By Abby Olena
Scientists find vancomycin-resistant Enterococci in crow fecal samples from across the U.S.
Excerpt: “…the various ways that bacteria gain resistance genes are still not well understood.”
My comment: One way that may not be understood is the thermodynamically regulated organism-level thermoregulation of antibiotic resistance. It facilitates Evolution of Escherichia coli rifampicin resistance in an antibiotic-free environment during thermal stress.The evolution of resistance in an antibiotic-free environment was attributed to beneficial mutations.
No experimental evidence suggests that mutations are fixed in the organized genome of any species from microbes to man. All evidence suggests that antibiotic resistance, like other benefits manifested at the cellular and organismal levels, involves the nutrient-dependent pheromone-controlled physiology of reproduction. Thus, attributing rifampicin resistance to mutations would be as likely a missattribution as any other antibiotic resistance attributed to mutation-driven evolution.
If the observed potential for the evolution of ecological specialization of the niche occupied by rifampicin resistant E. coli is nutrient-dependent and pheromone-controlled, ecological and social niche construction can be placed into the proper context and its antibiotic resistance understood. In the proper context, the epigenetic effects of nutrients and their metabolism to species-specific pheromones controls reproduction in species from microbes to man, which means that antibiotic resistance is both nutrient-dependent and pheromone-controlled in microbes. That understanding of cause and effect in the context of epistasis might benefit our understanding of antibiotic resistance in other organisms. See for example: The cost of antibiotic resistance depends on evolutionary history in Escherichia coli