Drug gradients may give bacteria an evolutionary boost towards antibiotic resistance.
Since Alexander Fleming discovered in 1928 that a substance secreted by a mold could kill bacteria, we have become used to the ease of administering cocktails of antibiotics to fight bacterial infections. However, the use and misuse of antibiotics in human medicine and livestock farming over many decades has had the serious side effect of selecting for bacteria that survive drug attack: many bacterial strains have emerged that are resistant to antibiotics, most famously the multi-drug-resistant Staphylococcus aureus strain, the source of Staph infections, that represents a major threat to hospital patients. The pool of effective antibiotics is running out, and finding new strategies to prevent the rapid evolution of drug resistance has become a pressing challenge for global health.
Now, two independent theoretical studies, one published in Physical Review Letters by Philip Greulich at the University of Edinburgh, UK, and colleagues , and the other by Rutger Hermsen at the Center for Theoretical Biological Physics, San Diego, and colleagues in Proceedings of the National Academy of Sciences , address how the evolution of drug resistance can be profoundly influenced by how drugs are distributed in biological tissues. Once administered, drugs do not spread evenly throughout the human body, which is compartmentalized and composed of tissues that have different affinity for retaining the drugs. The new research suggests that variations in the drug concentration may play an important role in selecting bacterial strains that are able to survive exposure to antibiotics.