Disseminated Coccidioidomycosis Complicated by Bronchopulmonary Fistula and Viridans Streptococci Empyema

Abstract

SESSION TITLE: Fungal Infections 1 SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: Coccidioidomycosis is typically a self-limited mild disease. Approximately 5-10% of patients with primary pulmonary coccidioidomycosis develop residual pulmonary sequelae such as fibrocavitary disease, which can rarely lead to bronchopulmonary fistulae (BPF). Although viridans streptococci (VS) has been documented to cause empyema, its coinfection in the setting of BPF complicating disseminated coccidioidomycosis infection has not been well described. CASE PRESENTATION: A 62-year-old Latino male farm worker with uncontrolled type II diabetes presented with acute left knee pain, progressively worsening over the course of three weeks. His history was also notable for a left arm nodule and a productive cough. Serum coccidioidal IgM was negative, IgG was positive, and complement fixation was 1:128. Synovial joint fluid from the left knee grew Coccidioides immitis and Coccidioides posadasii. Synovial tissue from the knee showed necrosis and multiple granulomata with coccidioidomycosis. Chest CT demonstrated a left-sided hydropneumothorax with associated BPF and pleural thickening. Additionally seen were innumerable bilateral centrilobular micronodules and left pleural-based cavity. Chest tube thoracostomy revealed purulent material and cultures with positive for VS. He subsequently underwent thoracoscopic debridement and decortication. Histopathology confirmed the presence of coccidioidomycosis. DISCUSSION: VS has been described the main virulent agent in community acquired pneumonia as well as in empyema and lung abscesses. Aspiration of oral secretions is hypothesized to be the etiology of VS respiratory infections. In our patient, rupture of the left-sided coccidial cavity abutting the pleura led to the development of a hydropneumothorax, and ultimately to the formation of a BPF, allowing for a contiguous pathway from the oral pharyngeal space into the pleural space. We hypothesize that the mechanism of VS empyema in our patient was via direct translocation of VS bacteria from the oral cavity through the fistula leading to inoculation of the coccidial pleural effusion. CONCLUSIONS: BPF is a rare complication of disseminated coccidioidomycosis infection. VS empyema has not been previously described in the setting of coccidioidomycosis infection and may be a more important pathogen in pleural pulmonary disease than previously recognized. A BPF may be a potential route of translocation for VS rather than aspiration when it is shown to be the sole pathogen in empyema. Reference #1: Thompson et al. Pulmonary Coccidioidomycosis. Semin Respir Crit Care Med 2011; 32(6): 754-763. 2011 Dec13 Reference #2: Choi SH, Cha SI, Choi KJ, Lim JK, Seo H, Yoo SS, Lee J, Lee SY, Kim CH, Park JY. Clinical Characteristics of Community-Acquired Viridans Streptococcal Pneumonia. Tuberc Respir Dis (Seoul). 2015 Jul;78(3):196-202. Reference #3: Jerng JS, Hsueh PR, Teng LJ, Lee LN, Yang PC, Luh KT. Empyema thoracis and lung abscess caused by viridans streptococci. Am J Respir Crit Care Med. 1997 Nov;156(5):1508-14. DISCLOSURE: The following authors have nothing to disclose: Margaret Wei, Nader Kamangar No Product/Research Disclosure Information