Researchers
at Washington University School of Medicine in St. Louis have figured out a key
step in the transmission of antibiotic resistance from one Acinetobacter
bacterium to another, insight that sheds light on how antibiotic resistance
spreads through a hospital or community. This could open up a new strategy to
safeguard our ability to treat bacterial infections with antibiotics. The
research indicates that the effectiveness of current antibiotics may be
somewhat preserved by curtailing the spread of antibiotic-resistance genes.
Spotless
surfaces in hospitals can hide bacteria that rarely cause problems for healthy
people but pose a serious threat to people with weakened immune systems.
Acinetobacter baumannii causes life-threatening lung and bloodstream infections
in hospitalized people. Such infections are among the most difficult to treat
because these bacteria have evolved to withstand most antibiotics.
The
plasmids' reproductive strategy requires close contact between two bacteria.
But that raises a question: How do two bacteria ever get near enough to
transmit plasmids to each other? Most Acinetobacter guard against strangers
with a system that injects lethal proteins into any unrelated bacteria that
approach too closely, thus reducing the changes of spreading
antibiotic-resistance genes.
The
researchers found that plasmids disable bacteria's self-defense systems so that
plasmids can inject copies of themselves into neighboring bacteria, conferring
drug resistance on the unwitting bacterial neighbors. By forcing the bacteria
in which they reside to lay down their weapons, the plasmid ensures that nearby
bacteria aren't killed before the plasmids can infect them. The researchers
found that mutating plasmids so they could not interfere with the bacteria's defenses
- or mutating the bacteria so the defenses could not be lowered -- prevented
plasmids from spreading.
These
findings provide a novel opening to interrupt the spread of drug resistance,
the researchers said. The genes involved have been identified. Now researchers
have to find compounds that prevent plasmids from disrupting bacterial-defense
systems.
See:
Posted by Dr. Tim Sandle, Pharmaceutical Microbiology
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