As many know, antibiotics are at the front line of medical treatment when it comes to many deadly bacterial infections such as pneumonia, dysentery, and others.  Dr. Miguel Valvan and Omar Halfawy have showed that antibiotic resistance can come from more than just an acquired trait within the cell. They observed that large populations of antibiotic resistant strains share small molecule metabolites with other non-resistant cells.

Many of these mechanisms are well defined.  Examples of these mechanisms include pumping the antibiotic out of the cell and secreting chemicals to degrade the antibiotic.  However, Dr. Miguel Valvan and Omar Halfawy have showed that antibiotic resistance can come from more than just an acquired trait within the cell. 

They observed that large populations of antibiotic resistant strains share small molecule metabolites with other non-resistant cells.   These small, secreted molecules are amino acid derivatives and protect not only the cells that synthesize them but also cells that live in the same environment.

The species under examination were B. cenocepacia and Pseudomonas aeruginosa.  B. cenocepacia is the antibiotic producer while Pseudomonas aeruginosa reaps the benefits of the secreted antibiotic resistances.

This novel form of bacterial communication could have broad implications for medicine and antimicrobials.  These two bacteria are known to cause problems in people with Cystic Fibrosis (CF).  Part of the problem of treating this infection is conventional antibiotics are ineffective at destroying the bacteria.  With this new discovery, novel antibiotics (that aren’t sensitive to this degradation) could be synthesized. 

Treating these antibiotic resistant microbes in CF patients may be the first step to decreasing the incidence by which people are infected with these bacteria.