Erm(41)-dependent inducible resistance to azithromycin and clarithromycin in clinical isolates of Mycobacterium abscessus

Maurer, Florian P.; Castelberg, Claudio; Quiblier, Chantal; Böttger, Erik C.; Somoskövi, Ákos

doi:10.1093/jac/dku007

Cited by 91 publications

(100 citation statements)

References 19 publications

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“…massiliense were susceptible to clarithromycin and harbored an erm (41) (41) sequevars with regard to a T/C polymorphism at nucleotide 28: erm(41) sequevar T28 (Trp 10 codon) associated with inducible resistance and erm(41) sequevar C28 (Arg 10 codon) associated with clarithromycin susceptibility. These results were confirmed using isolates from other countries (19)(20)(21)(22).…”

supporting

confidence: 65%

Selection of Resistance to Clarithromycin in Mycobacterium abscessus Subspecies

Mougari

Bouziane

Crockett

et al. 2017

Antimicrob Agents Chemother

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Mycobacterium abscessus is an emerging pathogen against which clarithromycin is the main drug used. Clinical failures are commonly observed and were first attributed to acquired mutations in rrl encoding 23S rRNA but were then attributed to the intrinsic production of the erm(41) 23S RNA methylase. Since strains of M. abscessus were recently distributed into subspecies and erm(41) sequevars, we investigated acquired clarithromycin resistance mechanisms in mutants selected in vitro from four representative strains. Mutants were sequenced for rrl, erm(41), whiB, rpIV, and rplD and studied for seven antibiotic MICs. For mutants obtained from strain M. abscessus subsp. abscessus erm(41) T28 sequevar and strain M. abscessus subsp. bolletii, which are both known to produce effective methylase, rrl was mutated in only 19% (4/21) and 32.5% (13/40) of mutants, respectively, at position 2058 (A2058C, A2058G) or position 2059 (A2059C, A2059G). No mutations were observed in any of the other genes studied, and resistance to other antibiotics (amikacin, cefoxitin, imipenem, tigecycline, linezolid, and ciprofloxacin) was mainly unchanged. For M. abscessus subsp. abscessus erm(41) C28 sequevar and M. abscessus subsp. massiliense, not producing effective methylase, 100% (26/26) and 97.5% (39/40) of mutants had rrl mutations at position 2058 (A2058C, A2058G, A2058T) or position 2059 (A2059C, A2059G). The remaining M. abscessus subsp. massiliense mutant showed an 18-bp repeat insertion in rpIV, encoding the L22 protein. Our results showed that acquisition of clarithromycin resistance is 100% mediated by structural 50S ribosomal subunit mutations for M. abscessus subsp. abscessus erm(41) C28 and M. abscessus subsp. massiliense, whereas it is less common for M. abscessus subsp. abscessus erm(41) T28 sequevar and M. abscessus subsp. bolletii, where other mechanisms may be responsible for failure.

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supporting

confidence: 65%

Selection of Resistance to Clarithromycin in Mycobacterium abscessus Subspecies

Mougari

Bouziane

Crockett

et al. 2017

Antimicrob Agents Chemother

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“…Interestingly, these strains showed increasing MIC levels during prolonged incubation with CLR, but not >4 g/mL at 14 days of incubation; however, the MICs were much lower than those for M. abscessus T28 sequevars. This decrease in susceptibility after prolonged incubation was previously observed and was associated with an increase in mRNA transcripts upon exposure to macrolides [9,21]. [26].…”

Section: Discussionsupporting

confidence: 77%

Molecular mechanisms of clarithromycin resistance in Mycobacterium abscessus complex clinical isolates from Venezuela

Ramírez

Waard

Araque

2015

Journal of Global Antimicrobial Resistance

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“…If the results of prolonged DST suggest a susceptibility of M. abscessus species to macrolides, one of the macrolides, preferably azithromycin, should always be part of the drug regimen. Clarithromycin might induce macrolide resistance in the M. abscessus complex more frequently than azithromycin [147], but this finding is not consistent [148]. The choice of companion drugs that will protect the macrolide from resistance is controversial.…”

Section: Managementmentioning

confidence: 99%

Pulmonary Disease Caused by Non-Tuberculous Mycobacteria

Wassilew¹,

Hoffmann²,

Andréjak³

et al. 2016

Respiration

127

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Non-tuberculous mycobacteria (NTM) include more than 160 ubiquitous, environmental, acid-fast-staining bacterial species, some of which may cause disease in humans. Chronic pulmonary infection is the most common clinical manifestation. Although patients suffering from chronic lung diseases are particularly susceptible to NTM pulmonary disease, many affected patients have no apparent risk factors. Host and pathogen factors leading to NTM pulmonary disease are not well understood and preventive therapies are lacking. NTM isolation and pulmonary disease are reported to rise in frequency in Europe as well as in other parts of the world. Differentiation between contamination, infection, and disease remains challenging. Treatment of NTM pulmonary disease is arduous, lengthy, and costly. Correlations between results of in vitro antibiotic susceptibility testing and clinical treatment outcomes are only evident for the Mycobacterium avium complex, M. kansasii, and some rapidly growing mycobacteria. We describe the epidemiology of NTM pulmonary disease as well as emerging NTM pathogens and their geographical distribution in non-cystic fibrosis patients in Europe. We also review recent innovations for the diagnosis of NTM pulmonary disease, summarize treatment recommendations, and identify future research priorities to improve the management of patients affected by NTM pulmonary disease.

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Erm(41)-dependent inducible resistance to azithromycin and clarithromycin in clinical isolates of Mycobacterium abscessus

Cited by 91 publications

References 19 publications

Selection of Resistance to Clarithromycin in Mycobacterium abscessus Subspecies

Selection of Resistance to Clarithromycin in Mycobacterium abscessus Subspecies

Molecular mechanisms of clarithromycin resistance in Mycobacterium abscessus complex clinical isolates from Venezuela

Pulmonary Disease Caused by Non-Tuberculous Mycobacteria

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