Excerpt: By gaining mutations in two genes, a strain called H30 gave rise more than a decade ago to the H30-R clone, which became fully resistant to the then-wonder-drug known as Cipro. Soon after, a new clone evolved from H30-R called H30-Rx, which is resistant to several extended-spectrum antibiotics, such as third-generation cephalosporins.
My comment: In my model, the H30 strain gave rise to the H30-R clone via adaptations, not by gaining mutations. The initial strain adapted to the thermodynamic challenge of maintaining its nutrient-dependent pheromone-controlled organism-level thermoregulation, which was required for it to adapt to changes in the cell wall caused by the antibiotic.
Adaptations must continue to occur, when new antibiotics are introduced. Nutrient-dependent alternative splicings continue to enable organisms to better tolerate the increased body temperature associated with “fever” in humans. Nutrient-dependent changes in the epigenetic landscape of the bacteria enable the physical landscape of DNA in its organized genome to incorporate pheromone-controlled epigentically-effected alternative splicings that increase the thermodynamic stability of the cell type. The increased thermodynamic stability of the unicellular cell type may enable it to overtake the immune system defenses of any organism that would otherwise kill it via an increase in body temperature. However, an adapted strain of what once was a non-pathogen associated with the metabolism of nutrients may become a killer in immuno-compromised patients, like those who are hospitalized with infections.
However, Randy Nesse addressed a larger problem (in a lecture I attended last August) that may be responsible for part of the problem with infections in immuno-compromised patients. Prescription antibiotics typically may not be required to kill a pathogen that is causing an uncomfortable fever in a patient. Antibiotic use may relieve their discomfort and reduce the fever by killing most but not all of the organism that is causing the problem. Later in life, patients succumb to strains of the organism with increased organism-level thermoregulatory capacity that has developed due to past antibiotic use. I discussed that fact in this video of the poster presentation I made at that conference.
James V. Kohl detailedl how quantized energy-dependent microRNA biogenesis links the pheromone-controlled physiology of reproduction to biophysically constrained viral latency and healthy longevity. Links from what organisms eat to the enzyme-dependent metabolism of food also link metabolic networks to microRNA-mediated genetic networks in the context of RNA interference. Drug therapies alter RNA interference by altering cell type differentiation in all cells of all individuals of all species. For comparison, during the past 26 years, Kohl has detailed how the chemistry of protein folding is biophysically constrained at every level of biological organization by conserved molecular mechanisms.