London: Scientists have developed what they call a “suicide bomber” bacterium which can detect and destroy a hospital superbug resistant to antibiotics.
Researchers in the Nanyang Technological University in Singapore engineered a strain of E. coli that can detect signs of Pseudomonas aeruginosa, a leading cause of infection that can be fatal to patients with weak immune systems.
The specially designed bacteria produces a toxin that is lethal to the superbug, before blowing themselves apart like bombs and splattering the substance over the surrounding area, the Daily Telegraph reported.
When added to a culture of P. aeruginosa in lab tests, the artificial E.coli destroyed 99 percent of its targets and prevented the formation of biofilms -- slimy communities of bacteria which are difficult to destroy -- by up to 90 percent, the researchers said.
The method has not been tested in trials on humans or animals, but the researchers indicated that it could provide a new approach to tackling drug-resistant infections, where progress using current techniques has ground to a halt.
Detailing their findings in the journal Molecular Systems Biology, the researchers wrote:
"In summary, we engineered a novel biological system, which comprises sensing, killing, and lysing devices, that enables E. coli to sense and eradicate pathogenic P. aeruginosa strains by exploiting the synthetic biology framework."
P. aeruginosa strains which generally found in hospitals infect the lungs and digestive system particularly in patients who are critically ill or have weakened immune systems.
The new E.coli strain developed by the researchers in Singapore uses a protein called LasR to detect chemical signals given off by P. aeruginosa cells while communicating with each other.
P. aeruginosa naturally produces a toxin known as pyocin, but the scientists engineered the E.coli to produce the same weapon when the pathogen is detected nearby.
The E.coli bacteria then burst themselves open and cover the P. aeruginosa bacteria with pyocin, which eats away at the outer cell wall and causes the insides to spill out.