London, Mar 2 (ANI): Scientists have achieved a major breakthrough that may pave the way for new approaches to combat superbug Clostridium difficile (C-diff), a spore-forming bacterium that was discovered in 1978 to be the cause of antibiotic-associated diarrhoea and colitis.
The researchers behind this work say that, since a long time, scientists have been focusing on the wrong toxin that is released by the bacteria in the colon.
The toxin was known to cause severe diarrhoea and life-threatening colitis that could lead to the surgical removal of the colon.
"For 20 years, we have been focusing on Toxin A. But it turns out the real culprit is Toxin B. This is a major finding in how C-diff causes disease in humans. It completely flips our whole concept of what the important toxin is with this disease," Nature magazine quoted study co-author Dr. Dale Gerding as saying.
When the normal bacteria that live in the colon are disturbed, usually as a result of antibiotic treatment, and a patient ingests C-diff spores, the bacteria can multiply and release the two toxins.
The epidemic strain now rivals the superbug known as MRSA as one of the top emerging disease threats to humans. Since its discovery, C-diff has grown increasingly resistant to antibiotics.
C-diff infection is spread by spores that contaminate the hospital environment, or by hands of healthcare workers who can transmit the spores to patients.
But the resistance of the spores to hospital cleaning agents, and to alcohol hand disinfectants, makes it extremely difficult to eradicate.
Gerding pointed out that a human clinical trial using a drug that bound Toxin A more than it bound Toxin B failed to treat C-diff effectively.
"There's probably a good reason why the trial failed. We now know that Toxin B should have been the primary target," said Gerding.
The researchers claimed that the study has major implications for the future development of treatments and preventative measures for C-diff.
"The more you understand the way an organism causes disease, the better you can target treatment or preventative measures," said one of the co-authors of the study.
The breakthrough in the study came after co-authors in Australia engineered mutant strains of the bacteria that were tested by Gerding and other Loyola researchers.
"It turns out that in the strain in which Toxin A was knocked out, the organism was fully virulent. It caused disease. When they knocked the Toxin B out in another set of experiments, the organism didn't cause disease. This is probably the best evidence to date about the relative importance of these two toxins," said the authors.
The study has been published in the journal Nature. (ANI)