Mycobacterium abscessus Smooth and Rough Morphotypes Form Antimicrobial-Tolerant Biofilm Phenotypes but Are Killed by Acetic Acid

Authors:
Open Access
Publisher website
Google Scholar
Abstract
Mycobacterium abscessushas emerged as an important pathogen in people with chronic inflammatory lung diseases such as cystic fibrosis, and recent reports suggest that it may be transmissible by fomites.M. abscessusexhibits two major colony morphology variants: a smooth morphotype (MaSm) and a rough morphotype (MaRg). Biofilm formation, prolonged intracellular survival, and colony variant diversity can each contribute to the persistence ofM. abscessusand other bacterial pathogens in chronic pulmonary diseases. A prevailing paradigm of chronicM. abscessusinfection is thatMaSmis a noninvasive, biofilm-forming, persistent phenotype andMaRgan invasive phenotype that is unable to form biofilms. We show thatMaRgis hyperaggregative and forms biofilm-like aggregates, which, likeMaSmbiofilm aggregates, are significantly more tolerant than planktonic variants to acidic pHs, hydrogen peroxide (H2O2), and treatment with amikacin or azithromycin. We further show that both variants are recalcitrant to antibiotic treatment inside human macrophage-like cells and thatMaRgis more refractory thanMaSmto azithromycin. Our results indicate that biofilm-like aggregation and protracted intracellular survival may each contribute to the persistence of this problematic pathogen in the face of antimicrobial agents regardless of morphotype. Biofilms of eachM. abscessusvariant are rapidly killed, however, by acetic acid, which may help to prevent local fomite transmission.

This publication has 65 references indexed in Scilit: