B47-23 Pulmonary MAC in Cystic Fibrosis: Challenges in Treatment

Abstract Introduction Nontuberculous mycobacteria (NTM), particularly Mycobacterium avium complex (MAC), are increasingly recognized as important pathogens in patients with structural lung disease, including cystic fibrosis (CF). While Pseudomonas aeruginosa and Staphylococcus aureus are more common in CF infections, NTM pose unique diagnostic and therapeutic challenges. Treatment is complicated by prolonged multidrug therapy, frequent intolerance, and difficulty distinguishing infection from colonization. Case Description A 65-year-old woman with cystic fibrosis, bronchiectasis, gastroparesis, and asthma was found to have a right upper lobe pulmonary nodule ten years prior. Bronchoscopy with lavage cultures grew Mycobacterium avium complex. She was started on erythromycin, rifampin, and ethambutol but developed severe gastrointestinal intolerance, leading to early discontinuation. She remained clinically stable and untreated for six years. She later presented with progressive cough and dyspnea. CT imaging showed new right upper lobe consolidation and tree-in-bud nodularity, raising concern for bacterial pneumonia superimposed on chronic MAC infection. She received an eight-week course of intravenous ceftazidime, tigecycline, amikacin, and rifampin. One year later, she was readmitted for a CF exacerbation with new left lower lobe consolidation, treated empirically with a six-week course of piperacillin-tazobactam. After recovery, she resumed MAC therapy with azithromycin, ethambutol, and inhaled amikacin. This regimen was well tolerated and led to interval improvement in right lung opacities. Over the next year, sputum cultures for acid-fast bacilli remained negative, prompting discontinuation of therapy. She has since remained clinically stable without radiographic progression. Discussion This case illustrates the challenges of managing pulmonary Mycobacterium avium complex (MAC) infection in cystic fibrosis. In CF, chronic bronchiectasis fosters colonization by diverse pathogens, including nontuberculous mycobacteria, making it difficult to distinguish active infection from colonization or concurrent bacterial exacerbations. A major barrier to treatment in this patient was intolerance to standard macrolide-based triple therapy, which led to early discontinuation and underscores the limitations of systemic regimens in individuals with gastrointestinal comorbidities. The subsequent use of inhaled amikacin—approved for refractory MAC pulmonary disease—provided an effective and well-tolerated alternative, achieving culture conversion and sustained clinical stability. This case highlights the importance of individualized treatment strategies in CF-associated MAC infection. Incorporating inhaled antimicrobials can expand therapeutic options for patients unable to tolerate systemic therapy while maintaining disease control and improving quality of life. Ultimately, this case demonstrates that flexibility in regimen design, supported by close clinical and microbiologic monitoring, is essential for successful long-term outcomes. This abstract is funded by: None