“A chief cause of the resistance of biofilms is that bacteria on the outside of the clusters have the first shot at the nutrients that diffuse in,” said Pradeep Singh, associate professor of medicine and microbiology at the University of Washington.
“This produces starvation of the bacteria inside clusters, and severe resistance to (their) killing,” added the senior study author, the journal Science reports.
“Bacteria become starved when they exhaust nutrient supplies in the (infected) body, or if they live clustered together in groups known as biofilms,” said study co-author Dao Nguyen, assistant professor of medicine at Montreal’s McGill University.
Preventing pathogenic bacteria from sensing nutrient starvation may present a new therapeutic approach to increasing antibiotic efficacy and preventing drug resistance, researchers claim. A team led by McGill University investigators has found that blocking an active mechanism used by bacteria to respond to starvation by slowing their growth significantly reduces the natural tolerance to antibiotics that infectious organisms develop when nutrient supplies become low.
The investigators work is reported in Science in a paper titled “Active Starvation Responses Mediate Antibiotic Tolerance in Biofilms and Nutrient-Limited Bacteria.” Pradeep K. Singh, Ph.D., Dao Nguyen, Ph.D., and colleagues
Bacteria become highly tolerant to antibiotics when nutrients are limited. The inactivity of antibiotic targets caused by starvation-induced growth arrest is thought to be a key mechanism producing tolerance. Here we show that the antibiotic tolerance of nutrient-limited and biofilm Pseudomonas aeruginosa is mediated by active responses to starvation, rather than by the passive effects of growth arrest. The protective mechanism is controlled by the starvation-signaling stringent response (SR), and our experiments link SR-mediated tolerance to reduced levels of oxidant stress in bacterial cells. Furthermore, inactivating this protective mechanism sensitized biofilms by several orders of magnitude to four different classes of antibiotics and markedly enhanced the efficacy of antibiotic treatment in experimental infections.
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