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Progressive cavitary Mycobacterium abscessus pulmonary disease with inducible macrolide resistance — SCE Respi

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HardTuberculosis and Nontuberculous MycobacteriaProgressive cavitary Mycobacterium abscessus pulmonary disease with inducible macrolide resistanceSCE Respiratory

A 61-year-old woman with bronchiectasis reports worsening productive cough, fatigue and 5 kg weight loss over 6 months despite optimised airway clearance. CT shows progressive tree-in-bud nodularity and a new 2.5 cm right upper-lobe cavity. Three sputum samples are smear-positive and culture Mycobacterium abscessus subsp. abscessus. An NTM multidisciplinary team confirms that treatment is indicated. The isolate is susceptible to clarithromycin on day 3 of incubation but resistant on day 14. Sequencing demonstrates a functional erm(41) gene without an rrl mutation. The amikacin MIC is 16 mg/L, with no rrs mutation. Baseline renal and hepatic function, audiometry and ECG permit all the agents listed. Which initial antibiotic strategy is most appropriate?

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Correct answer: E — Start intravenous amikacin, tigecycline and imipenem with oral azithromycin, without counting azithromycin as an active drug

Explanation lettering: B = shown as A · C = shown as B · D = shown as C · A = shown as D

The clinical, radiological and microbiological progression establishes M. abscessus pulmonary disease requiring treatment rather than observation. Clarithromycin susceptibility at day 3 followed by resistance at day 14, together with a functional erm(41) gene and no rrl mutation, identifies inducible rather than constitutive macrolide resistance. BTS guidance recommends an initial phase of at least 4 weeks of intravenous amikacin and tigecycline, with intravenous imipenem and an oral macrolide where tolerated. Severe cavitary, smear-positive disease may justify a longer intravenous phase according to response and toxicity. The ERS-endorsed guideline clarifies that a macrolide may remain in the regimen for potential immunomodulatory benefit when inducible resistance is present, but it must not be counted as microbiologically active. A is a regimen for severe MAC pulmonary disease, not M. abscessus. B resembles older or individualised regimens but omits tigecycline and incorrectly treats azithromycin as active. C would fit the BTS approach to constitutive macrolide resistance, which would produce early and persistent resistance, usually through an rrl mutation. D provides too few reliably active initial drugs and incorrectly relies on azithromycin despite functional erm(41).

Reference: British Thoracic Society Guideline for the management of non-tuberculous mycobacterial pulmonary disease: summary of recommendations (November 2017) — https://www.brit-thoracic.org.uk/document-library/guidelines/ntm/bts-ntm-guideline-summary-of-recommendations/ British Thoracic Society guidelines index (Checked 18 August 2026) — https://www.brit-thoracic.org.uk/clinical-resources/guidelines/ Treatment of nontuberculous mycobacterial pulmonary disease: an official ATS/ERS/ESCMID/IDSA clinical practice guideline (2020) — https://publications.ersnet.org/content/erj/56/1/2000535