SESSION TITLE: Infectious Disease Student/Resident Case Report Posters III
SESSION TYPE: Medical Student/Resident Case Report
PRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PM
INTRODUCTION: This case report describes a rare presentation of histoplasmosis and emphasizes the importance of maintaining suspicion in endemic areas.
CASE PRESENTATION: A 62 year old veteran from mid-Missouri was admitted with a one month history of SOB, cough productive of green sputum, and weight loss of 2.2 kg. He had no medical history because he had not seen a physician in over ten years. He had a 100 pack year smoking history and was a chronic alcoholic. He denied illicit drug use, contact with sick persons, exposure to animals, history of exotic travel, or unusual hobbies. Review of symptoms was positive for fevers, chills, night sweats, and loose stools. The physical examination showed a cachectic male. Vital signs were HR 90 bpm, resp 20, BP 130/85 mmHg, temp 38.9 C, and O2 sat 96% on RA. He had decreased air entry in lungs bilaterally with expiratory wheezes throughout upper lung fields. Cardiac examination revealed regular rate and rhythm with no murmurs. Admission labs showed leukocytosis of 11.6 WBCs. Chest x-ray was obtained and showed bilateral upper lobe cavitary lesions. CT scan of the chest showed upper lung zone consolidations with thick-walled cavities and soft tissue nodules. Blood cultures, sputum cultures with acid-fast stain, and further work up were negative for mycobacteria, Legionella, Blastomycosis, and Cryptococcus. His urine was tested for Histoplasmosis antigen and was positive. He was started on Itraconazole 200mg. Bronchoalveolar lavage was obtained and samples were submitted for fungal culture. Specimens grew a mold after 2 weeks of incubation with features consistent with H. capsulatum.
DISCUSSION: Acute symptomatic H. capsulatum infection is observed in less than 1% of infected patients, and usually has a self-limited course. In hosts with immunosuppression, or those with underlying parenchymal disease, H. capsulatum can cause chronic cavitary pulmonary histoplasmosis or disseminated disease. The presentation in this patient was unique because he had no apparent immunosuppression and no history of parenchymal disease. A fast and cost effective method of diagnosing H. capsulatum is by detection of circulating polysaccharide antigens in urine. Our patient responded well to Itraconazole treatment and his current Histoplasma antigen levels remain below detection upon urine testing.
CONCLUSIONS: This patient’s presentation was unique in that H. capsulatum caused cavitary lung lesions in an immunocompetent host. This case highlights the importance of including histoplasmosis in the differential diagnosis of cavitating lung lesions and using the urine antigen-detection test early on during workup.
Reference #1: Gadkowski LB and Stout JE. Cavitary pulmonary disease. Clinical Microbiology Reviews 2008;21:305-333.
Reference #2: Kauffman, C. Histoplasmosis: a Clinical and Laboratory Update. Clinical Microbiology Reviews 2007;20:115-132.
Reference #3: Santos JW, et al. Chronic cavitary pulmonary histoplasmosis [in English and Portuguese]. J Bras Pneumol 2009; 35:1161-1164.
DISCLOSURE: The following authors have nothing to disclose: Donica Liu-Baker, Mittal Mayank, Will Roland
No Product/Research Disclosure Information