C69-08 An Elusive Diagnosis of Strongyloides Infection Masquerading as Daptomycin-Induced Eosinophilic Pneumonitis

Abstract Introduction Strongyloides stercoralis is a nematode endemic to tropical and subtropical regions that can persist subclinically for years, completing it’s lifecycle in the host. For immunocompromised patients such as cirrhotics, HIV-positive individuals, and patients on chronic steroids, this autoinfection cycle can accelerate, leading to disseminated disease. Characteristic laboratory findings include eosinophilia, Gram-negative or polymicrobial bacteremia from enteric translocation, and elevated IgE levels. Pulmonary manifestations such as diffuse nodular infiltrates, pleural effusions, or eosinophilic pneumonitis may mimic drug reactions, delaying diagnoses. We present a case of strongyloides hyperinfection in a patient that initially presented similarly to drug-induced eosinophilic pneumonitis. Case Presentation A 44-year-old man with history of alcoholic cirrhosis, and esophageal varices who travels frequently to Mexico presented with a rapidly progressive, flaking, blistering rash four days after discharge from a prior hospitalization for a gastrointestinal infection treated with ciprofloxacin and metronidazole. The eruption began on the face and trunk, spreading to the lower extremities with oral and ocular discomfort. On presentation, he was afebrile but developed sepsis and polymicrobial bacteremia, including ESBL E. coli, K. pneumoniae, L. rhamnosus, and VRE faecium, and was started on daptomycin per infectious disease. Skin biopsy revealed epidermal necrosis and lymphocytic-eosinophilic infiltrates consistent with a drug reaction, and IVIG was initiated for suspected Steven-Johnson Syndrome. During his hospitalization, the patient developed worsening eosinophilia, and new pulmonary nodules on CT chest, initially attributed to daptomycin-induced eosinophilic pneumonitis. However, persistent leukocytosis and polymicrobial bacteremia raised concern for Strongyloides stercoralis hyperinfection. Bronchoscopy with bronchealveolar lavage was performed, and empiric antiparasitics were initiated. His strongyloides antibody test was ultimately positive, and he received ivermectin 200 µg daily for four weeks and albendazole 400 mg twice daily for seven days. After treatment initiation, the patient’s fevers abated, leukocytosis resolved, and he was discharged on continued antiparasitic and antibiotic therapy with outpatient hematologic and infectious disease monitoring. Discussion This case illustrates the diagnostic challenges of Strongyloides hyperinfection in an immunocompromised cirrhotic host. Initially attributed to drug-induced eosinophilic pneumonitis, the persistence of eosinophilia, pulmonary nodules, and polymicrobial bacteremia ultimately pointed to disseminated strongyloidiasis. The parasite’s autoinfective cycle allows larvae to migrate through the intestinal and pulmonary vasculature, facilitating translocation of enteric bacteria such as E. coli and Klebsiella into the bloodstream. Pulmonary manifestations can mimic bacterial pneumonia or drug reactions, delaying diagnosis. Thus, a high index of suspicion for strongyloides should be maintained for eosinophilic patients with appropriate risk factors. This abstract is funded by: None