Disseminated Bartonella or Post‐Transplant Lymphoproliferative Disease in Pediatric Transplant Patients: A Diagnostic Challenge

BACKGROUND: Post transplant lymphoproliferative disease (PTLD) and infection remain the two most common complications of solid organ transplant and carry a risk of significant morbidity and mortality. PTLD is a highly variable disease with clinical signs and symptoms that are non-specific and require a high degree of suspicion to detect. The most common presenting symptoms of PTLD are malaise, fatigue, fever, and a mononucleosis-like picture; night sweats, weight loss, and lymphadenopathy are also frequent manifestations. An infection with Bartonella Henselae is another known cause of local lymphadenopathy. However, in immunocompromised individuals, Bartonella Henselae is far more likely to cause a systemic response that may mimic PTLD. The specifics regarding differentiating systemic bartonella and PTLD in pediatric solid organ transplant patients are not well described. There have been more detailed descriptions of disseminated bartonella mimicking PTLD in solid organ transplants in adult patients, but this has not been thoroughly reported or described in the pediatric population. Upon literature review, only five cases of disseminated bartonella in pediatric kidney transplant recipients have been described, with three of them possibly associated with PTLD. The past cases described antimicrobial diagnostics for bartonella and other infections, but none of these reported full histopathological findings or associated imaging studies for work-up of PTLD. In addition, past cases have only been described in Epstein-Barr virus (EBV) and Cytomegalovirus (CMV) negative children. There is no consensus for treatment duration and antibiotic choice for confirmed systemic bartonella infection in pediatric kidney transplant patients due to concerns of nephrotoxicity and drug interactions. METHODS: This patient who presented with fever, lymphadenopathy, nausea, vomiting, and abdominal pain was worked up and treated for both Bartonella Henslae and PTLD. PET Scan and biopsies were taken for the diagnosis of PTLD and the patient had Bartonella serologies and PCR testing done as part of a broader infectious workup. Clinical decisions regarding his treatment plan and the cause of his symptoms were made based on response to treatment and the likelihood of underlying etiology based on the timeline which his symptoms improved. RESULTS: After an extensive workup for PTLD and altering immunosuppressive regimens temporarily for possible PTLD we ultimately determined the cause of the patients' symptoms to be secondary to B. henselae infection. The patient was treated appropriately for disseminated Bartonella and improved significantly. He has followed up as an outpatient with continued improvement in symptoms and resumed his previous immunosuppression regimen as PTLD has been ruled out. CONCLUSION: Bartonella and PTLD are diagnoses that need to be carefully considered and treated in vulnerable populations. Pediatric patients should be managed cautiously with both etiologies under consideration, and more research is needed for specific recommendations regarding differentiating and treating the two simultaneously when clinical presentation is questionable. Given the overlapping symptoms, a thorough workup to rule out and treat PTLD if necessary is recommended given its significant mortality if missed. With biopsy being the gold standard, we recommend careful consideration of performing a biopsy while treating underlying infectious concerns in cases where PTLD is a possibility in pediatric populations.