Background: Clinical manifestations of leishmaniasis vary depending on parasite virulence and host immune response. While immunocompetent individuals have an effective Leishmania-specific response that makes the infection asymptomatic or at least subclinical in most cases, immunosuppressed patients are at risk of developing the disease. TNF-alfa mediated response is crucial for the control of several opportunistic infections caused by intracellular microorganisms such as Leishmania. Some cases of cutaneous as well as visceral leishmaniasis have been described in patients under antiTNF therapy. We have reported a case of an ulcerative colitis patient treated with infliximab in our Unit who developed cutaneous leishmaniasis.
The aim of this study was to detect asymptomatic infection in patients with inflammatory bowel disease (IBD) receiving anti TNF-α therapy from Catalonia area (Spain), where L. infantum is endemic and can cause cutaneous and visceral disease.
Methods: 192 patients with Crohn disease (n=126) or ulceratice colitis (n=46) receiving antiTNF treatment were recruited consecutively from May 2016 to October 2016 at the Crohn's and Colitis attention Unit (Hospital Vall d'Hebron). Anti-Leishmania antibodies were tested by ELISA and Western Blotting (WB) and Leishmania DNA was detected in peripheral blood mononuclear cells (PBMCs) by real time qPCR. Epidemiological and clinical data were also recorded in a clinical interview.
Results: One hundred and ninety-two patients were included, 126 with Crohn's disease (CD) and 46 with Ulcerative Colitis (UC). Ninety six patients were receiveng infliximab, 89 Adalimuab and 7 Golimumab. There was no previous history of leishmaniasis recorded in any patient. Fourteen patients (7.3%, 95% CI 4.3–11.9%) were positive for leishmaniasis, 7 of them treated with IFX and 7 with ADA. Eleven patients had CD and 3 UC.
Serology for leishmaniasis was positive in 12 patients, determined by ELISA in ten patients (5.2%) and in six patients by WB (3.1%). All patients with positive serology had a negative qPCR.
Leishmania DNA was detected by qPCR in 2 patients, indicating active infection. None of the patients had clinical symptoms suggestive of leishmaniasis.
Conclusions: Prevalence of asymptomatic carriers of Leishmania in IBD patients receiving antiTNF is relevant in our area. This population is, therefore, at high risk of developing clinical leishmaniasis. Screening for presence of Leishmania in this group of patients could be recommended before initiating therapy.