Delayed Microbiological Diagnosis and Fluoroquinolone-Associated Tendon Rupture in Pulmonary Nocardiosis Complicating...

This report describes pulmonary nocardiosis in autoimmune pulmonary alveolar proteinosis (PAP), characterized by delayed microbiological diagnosis and a severe fluoroquinolone-associated adverse reaction. The autoimmune form, mediated by anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) antibodies, predisposes patients to opportunistic infections due to impaired alveolar macrophage function. We describe a 48-year-old male smoker with a history of recurrent respiratory infections who presented with fever and hypoxemic respiratory failure. High-resolution CT demonstrated bilateral ground-glass opacities with superimposed interlobular septal thickening, consistent with a diffuse crazy-paving pattern predominantly involving the lower lobes, associated with focal consolidations in the left lower and right upper lobes. Despite initiation of broad-spectrum antimicrobial therapy, the patient exhibited clinical deterioration characterized by recurrence of fever, rising inflammatory markers (C-reactive protein (CRP) 298 mg/L), worsening hypoxemia with a decline in the PaO₂/FiO₂ ratio to 168, and radiological progression on repeat high-resolution computed tomography (HRCT), demonstrating increased areas of consolidation and expansion of ground-glass opacities. A milky-appearing bronchoalveolar lavage (BAL) initially yielded negative cultures; however, after 14 days of incubation, it revealed growth of Nocardia wallacei, identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). A diagnosis of autoimmune PAP was confirmed through the detection of anti-GM-CSF antibodies. The clinical course was complicated by relapse and a left-sided tendon rupture occurring after 10 days of fluoroquinolone therapy. The patient eventually achieved stability through a multidrug regimen followed by long-term secondary prophylaxis with cotrimoxazole for a total of 12 months. This case underscores the diagnostic challenge posed by slow-growing pathogens in patients with underlying rare lung diseases and highlights the necessity of maintaining a high index of suspicion for opportunistic infections when standard treatments fail.