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Dysphagia as a Rare Presentation of Pulmonary Coccidioidomycosis Infection FREE TO VIEW

Keren Fogelfeld, MD; Nader Kamangar, MD
Chest. 2011;140(4_MeetingAbstracts):22A. doi:10.1378/chest.1118171
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INTRODUCTION: Coccidioidomycosis infection is endemic in the Southwestern United States and is usually asymptomatic. Pulmonary coccidioidomycosis classically presents with cough and a flu-like illness. We report an unusual case of a patient who presented with significant dysphagia and weight loss secondary to bulky mediastinal lymphadenopathy caused by coccidioidomycosis.

CASE PRESENTATION: A 60-year-old Caucasian male presented to the emergency department with complaints of progressive dysphagia to solids accompanied by nausea, weight loss and cough with blood-streaked sputum that developed within 3 months. He also reported night sweats, fatigue and dyspnea on exertion. He was a resident of Southern California, a lifelong non-smoker, and had no TB risk factors. He was evaluated with a CT chest which revealed extensive pretracheal, subcarinal and right hilar lymphadenopathy and apparent narrowing of his esophagus. Also present was post-obstructive atelctasis of the superior segment of the right lower lobe with a small hypodense area within the atelectatic segment. Laboratory data were equivocal with positive coccidioidomycosis antibodies and negative complement fixation. Because of the hemoptysis and the suspicion for malignancy, a bronchoscopy was performed which revealed a splayed carina and hyperemic airways but no extrinsic compression or endobronchial lesions. Subcarinal transbronchial needle aspiration and transbronchial biopsies of the right lower lobe were negative for malignancy, granulomas, or organisms. The bronchoalevolar lavage showed spherules and the cultures returned positive for C. immitis. Fluconazole treatment was initiated and the patient was discharged from the hospital shortly thereafter. A follow up CT chest a month and a half later showed slight improvement of the lymphadenopathy, mild increase in the hypodense lesion within the right lower lobe, and new small right pleural effusion. The patient remained symptomatic with persistent dysphagia, cough and dyspnea while on lengthy treatment. Subsequently, the patient was re-admitted to the hospital with acute shortness of breath, fever and pleuritic chest pain. Chest imaging confirmed the presence of a loculated pleural effusion due to rupture of a right lower lower subpleural fluid-filled cavity. The patient clinically deteriorated requiring ICU admission for hypoxemia and increased work of breathing. A tube thoracostomy was performed and the patient's antifungal regimen was broadened to liposomal amphotericin B. The patient improved after one week and was transitioned to oral posiconazole upon discharge.

DISCUSSION: Despite the prevalence of coccidioidomycosis infection in Southern California, its course and presentation are not always predictable. Cocciodioidomycosis is a great imitator of other pulmonary diseases. Our patient's initial presentation with dysphagia, hemoptysis and bulky mediastianal and hilar adenopathy was more consistent with bronchogenic carcinoma or other malignancies such as lymphomas. In this patient, the diagnosis of cocciodioidomycosis infection was not initially apparent. Although the coccidioidal antibodies were positive, it is not uncommon for patients living in endemic areas to have seroconversion without clinically evident disease. The complement fixating antibody is a more sensitive and specific test for the diagnosis of active infection, but was negative in our patient. Malignancy was ruled out by bronchoscopy, however, the diagnosis of coccidioidomycosis infection was confirmed one week later via positive culture for c.immitis. The dysphagia in this patient was caused by the unusually bulky lymphadenpathy that was impinging on the distal esophagus. Other reported cases of dysphagia associated with cocciodioidomycosis infection had been attributed to laryngeal involvement. Another interesting aspect of this case was the patients clinical deterioration while on treatment with fluconazole. In most cases, fluconazole is sufficient to achieve clinical resolution, however, our patient's course was further complicated by the the rupture of a right lower lobe pleural-based fluid-filled coccidioidomycosis cavity, causing a large pleural effusion, necessitating chest tube thoracostomy and initiation of intravenous liposomal amphotericin B.

CONCLUSIONS: Our case exemplifies that pulmonary coccidioidomycosis, while common in certain endemic areas, can present atypically. To our knowledge, this is the first reported case of pulmonary coccidioidomycosis infection presenting with dysphagia due to the mediastinal lymphadenopathy, with initial radiographic findings mimicking malignancy.

Reference #1 Coccidioidomycosis with Endolaryngeal Involvement. Harkishen Singh, D.M.D., M.D.; Charles J. Yast, M.D.; John H. Gladney, M.D.; AMA Arch Otolaryngol. 1956;63(3):244-247.

Reference #2 Unusual presentations of coccidioidomycosis: a case series and review of the literature. Crum-Cianflone NF, Truett AA, Teneza-Mora N, Maves RC, Chun HM, Bavaro MF, Hale BR. Medicine (Baltimore). 2006 Sep;85(5):263-77.

DISCLOSURE: The following authors have nothing to disclose: Keren Fogelfeld, Nader Kamangar

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