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Identification of Virulence Markers of Mycobacterium abscessus for Intracellular Replication in Phagocytes

Identification of Virulence Markers of Mycobacterium abscessus for Intracellular Replication in Phagocytes

Published on: September 27, 2018

Amikacin exposure and susceptibility of macrolide-resistant Mycobacterium abscessus

Shelby Daniel-Wayman¹, Shamira Shallom², Nabila Azeem²

¹Epidemiology Unit, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

ERJ Open Research

|June 1, 2019

Abstract:

Mycobacterium abscessus is associated with antibiotic resistance and poor treatment outcomes. We described within-patient changes in M. abscessus resistance to clarithromycin and amikacin. Patients with amikacin exposure and a >50-month interval between M. abscessus isolates were identified. Antimicrobial susceptibility testing was performed on the first and last isolates by broth microdilution, and genetic markers of resistance were identified. 16 patients were identified with a median amikacin exposure of 2.3 years (range 0.6-8.6 years). 15 patients also received macrolides (median 7.2 years, range 1.3-10.7 years). All initial isolates were resistant to clarithromycin (minimum inhibitory concentration (MIC) ≥8 µg·mL^-1). Two patients had later susceptible isolates, which were of a different subspecies (M. abscessus subsp. massiliense) than the initial isolates (M. abscessus subsp. abscessus). All initial isolates were susceptible or intermediately resistant to amikacin, and only one patient had a resistant final isolate (MIC >64 µg·mL^-1), accompanied by an A→G mutation at position 1408 of the 16S ribosomal RNA. Forced expiratory volume in 1 s decreased significantly over the study period, while smear quantity and the proportions of patients with elevated C-reactive protein or cavitary lesions all increased significantly. Despite prolonged, mostly inhaled amikacin exposure, development of amikacin resistance was uncommon in this patient population; however, disease progression continued.

Insights

Mycobacterium abscessus resistance to clarithromycin is common. Amikacin resistance remained rare despite prolonged exposure, but lung disease worsened in patients with Mycobacterium abscessus infections.

Area of Science:

Medical Microbiology
Infectious Diseases
Pulmonology

Background:

Mycobacterium abscessus infections are challenging due to antibiotic resistance and poor treatment outcomes.
Understanding within-patient resistance development is crucial for optimizing therapy.
Clarithromycin and amikacin are key drugs for M. abscessus treatment.

Purpose of the Study:

To investigate changes in Mycobacterium abscessus susceptibility to clarithromycin and amikacin over time within individual patients.
To identify genetic markers associated with resistance development.
To correlate antimicrobial resistance patterns with clinical disease progression.

Main Methods:

Retrospective analysis of 16 patients with M. abscessus isolates and prolonged amikacin exposure (>50 months).
Broth microdilution antimicrobial susceptibility testing on initial and final isolates.
Identification of genetic resistance markers, including 16S rRNA mutations.
Assessment of clinical parameters: lung function (FEV1), bacterial load, inflammation (CRP), and radiological findings (cavitation).

Main Results:

All initial M. abscessus isolates were resistant to clarithromycin; two later isolates shifted to susceptible due to subspecies change (M. abscessus subsp. massiliense).
Initial isolates were susceptible or intermediately resistant to amikacin; only one patient developed amikacin resistance (with a specific 16S rRNA mutation).
Despite amikacin treatment, patients showed significant decline in lung function and increased markers of disease severity.

Conclusions:

Clarithromycin resistance is prevalent in M. abscessus isolates, potentially linked to subspecies.
Development of amikacin resistance is infrequent even with extended exposure, suggesting its continued utility.
Prolonged M. abscessus infection leads to clinical deterioration regardless of amikacin resistance patterns.

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