Scientists claim that sea sponges contain a chemical, algeferin, that thwarts bacterial reistance to antibiotics, as demonstrated in the lab. When antibiotic-resistant bacteria are treated with algeferin they become vulnerable again and antibiotics kill them. The bacteria so far tested include those that cause ear infections, whooping cough, septicemia, food poisoning, MRSA (resistant staph), and pseudomonas aeruginosa, which causes devastating infections in wounded soldiers. So far it has worked on every bacteria tried. Biofilms, usually very resistant to treatment, dissolve. Reseachers found sponges living where other life had been wiped out by bacteria, and began to investigate. (Report from the Hollings Marine Lab in Charleston, presented at the AAAS meeting Feb. 14, review by Science News)
From Science News online
Sponge’s secret weapon restores antibiotics’ power
Bacteria treated with compound lose their resistance
By Laura Sanders
Web edition : Saturday, February 14th, 2009
CHICAGO — A chemical from an
ocean-dwelling sponge can reprogram antibiotic resistant bacteria to make them
vulnerable to medicines again, new evidence suggests.
Ineffective antibiotics become lethal once again for bacteria treated with the sponge compound, chemist Peter Moeller reported February 13 at the American Association for the Advancement of Science annual meeting.
“The potential is outstanding. This could revolutionize our approach to thinking about how infections are treated,” comments Carolyn Sotka of the National Oceanic and Atmospheric Administration’s Oceans and Human Health Initiative in Charleston, S.C.
Everything living in the ocean survives in a microbial soup, under constant bombardment from bacterial assaults. Researchers led by Moeller, of Hollings Marine Laboratory in Charleston, found a sponge thriving in the midst of dead organisms. This anomalous life amidst death raised an obvious question, says Moeller: “How is this thing surviving when everything else is dead?”
Chemical analyses of the sponge’s chemical defense factory pointed to a compound called algeferin. Biofilms, communities of bacteria notoriously resistant to antibiotics, dissolved when treated with fragments of the algeferin molecule. And new biofilms did not form.
So far, the algeferin offshoot has, in the lab, successfully treated bacteria that cause whooping cough, ear infections, septicemia and food poisoning. The compound also works on Pseudomonas aeruginosa, which causes horrible infections in wounded soldiers, and MSRA infections, which wreak havoc in hospitals. “We have yet to find one that doesn’t work,” says Moeller.
And the results may not just apply to bacteria in communities. The compound is able to reprogram antibiotic-resistant bacteria that don’t form biofilms. When bacteria are treated with the compound, antibiotics that usually have no effect are once again lethal. This substance may be the first one that can restore bacterial vulnerability, Moeller says. “This resensitization is brand new.”
And the problem of perpetuating a bacterial-resistance arms race, in which bacteria rapidly develop countermeasures against new antibiotics, may be avoided entirely with the new compound. “Since the substance is nontoxic to the bacterium, it’s not throwing up any red flags,” says Moeller.
Other than “doing something really funky that we’re excited about,” researchers don’t yet know how this compound interferes with bacterial resistance to antibiotics, says Moeller. The compound may sneak by bacteria’s sensors that trigger new ways to combat antibiotics. Bacteria continually treated with this compound for three months are still susceptible to antibiotics.
The research is still in very early phases.
“Everyone would like to see this in antibiotic trials tomorrow,” Moeller says, but treatments for human infections are a long way off.
Sotka agrees. “Of course, we need clinical trials to take it to the next level,” she says.