A Successfully Treated Case of Mycobacterium chelonae Pulmonary Infection and a Literature Review (1990–2025)

Introduction

Mycobacterium chelonae is a species of non-tuberculous mycobacteria (NTM) predominantly associated with skin and soft tissue infections, whereas pulmonary involvement is exceedingly uncommon. Over the past 35 years, sporadic reports have documented its role as an atypical pulmonary pathogen. With the advancement of molecular diagnostic technologies and heightened clinical awareness, understanding of its microbiological characteristics, diagnostic approaches, and therapeutic strategies has steadily improved.¹ A review of 16 English-language case reports retrieved from the PubMed database revealed that the majority of affected patients presented with underlying chronic pulmonary disorders.² Taxonomically, M. chelonae is classified within the Mycobacterium abscessus–chelonae complex, a subgroup of rapidly growing mycobacteria.³ Disseminated disease is rare and generally confined to severely immunocompromised individuals. Notably, M. chelonae demonstrates substantial in vitro resistance to multiple antimycobacterial agents,⁴ and conventional chemotherapeutic eradication has often proven unsuccessful. Herein, we present a rare case of pulmonary M. chelonae infection in a patient without pre-existing chronic lung disease, which was successfully managed with an oral combination regimen of azithromycin (0.5 g once daily) and moxifloxacin (0.4 g once daily).

Clinical Data

A 59-year-old Chinese woman presented with a 2-week history of pronounced fatigue and a 1-day history of fever with chills and dizziness. On examination, temperature was 38.3°C and pulse rate 118 beats/min. Laboratory tests showed: white blood cell count 6.38×10^9/L, neutrophils 84.8%, high-sensitivity C-reactive protein 7.46 mg/L, procalcitonin 1.12 μg/L, and interleukin-6234.7 pg/mL. Gram stain and fungal smear were negative; respiratory nucleic acid assays for influenza A/B, rhinovirus, Mycoplasma pneumoniae, adenovirus and respiratory syncytial virus were negative. Blood culture showed no bacterial growth after 5 days, and bronchoalveolar lavage fluid (BALF) culture yielded only normal respiratory flora. A tuberculosis RNA test was reported as positive; however, the overall clinical-radiologic picture and the subsequent clinical course did not support active tuberculosis. We therefore interpreted this result as possibly reflecting non-viable nucleic acid detection or contamination; confirmatory tuberculosis testing was not available for this report and is acknowledged as a limitation.

Three years earlier, a solitary pulmonary nodule in the left lower lobe was discovered during routine screening and remained stable during follow-up. One year prior, chest computed tomography (CT) revealed an irregular ground-glass nodule in the dorsal segment of the left lower lobe, highly suggestive of invasive adenocarcinoma. The patient underwent single-port laparoscopic left lower lobectomy with mediastinal lymph node dissection, with an uneventful postoperative course. Postoperative adjuvant chemotherapy with pemetrexed and carboplatin was completed in four cycles.

Three months before the current presentation, the patient noticed enlargement of right cervical lymph nodes; biopsy confirmed metastatic lung adenocarcinoma. She subsequently received combination chemotherapy with carboplatin, paclitaxel, and toripalimab. One month prior to presentation, follow-up evaluation indicated immune-related pneumonia, necessitating corticosteroid therapy and temporary suspension of immunotherapy. The second cycle of carboplatin plus paclitaxel chemotherapy was then administered. The current symptoms developed 14 days after the last chemotherapy cycle.

The patient’s medical history was notable for hypertension of one year’s duration and type 2 diabetes mellitus for 15 years, both managed with stable pharmacological therapy.

PTseq analysis of BALF identified: Mycobacteroides chelonae (62 sequences), Tropheryma whipplei (6 sequences), and human gammaherpesvirus 4 (EBV) (4461 sequences). Upon consultation, clinical pharmacists-considering the patient’s oncologic status and microbiological findings-suspected a high probability of M. chelonae infection. Following relevant NTM treatment guidelines, they recommended oral azithromycin (0.5 g once daily) plus moxifloxacin (0.4 g once daily). After initiation of therapy, the patient’s body temperature normalised by day 3, and at 14-day follow-up all infection markers had normalised (Table 1).

Table 1 Conditions for Treatment Recommended by Clinical Pharmacists

Literature Review

We conducted a comprehensive PubMed search for reports of pulmonary infection caused by Mycobacterium chelonae from January 1, 1990, to December 31, 2025, using combinations of the keywords “Mycobacterium chelonae”, “pulmonary”, “lung”, and “mycobacterium”. Titles/abstracts were screened, followed by full-text assessment. Duplicate records were removed. We included case reports/series that provided patient-level pulmonary involvement with species-level identification of M. chelonae; we excluded non-pulmonary infections, reports with unclear species identification, and studies without sufficient case information. Using these criteria, 16 individual pulmonary cases were identified from 16 published articles.^5–20 Including the present case, 17 cases have been reported in the literature within this time window. Due to heterogeneity and incomplete reporting across cases, we summarized patient demographics, clinical presentations, diagnostic approaches, treatment regimens, and outcomes descriptively, without making formal comparative inferences (Table 2).

