Strongyloides stercoralis Infection as a Manifestation of Immune Restoration Syndrome

Sir—A 34-year-old African male immigrant from the Ivory Coast with a history of malaria presented to Bellevue Hospital (New York) with headache and altered mental status. He denied receiving any medications, having allergies, or consuming alcohol and admitted having a remote history of injection drug use. A large number of ring-enhancing lesions (diameter, 1–2 cm) associated with extensive edema involving the corticomedullary junction and cortex, the right basal ganglia, and the medial right occipital lobe with moderate mass effect and right-to-left shift were seen on a head CT scan. The patient refused to undergo lumbar puncture. Results of ELISA for HIV-1 antibody were positive. Empirical dexamethasone, pyrimethamine, and sulfadiazine therapy was initiated for cerebral toxoplasmosis. The CD4+ T lymphocyte count and HIV load were 32 cells/mm3 and >750,000 copies/mL, respectively. After radiographic improvement, prophylactic treatment with zidovudine/lamivudine, lopinavir/ritonavir, and azithromycin for Mycobacterium avium infection was started. Two and one-half weeks after discharge (23 days after initiation of antiretroviral therapy [ART]), the patient presented with fever (temperature, 38.4°C) and no other symptoms. Vital signs and findings of physical examination were normal. Laboratory data revealed new eosinophilia, with an absolute eosinophil count (AEC) of 784 × 106 cells/L (baseline AEC, 270 × 106 cells/L). Levels of hepatic transaminases were >10 times higher than normal levels and >5 times higher than baseline levels, with an aspartamine transferase level of 206 U/L (normal range, 10–35 U/L), an alanine aminotransferase level of 342 U/L (normal range, 10–33 U/L), and an alkaline phosphatase level of 314 U/L (normal range, 30–90 U/L). The HIV load decreased to 900 copies/mL. CD4+ T lymphocyte testing was not performed again. CT of the head revealed interval improvement of vasogenic edema, with mild communicating hydrocephalus. CT of the chest showed no adenopathy and a 3-mm nodule in the right upper lobe of the lung. Results of serological tests for hepatitis viruses and PCR for hepatitis C RNA were all negative. Drug toxicity was suspected, and all medications were stopped. After 1 week, the patient continued to have fever, with persistent hepatitis and peripheral eosinophilia. On hospital day 6, the AEC count peaked at 6837 × 106 cells/L, with continued hepatitis. Tests of peripheral blood were successively negative for malaria. Examination of a stool specimen revealed larval forms of Strongyloides stercoralis. Institution of ivermectin therapy resulted in resolution of fever and improvement of eosinophilia and hepatitis. Toxoplasmosis was treated with clindamycin and pyrimethamine. Two weeks after discharge from the hospital, the patient reinitiated ART, with lamivudine, tenofovir, and efavirenz, and Pneumocystis pneumonia prophylaxis, with dapsone. Follow-up studies showed the absence of S. stercoralis larvae in stool specimens and resolution of peripheral eosinophilia. After initiation of effective ART, patients with low CD4+ T lymphocyte counts are at risk of developing inflammatory reaction against presumably preexisting or subclinical infection. This manifestation of the immune restoration of the CD4+ T lymphocyte response has evolved into a well-described syndrome of immune restoration or immune restitution disease [1–5]. Until now, most infections with S. stercoralis in patients with AIDS have been associated with the syndrome of hyperinfection or disseminated infection. To our knowledge, we report here the first documented case of S. stercoralis infection as the presenting clinical manifestation of immune restoration syndrome. Although a second CD4+ T lymphocyte count was not obtained during the second hospitalization, we believe that the patient was adherent to ART, because of the significant reduction in the virus load. The temporal course of fever, eosinophilia, and hepatitis 23 days after initiation of ART suggests possible drug toxicity. However, all 3 manifestations persisted, despite withdrawal of all medications. Clinical improvement did not occur until initiation of ivermectin therapy, which suggests a possible case of immune restitution syndrome due to S. stercoralis infection.

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