Gene researchers have ripped the mask off a strain of hospital superbug that is becoming resistant to all but the toughest antibiotics.
They have identified a cluster of genes in Enterococcus faecalis that enable the bacterium to develop into a colony and exude a potentially lethal toxin, cytolisin, the British weekly Nature reports in Thursday’s issue.
E. faecalis, part of the Enterococcus group of intestinal bacteria, plays a vital role in human health when it is confined to the gut, but is highly infectious if it enters a wound.
Over the years, antibiotic-resistant strains of E. faecalis have built up, becoming one of the most worrying problems for hospital doctors.
The strain whose genome was unravelled by University of Oklahoma researchers was taken from a sample, isolated from a chronically ill US patient in the 1980s, that is resistant to vancomycin, a closely-hoarded antibiotic of last resort.
Tiny differences within the so-called ”pathogenicity island” of genes are what makes this strain so lethal and hard to beat, the team say.
The research is the latest in a series of studies to unlock useful knowledge about superbugs, although a long road lies ahead before the discovery can be made practicable.
Last month, British scientists said they had drawn up a DNA map of Streptomyces coelicolor, a bug that occurs naturally in the soil and is industrially fermented to produce an enormous range of drugs.
More than two-thirds of antibiotics derived from natural sources come from S. coelicolor and its relatives, including streptomycin, tetracyclin and erythromycin.
Understanding how S. coelicolor works could open up the way to tweaking these drugs — making small but important changes to their molecules so that they are better armed to defeat resistant bacteria.
In another step forward, a protein called lactoferrin, which is abundant in tears and mother’s milk, has been found to block germs from forming colonies called biofilms.
Lactoferrin devours iron, depriving the bacteria of an essential nutrient and forcing them to wander across the surface for a new home instead of forming reproductive cell clusters.
The protein was tested on lab dishes sown with Pseudonomas aeruginosa, a germ that has become a serious problem with surgical implants and lethally infects the airways of people with cystic fibrosis. – Sapa-AFP