STRONGYLOIDIASIS AND THE HYPERINFECTION SYNDROME. H. Jneid 1 , N. Correia 1 , F. Michota 1 ; 1 Cleveland Clinic Foundation, Cleveland, Ohio LEARNING OBJECTIVES: 1. List the differential diagnoses for immunocompromised patients with chronic obstructive pulmonary disease and progressive dyspnea. 2. Recognize the risk factors and clinical features of strongyloidiasis. 3. Recognize the hyperinfection syndrome of strongyloidiasis. CASE INFORMATION: A 65-year-old retired coal miner presented with a 2-month history of progressive shortness of breath and nonproductive cough. He had a history of emphysema and coal worker' pneumoconiosis and had been using an inhaler and oxygen therapy. He had grown up in a rural Appalachian area of Ohio and stopped using tobacco 20 years ago. He had been started on cyclophosphamide and high-dose prednisone therapy for rapidly progressive glomerulonephritis 3 months previously. He was morbidly obese, with T 37.48C, BP 134/65 mm Hg, Pulse 100, RR 22/min, and SpO2 91% on 4 L of oxygen. Lung auscultation showed decreased air entry and diffuse wheezing. Initial chest x-ray showed no parenchymal lung disease. Review of his kidney biopsy revealed chronic interstitial nephritis, cyclophosphamide was stopped, and prednisone was gradually tapered. His dyspnea and oxygen requirement increased despite aggressive therapy with bronchodilators. Venous duplex ultrasound of the upper and lower extremities showed no thrombosis. V-Q scan revealed no mismatches. Computed tomography of the chest subsequently showed diffuse alveolar ground-glass appearance. The patient was started on broad-spectrum antibiotics, including intravenous Bactrim and amphotericin. Bronchoscopy was done, and Strongyloides stercoralis was diagnosed by transbronchial biopsy. The patient was started on intravenous thiabendazole. Prednisone was tapered quickly and stopped. His respiratory status deteriorated, and the patient eventually died. Autopsy found disseminated infection, with panlobar pulmonary infestation and patchy small and large bowel strongyloidiasis. DISCUSSION: Our immunocompromised patient had worsened respiratory symptoms despite inhaler therapy, which prompted us to seek other diagnoses. Initial work-up was negative for congestive heart failure and thromboembolism. His previous diagnosis of simple coal worker' pneumoconiosis was not supported by initial radiologic findings and would not have explained his rapid clinical deterioration and radiologic evolution. In this setting, opportunistic infections should be strongly suspected. Strongyloides is an intestinal parasite that is common in tropical and subtropical areas. Infection rates are highest among residents of the southern states and Appalachia, and among immigrants from endemic areas. Transmission occurs when infective larvae come in contact with the skin. The parasite has an autoinfection cycle that is usually contained by the host immune system; therefore, larval forms may persist in the body up to 50 years. Clinical manifestations of strongyloidiasis include abdominal upsets, lung manifestations such as wheezing and cough, and a pathognomonic skin eruption called larva currens. The autoinfection cycle accelerates inversely with the strength of the immune system and may yield to the highly lethal hyperinfection syndrome in immunosuppressed patients, characterized by massive dissemination to multiple organs and systems, such as the central nervous system, heart, liver, and endocrine glands. People at risk for Strongyloides infection should be screened before being given immunosuppressive therapy. Recognize the predisposing conditions and the treatment of cerebral arterial air embolism. CASE INFORMATION: A 50-year-old white woman presented with two transient 15-minute episodes of left upper extremity parasthesia, slurred speech, and diplopia. She had had inflammatory breast cancer 3 years previously, and had undergone right modified radical mastectomy, chemotherapy, and radiotherapy. Liver metastasis had recently been discovered. Neurologic exam on presentation was nonfocal. Computed tomography (CT) of the brain and lumbar puncture fluid analysis were normal. Magnetic resonance imaging found no leptomeningeal enhancement or focal lesions. Duplex ultrasound of her extracranial arteries showed no significant atherosclerotic stenoses, but 15 minutes of continuous Doppler monitoring showed active embolization (>1000 emboli /minute) to the brain. Venous duplex ultrasound of her upper and lower extremities showed no thrombosis, and CT scan of her abdomen showed no pelvic or inferior caval thrombosis. Holter monitoring showed no cardiac arrhythmias. Transesophageal echocardiography showed no valvular vegetations, intracardiac thrombi, or patent foramen ovale, but revealed spontaneous air bubbles in the left atrium. The patient' neurological status progressively worsened until she became comatose, entered respiratory arrest, and died. No autopsy was performed.