Case Presentation: A 76-year-old male was admitted to an outside hospital with several weeks of progressive dyspnea and wheezing. His past medical history was significant for ischemic cardiomyopathy, type 2 diabetes mellitus, and chronic kidney disease. His social history was significant for having lived in Somalia, Yemen, and Indonesia prior to immigrating to the United States five years earlier. At the outside hospital, he was treated for community acquired pneumonia without improvement. He was found to have rising eosinophilia to above 10,000 eosinophils/μL, for which he was administered glucocorticoids and transferred to our hospital for further evaluation.During his hospitalization, a broad evaluation was pursued to identify the etiology of his hypereosinophilia. Diagnostic testing was notable for a peak absolute eosinophil count of 10.6K eosinophils/μL, sputum eosinophil of 21% (normal < 3%), elevated IgE to 817 kU/L (< 214), creatinine 2.66 mg/dL (baseline 1.3-1.4), AST 273 U/L (7-55), ALT 125 U/L (8-48), and positive toxocara antibodies. The remainder of his allergic, infectious, rheumatologic, and hematologic evaluation was unrevealing. He was treated with albendazole for toxocariasis and inhaled corticosteroids for his wheezing. His clinical symptoms resolved and his eosinophilia, creatinine, and transaminases normalized over the subsequent months.
Discussion: Peripheral eosinophilia presents a diagnostic dilemma for hospitalists due to the infrequent clinical presentation and wide differential diagnosis that includes allergic, infectious, rheumatologic, neoplastic, and less commonly idiopathic disorders. Hypereosinophilic syndrome is defined by hypereosinophilia (≥1,500 eosinophils/μL) with end-organ dysfunction. We present a case of hypereosinophilic syndrome with pulmonary, renal, and hepatic dysfunction secondary to toxocariasis.The clinical approach to peripheral eosinophilia should begin with a broad multisystem evaluation to identify the underlying etiology. The most common causes of eosinophilia are medications (in the developed world) and parasitic infections (worldwide). Clinicians should also evaluate for end-organ involvement, bearing in mind hypereosinophilic syndrome most commonly involves the pulmonary, gastrointestinal, cardiac, renal, central nervous and/or cutaneous systems.Toxocariasis is an uncommon parasitic infection caused by the accidental ingestion of eggs shed by the roundworm parasites Toxocara canis and Toxocara cati. The incubation period averages weeks to months and while prevalence is highest in developing countries, domestic transmission can occur as in this case. The two most common clinical syndromes are visceral larva migrans and ocular larva migrans, though eosinophilia may be the primary symptom in mild infections. The diagnosis of toxocariasis is made with a positive Toxocara serology along with a compatible clinical and exposure history. Stool O&P is not a sensitive test as humans are the accidental host and the organism may not complete a full life cycle within the gastrointestinal tract. Toxocariasis is treated with albendazole and while symptoms often resolve rapidly, eosinophilia may take months to resolve due to ongoing antigenic stimulation from dead larvae.
Conclusions: The diagnostic workup for hypereosinophilia should systematically evaluate the wide number of potential etiologies. Toxocariasis is an uncommon cause of hypereosinophilic syndrome that clinicians should be keep on their differential.