To the Editors: A 7-year-5-month-old girl presented to a tertiary medical center in Taiwan with a 1-month history of persistent cough and progressive dyspnea. Four weeks prior, Mycoplasma pneumoniae (MP) pneumonia was laboratory-confirmed (serum MP immunoglobulin IgM positive; IgG 1:1280). Despite a course of doxycycline, her condition worsened. Upon emergency admission, she was hypoxemic with an SpO2 of 89%–92% on room air. Physical examination revealed bilateral diffuse wheezing, coarse crackles and subcostal retractions. Initial chest radiograph (Fig. 1A) showed peribronchial thickening with bilateral emphysematous changes suggestive of air trapping. Laboratory workup showed a white blood cell count of 11,900/μL and C-reactive protein <0.4 mg/dL. She failed to respond to empiric intravenous antibiotics and bronchodilators. Pulmonary function testing demonstrated very severe obstruction, with an forced expiratory volume in the first second at 24% of the predicted value. Advanced imaging was pursued to confirm the diagnosis of postinfectious bronchiolitis obliterans (PIBO). Chest high-resolution computed tomography (HRCT) (Fig. 1B) definitively confirmed the diagnosis by showing ground-glass opacities and a classic mosaic attenuation pattern in the right middle lobe and left lower lobe, characteristic of small airway obliteration. Nuclear medicine lung perfusion scan shows multiple perfusion defects over bilateral lung fields, which are compatible with HRCT findings of PIBO. Echocardiography confirmed no pulmonary hypertension with a fair ejection fraction.FIGURE 1.: Diagnostic imaging progression of postinfectious bronchiolitis obliterans (PIBO). A: Chest radiograph anteroposterior view reveals peribronchial thickening predominantly in the right lower lung and right upper lung. Besides, bilateral emphysematous changes and hyperinflation are noticed, indicating significant air trapping. B: Chest high-resolution computed tomography (HRCT) with transverse section reveals ground-glass opacities and a pathognomonic mosaic attenuation pattern in the right middle lobe and left lower lobe. This pattern combines bronchial wall thickening, air trapping and small airway obliteration.The patient was treated with mini-pulse steroid therapy (Methylprednisolone 10 mg/kg/d × 3 days/month for a total of 6 courses in the following 6 months) and the FAM protocol (fluticasone, azithromycin, and montelukast). She stabilized and was discharged on day 20 with an SpO2 improving to 93%–97%. At a 15-month follow-up, despite completing 6 steroid pulses, pulmonary function testings showed persistent small airway obstruction, but her clinical images kept improving, both chest X-ray and HRCT. She could exercise without tachypnea and no need for any oxygen supply. She remains under outpatient follow-up. This case is believed to be the first published report of MP-induced PIBO in Taiwan. While PIBO is a well-documented sequela of viral insults like adenovirus, MP is a potent atypical agent capable of inducing permanent airway obliteration through intraluminal fibrosis and an exaggerated immune response.1–5 PIBO is usually misdiagnosed as refractory asthma; however, a bronchodilator has no effect in PIBO case.6 In Taiwan, MP infection is common in children, and both macrolide resistance in laboratory studies and infection in younger age in epidemiology were noticed.7,8 Literature indicates that MP-related PIBO often follows a “latent” period where the patient appears to recover from pneumonia before developing chronic small airway obstruction. Diagnosis is often delayed more than 6 months because initial chest radiographs may only show nonspecific inflammatory signs or hyperinflation. Chest HRCT remains the gold standard for diagnosis, as the mosaic attenuation pattern accurately reflects regional air trapping.9,10 Early recognition of MP-related PIBO and comprehensive management are essential to mitigate long-term sequelae and may have better outcomes.
Chen et al. (Wed,) studied this question.