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Incidental Cavitary Pulmonary Mycobacterium avium Complex Disease With Possible Haemophilus influenzae Coinfection
Robert Alhaddadin1, Amal Qsous2, Parth Bhagat1
1Internal Medicine, Covenant HealthCare College of Medicine, Central Michigan University, Saginaw, USA.
Abstract:
Pulmonary disease caused by Mycobacterium avium complex (MAC) most often occurs in patients with structural lung disease or immunocompromising conditions and typically follows recognized fibrocavitary or nodular-bronchiectatic radiographic patterns. Advanced cavitary disease discovered incidentally in an asymptomatic patient represents an uncommon and diagnostically challenging presentation that may be initially attributed to malignancy, aspiration pneumonia, or endemic fungal infection. We report the case of a 45-year-old man without known immunodeficiency who had alcohol use disorder and active deep vein thrombosis treated with apixaban and presented with acute right groin pain secondary to a reducible inguinal hernia. Abdominal computed tomography performed during hernia evaluation incidentally demonstrated a 6.9 × 5.3 cm thick-walled cavitary opacity in the left lower lobe with an air-fluid level and bilateral reticulonodular opacities. The patient denied cough, dyspnea, hemoptysis, fever, night sweats, and weight loss. Serial sputum acid-fast bacillus smears were positive, and mycobacterial cultures grew MAC. In the setting of compatible cavitary imaging, these findings fulfilled the American Thoracic Society/European Respiratory Society/European Society of Clinical Microbiology and Infectious Diseases/Infectious Diseases Society of America (ATS/ERS/ESCMID/IDSA) diagnostic criteria for pulmonary MAC disease. Tuberculosis and HIV testing were negative. A respiratory molecular panel was also positive for Haemophilus influenzae. Because bacterial cultures showed no growth, this finding was interpreted as a possible coinfection rather than a confirmed bacterial infection. Given the leukocytosis and bilateral infiltrates, intravenous ceftriaxone was initiated empirically. However, MAC-directed multidrug therapy was complicated by two pharmacologic barriers: the risk of reduced apixaban exposure with rifabutin-containing therapy and a baseline corrected QT interval of 512 ms, limiting routine macrolide use. The patient was therefore transferred to a tertiary care center for multidisciplinary regimen selection. This case underscores that incidental cavitary pulmonary lesions demand systematic microbiologic evaluation regardless of symptom burden and that early pharmacologic risk assessment is essential when standard MAC therapy is constrained.
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