C69-11 Is Anything Stronger Than Strongyloides?

Abstract Introduction Strongyloides stercoralis is often asymptomatic; however, when this parasite invades an immunocompromised host, it can progress to life-threatening hyperinfection and disseminated disease. We present a case of Human T-lymphotropic virus 1 (HTLV-1) and Strongyloides coinfection presenting as chronic diarrhea, acute hypoxia, and altered mental status (AMS). Case A 72-year-old man from the Caribbean with recent pulmonary embolism (PE) and persistent diarrhea attributed to Enteropathogenic Escherichia coli and Blastocystis hominis presented to the emergency department for worsening abdominal pain, diarrhea, and vomiting despite treatment of existing stool pathogens. Imaging revealed new pulmonary nodules, bronchiolitis, and enterocolitis. He underwent paracentesis for concern of spontaneous bacterial peritonitis. By hospital day 3, he became obtunded, was emergently intubated, and admitted to the intensive care unit. Peritoneal, respiratory, and blood cultures grew multidrug-resistant Klebsiella pneumoniae. Respiratory studies and stool ova and parasites showed Strongyloides stercoralis rhabditiform larvae. He also had positive Immunoglobulin (Ig) G for Strongyloides. Eosinophil count was zero. Despite treatment of Klebsiella with Meropenem and Strongyloides with Ivermectin, his mental status remained poor. MRI brain showed dependent layering debris within the occipital horns of the lateral ventricles, likely infectious material. Lumbar puncture was consistent with parasitic infection. Cerebrospinal Strongyloides was not tested, but CNS infection was presumed. He was then treated with Albendazole and began to track, blink, and open his eyes to voice. Repeat MRI brain showed improvement to the prior debris seen at the occipital horns. His hospital course was further complicated by Aspergillosis and multidrug resistant ventilator-associated pneumonia, myocardial infarction, and new PE. Flow cytometry was notable for concern of a T-cell lymphoproliferative disorder. Discussion HTLV-1 is thought to upregulate CD4+ T cells via the Th1 immune pathways. This comes at the expense of Th2 pathway functions which is demonstrated by decreased eosinophils, IgE, and interleukins 4 and 5. This could explain our patient’s eosinophil count of 0 during a disseminated parasitic infection. Lower Th2 response also predisposes patients to increased risk of helminthic infections, hyperinfection from the higher quantity of larvae, and eventual dissemination with poor response to traditional anti-parasitics. In conclusion, clinicians should have higher suspicion for parasitic infection in those with HTLV-1. This abstract is funded by: None