Table 2 Clinical Characteristics of Reported Pulmonary Mycobacterium chelonae Cases

Discussion

Mycobacterium chelonae belongs to the class Actinomycetia, order Mycobacteriales, family Mycobacteriaceae. This polymorphic organism may present as long, slender rods or short, thick rods (0.2–0.5 × 1–6 μm), with occasional coccoid forms of approximately 0.5 μm in diameter also reported. Young colonies (<5 days) demonstrate strong acid-fast staining, which diminishes with prolonged cultivation. On most culture media, colonies are typically smooth, moist, and glossy, appearing within 3–4 days,²¹ and are nonpigmented or pale creamy yellow. Rough colony morphotypes may develop after approximately three weeks. M. chelonae is widely distributed in environmental reservoirs, including water, soil, dust, and healthcare settings. Human transmission occurs predominantly via environmental exposure, either through aerosol inhalation or via contact with contaminated water/food in the presence of skin breaches.^22,23 As an opportunistic pathogen, it frequently causes infections when skin barriers are compromised (eg, surgery, trauma, cosmetic procedures) or when host immunity is impaired. Clinically, cutaneous infections often manifest with localized swelling, erythema, warmth, pain, and purulent discharge. Pulmonary disease presents with features consistent with pneumonia, including persistent cough, chest pain, hemoptysis, and dyspnea. Pulmonary M. chelonae infections are exceedingly rare.^24,25 Given the rarity of pulmonary involvement and the necessity of tailoring diagnosis and treatment to the organism’s pathogenic profile, we systematically evaluated the reasons for consultation, therapeutic regimens, treatment duration, and clinical outcomes in the aforementioned cases, extracting essential diagnostic and management data to guide individualized therapeutic recommendations for such infections (see Table 1).

Rapidly growing mycobacteria (RGM) are environmental nontuberculous mycobacteria (NTM) that typically form visible colonies on solid media within approximately 7 days. Clinically important RGM include the Mycobacterium abscessus complex (subsp. abscessus, massiliense, and bolletii), Mycobacterium chelonae, and the Mycobacterium fortuitum group.²⁶ Importantly, M. abscessus complex and M. chelonae are distinct species with different clinical spectra and antimicrobial resistance patterns; for example, inducible macrolide resistance mediated byerm (41) is common in M. abscessus subsp. abscessus but is typically absent in M. chelonae.^3,26 Therefore, species-level confirmation by culture-based identification and, when feasible, antimicrobial susceptibility testing remain essential to guide management.^23,27,28

Non-tuberculous mycobacterial pulmonary disease (NTM-PD) is diagnosed by integrating compatible clinical symptoms and radiologic findings with microbiologic evidence, as outlined in commonly used ATS/IDSA criteria and subsequent updates (eg, repeated positive sputum cultures, or a positive bronchoalveolar lavage culture/biopsy with compatible pathology, together with exclusion of alternative diagnoses).^23,27,28 Importantly, detection of NTM nucleic acids alone cannot reliably distinguish colonization from true disease; therefore, sequencing results should be interpreted within the overall clinical context and in conjunction with imaging, AFB smear/culture, and definitive species identification.^23,27,28 In this setting, metagenomic sequencing/PTseq can support early hypothesis generation and facilitate antimicrobial stewardship, but it should be regarded as an adjunct tool and does not replace standard confirmation or susceptibility-guided management.^27–29 In addition, the clinical PTseq report did not provide assay reporting thresholds, negative-control results, or predefined quantitative cutoffs; therefore, the reported sequence counts were treated as semi-quantitative signals, and contamination or detection of non-viable nucleic acids cannot be excluded. Accordingly, we have framed the present case as a probable pulmonary M. chelonae infection with short-term clinical response, while acknowledging that classical microbiologic confirmation and longer follow-up would strengthen diagnostic certainty and treatment assessment.^23,27,28

This report has several limitations inherent to a single-case description and a literature-based synthesis of published reports.³⁰ Firstly, the predominance of cases from specific medical institutions introduces potential referral bias, thereby affecting the generalizability of findings. Secondly, missing critical information—such as environmental exposure history, immune status indicators, and detailed underlying disease trajectories—limits in-depth analysis of infection mechanisms and risk factors. Additionally, heterogeneity in specimen collection and diagnostic protocols over time and across institutions,^31,32 compounded by technological limitations before the year 2000, may have led to underdiagnosis or misclassification.³³ Other potentially influential factors—including prior NTM infection history, interspecies microbial interactions, and host genetic polymorphisms affecting antibiotic metabolism—remain unexplored and could impact both infection risk assessment and optimal therapeutic strategies.

To address these gaps, future investigations should adopt multicenter prospective designs to expand sample sizes, enhance data completeness (including standardized environmental exposure histories and longitudinal immune monitoring), and implement refined analytical methods such as metagenomic sequencing for detailed strain typing. Such approaches would facilitate a clearer understanding of M. chelonae infection characteristics and support optimization of management strategies.²⁹

Conclusions

We report a rare case of probable pulmonary Mycobacterium chelonae infection in a patient with lung adenocarcinoma, in whom BALF PTseq supported early hypothesis generation and antimicrobial stewardship.

The azithromycin-moxifloxacin regimen was associated with short-term clinical improvement without significant adverse events in this immunocompromised patient. Given the lack of classic microbiologic confirmation and limited follow-up, this report should not be interpreted as evidence of definitive cure or as a basis for generalized treatment recommendations. Future studies incorporating confirmatory culture/species identification, susceptibility testing and longer follow-up are needed.