A powerful new antibiotic compound developed by MIT scientists destroyed many of the world’s disease-causing bacteria, including strains that have become resistant to antibiotics in common use. The computer model used to identify the compound, halicin, can also be used to identify other antibiotic candidates; it can screen more than a hundred million chemical compounds in a matter of days, MIT News reported in an article announcing the findings.
A powerful new antibiotic compound developed by MIT scientists destroyed many of the world’s disease-causing bacteria, including strains that have become resistant to antibiotics in common use. The computer model used to identify the compound, halicin, can also be used to identify other antibiotic candidates; it can screen more than a hundred million chemical compounds in a matter of days, MIT News reported in an article announcing the findings.
But one of the collaborators in the study, Dr. Jonathan Stokes of the Broad Institute of MIT & Harvard, cautioned that the development of a line of antibiotics that can permanently overcome a bacterium’s resistance mechanisms may still not be on the horizon.
“For any antibiotic we discover, bacteria WILL evolve resistance,” Stokes wrote in an email response to questions from Current Science Daily. “It’s more a question of how long it will take for resistance to evolve, and what is the mechanism of resistance. But it will, without question, happen. “
Stokes added that it’s nearly impossible to say when a certain bacterium will develop that resistance – it employs numerous defense mechanisms.
“Either the bacterium has a protein that degrades the antibiotic; the bacterium pumps the antibiotic out of the cell; the bacterium mutates the target of the antibiotic so that the antibiotic cannot stick to the target to exert it’s antibacterial activity,” Stokes wrote.
As an example, he said that in the case of the antibiotic ciprofloxacin “the target is a protein that the bacterium can easily mutate such that ciprofloxacin cannot exert its activity.”
Or, as is the case for most antibiotics, bacteria can exchange resistance genes, "thereby causing the spread of resistance through such aforementioned mechanisms. In cases when you have a new antibiotic that doesn’t stick a common target or have a structure similar to clinical antibiotics, the acquisition of resistance is more difficult and therefore takes a little longer.”
Finally, Stokes said that halicin is not a natural product.
“There might be some enzyme in nature that can inactivate halicin, it’s not from a producer organism,” he wrote.