Antibiotics: 5 Myths Debunked

Brad Spellberg, MD


October 20, 2016

Myth 3: To Prevent Resistance, Patients Must Complete Every Dose of Antibiotics Prescribed, Even After They Feel Better

The origins of this myth are slightly obscure, but appear to date back to the 1940s.[6,7] Despite how widespread and deeply this belief is held, there are no data to support the idea that continuing antibiotics past resolution of signs and symptoms of infection reduces the emergence of antibiotic resistance.[7]

To the contrary, studies have repeatedly found that shorter-course therapies are less likely to select out for antibiotic resistance, which is consistent with fundamental principles of natural selection.[7] Every randomized clinical trial that has ever compared short-course therapy with longer-course therapy, across multiple types of acute bacterial infections (including cellulitis, acute bacterial sinusitis, community-acquired pneumonia, nosocomial pneumonia/ventilator-associated pneumonia, complicated urinary tract infections, and complicated intra-abdominal infections), has found that shorter-course therapies are just as effective.[7] When evaluated, shorter-course therapies have resulted in less emergence of resistance.

Implications of busting this myth. This myth needs to be replaced by a new antibiotic mantra: "Shorter is better!"[7] Patients should be told that if they feel substantially better, with resolution of symptoms of infection, they should call the clinician to determine whether antibiotics can be stopped early. Clinicians should be receptive to this concept, and not fear customizing the duration of therapy.

Continuing antibiotics past resolution of symptoms for acute bacterial infections (not chronic infections, such as osteomyelitis, tuberculosis [TB], or actinomycosis) does not afford patient benefit and probably selects for antibiotic resistance.

Myth 4: When Antibiotic Resistance Emerges, It Is Usually a Consequence of New Mutations at the Site of Infection

This myth possibly stems from the correct recognition that resistance in TB occurs at the site of infection, owing to spontaneous mutations targeting TB therapy.[8] However, TB has unique features distinct from those of most acute bacterial infections.

There is no environmental reservoir for TB, and TB is not part of our normal flora. Therefore, TB resistance can only occur at the site of infection in the body. TB cavities also contain very high densities of bacilli (ie, > 1012 per gram), which predispose to the emergence of resistance on monotherapy, on the basis of the statistical frequency of spontaneous mutations to such drugs as isoniazid and rifampin.

In contrast, when we use typical antibiotics (different from isoniazid, which is specific for TB), they inevitably cause selective pressure among a person's normal bacterial flora. In most cases, resistance emerges not at the site of infection during a course of therapy, but rather among bacteria in the gut or on the skin as a result of genetic sharing of preexisting resistance mechanisms (eg, plasmids, transposons, phages, naked DNA).[8]

Enrichment for resistant normal flora can result in future infections caused by the resistant pathogens, and spread of the resistant pathogens through contact with other people or fomites.

Implications of busting this myth. In most cases, we are not aware when resistance emerges in patients. The fact that the patient's infection resolves with prolonged or unnecessarily broad antibiotic therapy does not mean that you have escaped inducing resistance. To the contrary, it is very likely that after exposure to antibiotics, somewhere in the patient's body, strains of normal flora that are resistant to the antibiotics used have been enriched. Those strains can cause future infections, or spread to others in communities or hospitals.


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