A40-06 A Fulminant Case of Constrictive Bronchiolitis Caused by Mycoplasma Pneumoniae

Introduction Mycoplasma pneumoniae-associated constrictive bronchiolitis is a rare entity in the adult population. Case Report A 45-year-old man with a 17 pack-year smoking history (quit 15 years ago) and untreated systemic lupus erythematosus (SLE) presented with shortness of breath and acute hypoxemic respiratory failure (AHRF). One month earlier, he had been diagnosed with Mycoplasma pneumoniae (MP) community-acquired pneumonia. Two weeks later, he developed diffuse mucositis of the eyes, nose, mouth, and anorectal area, along with a widespread maculopapular rash. At presentation, he required 5 L/min of supplemental oxygen. Chest CT showed mosaic attenuation and upper-lobe-predominant ground-glass opacities (GGOs). Spirometry revealed severe, non-reversible obstruction (FEV1 1.3 L; FEV1/FVC 0.41) and marked air trapping (residual volume 244% predicted). Bronchoalveolar lavage (BAL) was positive for MP by PCR.He was treated with azithromycin and a prednisone taper over one month but was readmitted just two weeks after discharge with AHRF requiring intubation. Repeat BAL again detected MP and showed 77% bronchial lining cells, 19% monocytes, and 4% neutrophils. CT demonstrated persistent GGOs with new reticular changes and mild bronchiectasis. He was extubated after one day but showed minimal improvement in pulmonary function over the next month despite glucocorticoids, including pulse-dose steroids and ≥20 mg/day of prednisone, as well as ongoing azithromycin therapy. Retrospective review revealed that the apparent “GGOs” represented normal lung parenchyma and the “normal” areas reflected air trapping. He was clinically diagnosed with MP-associated constrictive bronchiolitis and referred for lung transplantation evaluation. Discussion Fulminant M. pneumoniae-associated constrictive bronchiolitis is rarely reported in the adult population (3,4). An instructive lesson from the management of this patient is the retrospective analysis that the “GGOs” were in fact the normal parts of the lung parenchyma and the “normal” areas were due to air trapping, the latter CT diagnosis more consistent with the obstructive physiology. Furthermore, we posit whether deficiency of T regulatory cell associated with SLE may have played a role in the heightened immune response to the M. pneumoniae infection, resulting in a severe small airway disease (2). This abstract is funded by: None