November 15, 2013
New Treatment May End Dangerous MRSA Superbug Infections
Rebekah Eliason for redOrbit.com – Your Universe Online
One of the most significant health threats people face today is antibiotic resistant bacteria. A new study by Professor of Biology Kim Lewis presents a groundbreaking method for treating and eliminating the deadly bacterium methicillin resistant staphylococcus aureus, commonly known as MRSA.
Referred to as a “superbug”, MRSA infects a staggering 1 million Americans every year. This bacteria is especially deadly as it leads to chronic infections such as osteomyelitis (bone infection), endocarditis (heart infection), or infections of implanted medical devices. Once these infections enter the body they are frequently incurable, even when aggressively treated with antibiotics.
MRSA and other similar bacteria have evolved to survive treatment with certain antibiotics. This fact has interested scientific and medical communities, but Lewis suspects there may be another adaptive function enabling these bacteria to be antibiotic resistant.
The new study is representative of over a decade worth of research focusing on the special cells all pathogens produce, known as persisters. Lewis explained that these cells were designed to survive. “Survival is their only function. They don’t do anything else.”
Lewis and colleagues theorized that if they could kill these excellent surviving cells, they might have a chance at curing chronic infections including the superbug MRSA.
Brian Conlon, a postdoctoral researcher in Lewis’ lab and first author on the paper, said, “If you can eradicate the persisters, there’s less of a chance that resistance will develop at all.”
Lewis discovered that persisters attain their ultimate goal of survival through entering a dormant state that survives treatment with traditional antibiotics. For regular bacterial infections, antibiotics work by attacking active cellular functions, but this is fruitless against persisters because they are entirely inactive and dormant. Persisters are the crucial aspects of superbugs that enable them to succeed as nasty chronic infections and biofilms. Once the drug treatment has ended the dormant cells simply reawaken and begin the infection all over again.
In this new groundbreaking study, which was also assisted by assistant professor Steve Leonard of the Department of Pharmacy Practice, the team discovered the use of a drug known as ADEP. This drug has the ability to awaken the dormant cells and at the same time initiate a self-destruct mechanism. In several laboratory experiments and, most excitingly, in a mouse model of chronic MRSA, the cells were completely eradicated by this approach.
Conlon explained that when ADEP is used in conjunction with traditional antibiotics the researchers wiped out the entire bacterial population.
It is likely that just as all other actively growing bacterial cells have developed immunity to antibiotics these cells will develop resistance to ADEP but Lewis said, “cells that develop ADEP resistance become rather wimpy.” This means that traditional drugs that treat infections such as rifampicin or linezolid will work well against these weaker, adapted cells. The new treatment will have the unique ability to kill persisters as well as eliminate ADEP-resistant mutant bacteria.
Dr. Richard Novick of New York University’s Langone Medical Center as well as leader in the field said this research is a “brilliant outgrowth of Kim Lewis’ pioneering work on bacterial persisters and represents a highly creative initiative in this era of diminishing antibiotic utility.”
Although ADEP specifically targets MRSA, Lewis and his team believe that compounds similar to it could be effective in the treatment of other infections. Also, they are excited about the potential for success using these compounds on other disease models, such as cancerous tumors, that can only be treated by destroying a population of rogue cells. The team is already in pursuit of other possible treatments.
This study was published Wednesday in the journal Nature.