New Molecule May Combat Dangerous Antibiotic-Resistant Bacteria Biofilms

First Posted: May 24, 2014 11:33 AM EDT

Scientists have made a promising find when it comes to combating antibiotic-resistant bacteria. They've discovered a molecule that prevents bacteria from forming biofilms, which is a frequent cause of infections.

"Currently there is a severe problem with antibiotic-resistant organisms," said Bob Hancock, one of the researchers, in a news release. "Our entire arsenal of antibiotics is gradually losing effectiveness."

In fact, more and more antibiotic-resistant bacteria are showing up in hospitals. These bacteria can cause infection and, in severe cases, lead to death since it's difficult to treat them.

Many bacteria that grow on skin, lung, heart and other human tissues surfaces actually form biofilms, which are highly structured communities of bacteria that are responsible for two-thirds of all human infections. Currently, there are no approved treatments for biofilm infections, and these infections can be quite resistant to standard antibiotics.

Yet this new finding may change things when it comes to combating biofilms. The researchers have found that the peptide known as 1018, which consists of about 12 amino acids, can destroy biofilms and prevent them from forming.

There are generally two different classes of bacteria: gram-positives and gram-negatives. The differences in their cell wall structures make them susceptible to different kinds of antibiotics. Yet 1018 actually worked on both classes of bacteria, and even on several major anti-biotic resistant pathogens.

"Antibiotics are the most successful medicine on the planet," said Hancock in a news release. "The lack of effective antibiotics would lead to profound difficulties with major surgeries, some chemotherapy treatments, transplants, and even minor injuries. Our strategy represents a significant advance in the search for new agents that specifically target bacterial biofilms."

The findings are published in the journal PLOS Pathogens.

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