Atypical Infection, Critical Consequences, Mycoplasma Pneumoniae-Associated ARDS in a Patient With Albright Hereditary Osteodystrophy

Document Type

Conference Proceeding

Publication Date

10-2025

Publication Title

Chest

Abstract

INTRODUCTION: Mycoplasma pneumoniae rarely causes fulminant respiratory failure with acute respiratory distress syndrome (ARDS), with severe presentations primarily documented in isolated case reports. The pathophysiology involves exaggerated immune responses and alveolar epithelial injury, manifesting as progressive hypoxemia with deteriorating radiographic findings. Patients with neuromuscular disorders such as Albright hereditary osteodystrophy (AHO) present unique ventilatory challenges due to restrictive pulmonary mechanics, impaired airway clearance, and chronic hypoventilation. We describe an adolescent with AHO who developed severe M. pneumoniae pneumonia with ARDS, highlighting the complexities of ventilatory management and liberation. CASE PRESENTATION: An 18-year-old woman with AHO, obstructive sleep apnea, and idiopathic intracranial hypertension presented with a four-day history of fever (39.4◦C), dyspnea, and intractable cough. On presentation, she exhibited respiratory distress with tachypnea (32 breaths/min), nasal flaring, and suprasternal retractions. Initial oxygen saturation was 89% on ambient air, requiring supplementation via nasal cannula at 4 L/min. Within hours, paroxysmal coughing precipitated hypoxemia, necessitating high-flow nasal cannula oxygen therapy (50 L/min, FiO₂ 1.0). Despite aggressive support, her oxygenation deteriorated further with an SpO₂/FiO₂ ratio of 120 and PaO₂/FiO₂ ratio< 100, consistent with severe ARDS. A trial of bilevel-positive airway pressure was unsuccessful, with oxygen saturation declining to 60%, prompting emergent intubation. Molecular diagnostics identified mycoplasma pneumoniae, with a pet parrot raising concern for chlamydia psittaci co-infection. Therapy was initiated with levofloxacin for mycoplasma, doxycycline for psittacosis, and piperacillin-tazobactam for potential superinfection. Bronchoalveolar lavage was negative for other infectious and inflammatory causes. CT angiography excluded pulmonary embolism and arteriovenous malformations. Mechanical ventilation with lung-protective strategy was initiated, with high PEEP and corticosteroids per ARDS protocol. On day eight, the patient passed spontaneous awakening and breathing trials; however, a coughing episode during weaning caused aspiration and hypoxemia, requiring PEEP escalation. On day ten, worsening respiratory failure necessitated deep sedation and neuromuscular blockade with cisatracurium. By day twelve, successful extubation to bilevel positive airway pressure was achieved, followed by intermittent bilevel positive airway pressure and high-flow nasal cannula due to desaturation episodes, attributed to neuromuscular disease and airway hyperreactivity. DISCUSSION: This case highlights several clinically significant observations. First, mycoplasma pneumoniae can cause fulminant ARDS in immunocompetent hosts, a presentation infrequently described in the literature. Second, restrictive lung physiology associated with AHO complicated ventilatory management, as neuromuscular impairment and chronic hypoventilation contributed to prolonged ventilator dependence. Third, the detailed exposure history facilitated consideration of psittacosis in the differential diagnosis, demonstrating the importance of epidemiological risk factor assessment in guiding antimicrobial therapy for community-acquired pneumonia. CONCLUSIONS: This report contributes to the growing recognition of mycoplasma pneumoniae as a potential etiology of severe ARDS. It emphasizes the necessity for individualized ventilatory strategies in patients with pre-existing neuromuscular disorders.

Volume

168

Issue

4S

First Page

3044A

Comments

American College of Chest Physicians CHEST Annual Meeting, October 19-22, 2025, Chicago, IL

Last Page

3044B

DOI

10.1016/j.chest.2025.07.1726

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