Abstract
A 53-year-old man was evaluated in the pulmonary clinic for ongoing asthma symptoms. Despite optimized treatment, he continued to experience a chronic productive cough. He was otherwise physically active, a lifelong non-smoker with no known occupational or environmental exposures. Pulmonary function tests demonstrated normal diffusing capacity and mild airflow obstruction. A chest computed tomography (CT) scan revealed basilar bronchiectasis, mediastinal lymphadenopathy, scattered nodules, and progressive ground-glass opacities (GGOs) in the bilateral lower lobes. Immunoglobulin (Ig) testing showed an isolated IgG3 deficiency, while other Ig subclasses were within normal limits. Additional laboratory workup, including alpha-1 antitrypsin levels, antinuclear antibody, and HIV serologies, was unremarkable. Bronchoscopy was performed, and bronchoalveolar lavage (BAL) cultures grew pan-sensitive Pseudomonas aeruginosa, prompting a course of levofloxacin. Despite an initial negative acid-fast bacilli (AFB) stain, cultures later identified Nocardia nova. Given this diagnosis, a head CT was obtained to assess for central nervous system involvement, which was negative. The patient was initially started on trimethoprim-sulfamethoxazole but developed an adverse reaction, necessitating a switch to an extended course of intravenous ceftriaxone, which was later changed to clarithromycin based on susceptibility testing. A repeat chest CT demonstrated resolution of nodularity, GGOs, and lymphadenopathy. His symptoms fully resolved, with no recurrence of cough or asthma-like exacerbations. Although Nocardia infections are commonly associated with immunosuppression, typically occurring in patients with solid organ or hematopoietic cell transplants, chronic glucocorticoid use, malignancy, or HIV with low CD4 counts, approximately one-third of cases are reported in immunocompetent individuals. While cellular immunocompromise is a well-established risk factor, isolated IgG3 deficiency is not. Asthma, particularly when treated with corticosteroids or accompanied by structural lung disease, is also recognized as a key predisposing respiratory condition. Pulmonary involvement is most frequent, though dissemination to the central nervous system and skin can also occur. This case underscores the need to consider pulmonary nocardiosis even in patients without an overtly immunocompromised state who present with unexplained respiratory symptoms. Diagnosis requires a high index of clinical suspicion and may necessitate bronchoscopy or other invasive procedures when initial treatments fail. Prompt identification and targeted antimicrobial therapy are essential for a favorable outcome.