SESSION TITLE: Chest Infections Case Report Posters
SESSION TYPE: Affiliate Case Report Poster
PRESENTED ON: Tuesday, October 27, 2015 at 01:30 PM - 02:30 PM
INTRODUCTION: We describe a unique case of Strongyloides hyperinfection after initiation of antiretroviral therapy (ART).
CASE PRESENTATION: A 45 year old Honduran female with HIV (CD4 count 204 cells/uL) presented with abdominal pain and diarrhea. CT scan of her abdomen revealed colitis. Stool studies were unrevealing, and she had no eosinophilia. Colonoscopy was unrevealing. Her diarrhea resolved, and she began ART. Three weeks later, she was readmitted with abdominal pain, nausea, diarrhea, shortness of breath and a purpuric rash on her abdomen. Chest radiograph revealed diffuse interstitial infiltrates, and CT scan of her abdomen showed progression of colitis. She was started on broad spectrum antibiotics and required high doses of vasopressors. On hospital day one, bronchoscopy revealed Strongyloides stercoralis filariform larvae (Image 1). Patient was started on ivermectin and albendazole. Furthermore, she had received two doses of stress corticosteroids, which were quickly discontinued. Her CD4 count had recovered to 1201 cells/uL, and ART was stopped. Bronchoalveolar cultures grew E. Coli,P. aeruginosa, and Influenza B. Patient persistently had poor lung compliance and ultimately developed bilateral pneumothoraxes. Chest tube placement and examination of pleural fluid revealed many S. stercoralis filariform larvae (Image 2). Repeated examinations of pleural fluid were positive for Strongyloides larvae. She passed away after 10 days of supportive care.
DISCUSSION: This is the sixth case of Strongyloidiasis infection as a manifestation of IRIS. Two of those cases were confounded by corticosteroid use. Furthermore, this is the first case where filariform larvae were persistently found in the pleural fluid. Interestingly, HIV itself has not been associated with hyperinfection despite a high prevalence of coinfection. One explanation is that HIV immunosuppression may create a host environment that favors the non-invasive phenotype of S. stercoralis. Restoration of the immune system triggers a switch to the more invasive female filariform phenotype. Our patient’s lack of fever, lactic acidosis, or renal failure despite profound shock, supports the theory that a shift to the more aggressive phenotype may be the primary means of decompensation rather than a robust host response.
CONCLUSIONS: Further prospective studies examining the life cycle of S. stercoralis in patients initiating ART are needed.
Reference #1: Viney ME, et al. Why does HIV infection not lead to disseminated strongyloidiasis? J Infect Dis 2004; 190:2175-2180.
DISCLOSURE: The following authors have nothing to disclose: Simon Yau, Diana Guerra
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