@article{mbs:/content/journal/jmm/10.1099/jmm.0.034942-0, author = "de Moura, Vinicius Calado Nogueira and da Silva, Marlei Gomes and Gomes, Karen Machado and Coelho, Fábrice Santana and Sampaio, Jorge Luiz Mello and Mello, Fernanda Carvalho de Queiroz and Lourenço, Maria Cristina da Silva and Amorim, Efigênia de Lourdes Teixeira and Duarte, Rafael Silva", title = "Phenotypic and molecular characterization of quinolone resistance in Mycobacterium abscessus subsp. bolletii recovered from postsurgical infections", journal= "Journal of Medical Microbiology", year = "2012", volume = "61", number = "1", pages = "115-125", doi = "https://doi.org/10.1099/jmm.0.034942-0", url = "https://www.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.034942-0", publisher = "Microbiology Society", issn = "1473-5644", type = "Journal Article", abstract = "Several outbreaks of infections caused by rapidly growing mycobacteria (RGM) were reported in many Brazilian states (2032 notified cases) from 2004 to 2010. Most of the confirmed cases were mainly associated with Mycobacterium massiliense (recently renamed as Mycobacterium abscessus subsp. bolletii) BRA100 clone, recovered from patients who had undergone invasive procedures in which medical instruments had not been properly sterilized and/or disinfected. Since quinolones have been an option for the treatment of general RGM infections and have been suggested for therapeutic schemes for these outbreaks, we evaluated the in vitro activities of all generations of quinolones for clinical and reference RGM by broth microdilution, and analysed the peptide sequences of the quinolone resistance determining regions (QRDRs) of GyrA and GyrB after DNA sequencing followed by amino acid translation. Fifty-four isolates of M. abscessus subsp. bolletii, including clone BRA100, recovered in different states of Brazil, and 19 reference strains of RGM species were characterized. All 54 M. abscessus subsp. bolletii isolates were resistant to all generations of quinolones and showed the same amino acids in the QRDRs, including the Ala-83 in GyrA, and Arg-447 and Asp-464 in GyrB, described as being responsible for an intrinsic low level of resistance to quinolones in mycobacteria. However, other RGM species showed distinct susceptibilities to this class of antimicrobials and patterns of mutations contrary to what has been traditionally defined, suggesting that other mechanisms of resistance, different from gyrA or gyrB mutations, may also be involved in resistance to high levels of quinolones.", }