Case Presentation: A 45yo soldier with a h/o visceral leishmaniasis (VL) and sarcoma of the thigh s/p excision presented with 2 weeks of lymphadenopathy (LAD), fevers, joint swelling, arthralgias, abdominal pain, and weight loss. Since his surgery for sarcoma 6 years prior, he had imaging to monitor for worsening LAD. Multiple lymph node biopsies were performed that were negative for malignancy, but showed fibrosis and non-necrotizing granulomas. He was deployed twice during this time and CT upon most recent return about 2 months prior to presentation showed increased iliac and inguinal LAD with avid uptake on PET CT. Abdominal US showed HSM.Repeat LN biopsy showed non-specific histiocytic and granulomatous inflammation. Leishmania donovani antibody test (rK39) was positive. The significance of the positive rK39 was unclear given his history of leishmaniasis. Tissue from earlier LN biopsy was sent to Walter Reed, where it was compatible with leishmaniasis due to the presence of amastigotes. He was treated with Amphotericin and initially improved, but returned to the hospital with recurrence of his daily fevers 3 weeks later. Chest CT showed worsening cervical and thoracic LAD with innumerable pulmonary nodules. Axillary LN biopsy revealed peripheral T cell lymphoma and he was started on chemotherapy.

Discussion: Visceral leishmaniasis is a protozoan infection caused by L. donovani or infantum and transmitted by the sand fly. It is endemic to the tropics and sub-tropics. The incubation period is typically 2-6 months, but up to 2 years. Symptoms include fever, fatigue, anorexia, weight loss, HSM, and LAD. Cases of VL diagnosed in military personnel deployed to Central or Southwest Asia have been reported. Our case highlights 2 questions: how to differentiate new infection or reactivation of leishmaniasis from an old (treated) infection and whether VL predisposes patients to lymphoma. Diagnosis of VL involves visualization of the amastigote form of the parasite on biopsy. This is subject to sampling error and while specific, has variable sensitivity. The rK39 test detects antibodies against proteins common to leishmania. While antibody levels decrease after successful treatment, they can remain detectable for several years, so diagnosing VL reinfection is difficult. In conversation with our military colleagues, rK39 is expected to be negative in a patient after 13 years, but re-infection is a relatively rare phenomenon that has not been adequately studied.Our patient was also diagnosed with T cell lymphoma, and similar reports exist of patients with VL being diagnosed with lymphoma shortly after treatment. The suggestion is that immunologic dysfunction resulting from leishmaniasis predisposes patients to the development of lymphoma, similar to patients with impaired cellular immunity (eg HIV). In our patient, it is hard to know whether his leishmaniasis led him to develop lymphoma or if alternatively, he had undiagnosed lymphoma that then put him at an increased risk for recurrent VL due to impaired cellular immunity.

Conclusions: We report a case of a soldier with recurrent visceral leishmaniasis and subsequent diagnosis of T cell lymphoma. This emphasizes the need for better diagnostic testing for leishmaniasis and raises the possibility of associations between VL and lymphoma due to immune dysregulation. Given the growing population of patients in the US who have had prior leishmaniasis infections after deployments, it will be important to consider these associations when taking care of this patient population.