develop alternatives, he said. " At this point, we have something in our back pocket, but that could change quickly "
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