.abstract img { width:300px !important; height:auto; display:block; text-align:center; margin-top:10px } .abstract { overflow-x:scroll } .abstract table { width:100%; display:block; border:hidden; border-collapse: collapse; margin-top:10px } .abstract td, th { border-top: 1px solid #ddd; padding: 4px 8px; } .abstract tbody tr:nth-child(even) td { background-color: #efefef; } .abstract a { overflow-wrap: break-word; word-wrap: break-word; }
A3216 - Unusual Cause of Pneumothorax: Invasive Aspergillosis in an Immunocompetent Host
Author Block: V. Pathak, J. Wininger, J. R. Lakey, E. Matheis; WakeMed Health and Hospitals, Raleigh, NC, United States.
Introduction: Invasive Aspergillosis rarely presents in an immunocompetent host. Patients who present with invasive aspergillosis are typically immunocompromised due to hematologic malignancy, high dose glucocorticoids, or are other immunosuppressive therapies. We present a case of a patient without typical risk factors who presented with pneumothorax due to a ruptured aspergilloma. Description: A 46-year-old female with well-controlled asthma on fluticasone actuation inhaler presented to the emergency department with sudden onset of sharp right-sided chest pain, tachycardia, and shortness of breath. Chest CT revealed a right-sided tension pneumothorax and multiple, bilateral, cavitary lung lesions. Her shortness of breath and tachycardia resolved after chest tube placement and she had no other clinical symptoms. Further investigation revealed she had possible dust and mold exposure 4 weeks earlier while cleaning out her garage. Approximately 3 days after cleaning the garage she endorsed brief symptoms of chills, headache, non-productive cough, and diarrhea. This prompted her to visit her primary care provider who prescribed a short course of prednisone. She noted resolution of her symptoms after completion of the steroid dose pack. Workup in the hospital revealed she was HIV negative and testing was negative for Tuberculosis, vasculitides, and sarcoidosis. Blood cultures were also negative. Respiratory cultures revealed light Aspergillus fumigatus. Bronchoalveolar washings also returned Aspergillus fumigatus. Medical cytology and surgical pathology were negative for malignancy but also showed Aspergillus fumigatus. The development of a bronchopleural fistula due to the ruptured aspergilloma required a right upper lobe and right middle lobe resection as well as a decortication. This procedure went well but required additional thorascopic evacuation of her pleural space due to a recurrent loculated effusion 3 days after her initial surgery. She was medically treated with micafungin and voriconazole. She was discharged home 18 days after her admission. Discussion: Invasive aspergillosis typically impacts those whose immune system is impacted by disease, medical treatment, or a combination of both. The mechanism by which this infection was seeded is unclear. Low dose inhaled steroids are associated with oral candidiasis and can increase the risk of respiratory viral infections but are not associated with invasive mold infection. It is possible that the dose pack prescribed by her primary care provider further perpetuated this infection but is only speculative. This case highlights that invasive mold infection should be on the differential for those deemed immune competent with a history of exposure.