201612-Bacteria-1

Resistance might be futile according to a US academic research AM resistance.

The Prof of Clinical Medicine at the University of Southern California, Brad Spellberg MD, has raised some interesting points about antibiotic resistance on a website posting. He says:

  • Bacterial antibiotic resistance is an inevitable part of Nature.
  • Yes, avoid prescribing antibiotics unnecessarily. When they are appropriate, prescribe the narrowest-spectrum agent and the shortest duration possible.
  • Do not tell patients to take every dose prescribed. Be available to coach patients, encouraging them to stop antibiotics early when symptoms resolve.
  • Prescribed antibiotics select for resistance in the patient’s microbiome.
  • When choosing antibiotics, cidal vs static is largely irrelevant.201612-Antibiotic sensitvity and resistance

His expanded comments say genetic analysis indicates that bacteria invented antibiotics about 2 billion years ago – killing each other with these weapons, and using resistance mechanisms to protect themselves. Resistance to modern antibiotics, including multi-drug resistance, was found in bacteria in a New Mexico cave that had no previous exposure to mankind.
Antibiotic use causes selective pressure by killing off bacteria, whether prescribing is appropriate or inappropriate. The difference is that inappropriate use offers no benefit. Eliminating inappropriate antibiotic use may slow the emergence of resistance (but does not cause resistance per se).
There are no data to support the idea that continuing antibiotics past resolution of signs and symptoms of infection reduces the emergence of resistance. Every randomised clinical trial that has ever compared short-course therapy with longer-course therapy, across multiple types of acute bacterial infections, has found shorter-course therapies are just as effective. In acute infections, if patients feel substantially better, with resolution of symptoms of infection, they can stop antibiotics early.
In most cases, resistance emerges not at the site of infection during therapy, but rather among bacteria in the gut or on the skin as a result of genetic sharing of pre-existing resistance mechanisms (e.g. plasmids, transposons, phages, naked DNA). Resistant strains can cause future infections, or spread to others in communities or hospitals.
Contrary to common belief, bacteriostatic (“static”) antibiotics do kill bacteria; they just require a higher concentration to do it. We define a bactericidal (“cidal”) antibiotic based on laboratory conventions, not on specific scientific principles. There is no clinical trial evidence of benefit of cidal agents over static agents (more to the contrary in fact!).
By Dr Rob McEvoy

 

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