Eosinophilia As a Marker of Strongyloides Infection

Abstract Abstract 4932 Eosinophilia as a marker of Strongyloides infection Aisha Zaidi, Nagendra Natarajan, Vivek R. Sharma Background: Peripheral blood eosinophilia can be categorized into secondary, clonal and idiopathic types. Secondary eosinophilia can occur due to parasitic infections, allergic or vasculitic conditions, drugs and malignancies. Presence of cytogenetic, histologic and molecular evidence of myeloid malignancy differentiates clonal from idiopathic type. Usually the first step in evaluation of eosinophilia is to exclude secondary causes. Complete work up to exclude secondary causes include careful and extensive review of travel history, medication list, physical examination, chest radiography, multiple stool oval and parasite testing, and serological testing for suspected pathogens (strongyloides stercolaris). Strongyloides infection is a particularly important secondary cause of eosinophilia that requires timely diagnosis and treatment to avoid life-threatening complications (hyperinfection syndrome) from interventions (corticosteroids) for treating the eosinophilia. We report a case highlighting this issue including the fact that such parasitic infection can occur in patients living in the United States (US) who have never traveled outside the country. Abstract: A 66 year old male with multiple comorbities including coronary artery disease, Chronic obstructive pulmonary disease, and stroke was evaluated in the hematology clinic for persistent eosinophilia. He has lived in the US his entire life and did not give any history of travel or change in his medication regimen. He had an itchy urticarial rash on the dorsal surface of his hands but denied any gastrointestinal symptoms. During his initial visit his CBC showed a white blood cell count of 8300 cells/mm3, with 28% eosinophils (Absolute eosinophil count of 2300). His hemoglobin was 13.5 mg/dl with an MCV 100.2 and the platelet count was 202,000 cells/mm3. Extensive work up including multiple stool ova and parasite testing, computed tomography of chest, abdomen and pelvis, cosyntropin test for adrenal insufficiency was unrevealing. His Bone Marrow evaluation revealed mild eosinophilia without dysplastic changes. Fluorescence in situ hybridization performed using tricolor probes targeting SCFD2/FIP1L1, LNX/CHIC2 and PDGFRA was normal. All interphase nuclei examined were negative for a deletion of LNX/ CHIC2 or rearrangement of PDGFRA often seen in association with hypereosinophilic syndrome/chronic eosinophilic leukemia or systemic mastocytosis. Finally, serological testing for strongyloides using ELISA that was ordered as part of the initial workup came back showing strongly positive IgG titer (3.84 ref > 2.11 is positive). He was treated with Ivermectin 200 mcg/kg/day for two days. At his 8 week follow up visit he had complete resolution of eosinophilia. He will be followed by serology within six months as Eosinophilia due to Strongyloidiasis is notoriously prone to fluctuations and may be absent in 20% of the patients with microscopically confirmed infection. Conclusion: This case highlights the importance of diagnosing asymptomatic or minimally symptomatic cases of strongyloides. Even though it is uncommon, it can be found in patients living in certain parts of the US especially the southeastern states. Diagnosis of asymptomatic cases is vital as it eliminates the risk of subsequent hyperinfection should the host's immunity be suppressed for example by corticosteroids used for treating the secondary eosinophilia. Disclosures: No relevant conflicts of interest to declare.