Leishmaniasis Reactivation in the Setting of Autoimmune Diseases and Immunosuppressive Therapy

Figure 1. Proposed relationship between immunosuppressive therapy and reactivation of leishmaniasis in patients with autoimmune and immune-mediated inflammatory diseases. Conventional synthetic, biologic, and targeted synthetic disease-modifying antirheumatic drugs, as well as glucocorticoids, may impair Th1-mediated immunity, macrophage activation, granuloma maintenance, and intracellular parasite control. In previously exposed individuals, particularly those from endemic or rural areas, this immunologic imbalance may favor the persistence and reactivation of latent Leishmania spp., resulting in cutaneous, mucosal, mucocutaneous, or visceral manifestations. Diagnosis may include polymerase chain reaction, direct microscopy, and histopathological examination. Management generally involves reassessment of immunosuppressive therapy, treatment with liposomal amphotericin B, and close clinical follow-up, with secondary prophylaxis considered in selected high-risk cases. Abbreviations: bDMARDs, biologic disease-modifying antirheumatic drugs; CL, cutaneous leishmaniasis; csDMARDs, conventional synthetic disease-modifying antirheumatic drugs; IL, interleukin; MCL, mucocutaneous leishmaniasis; ML, mucosal leishmaniasis; PCR, polymerase chain reaction; Th1, T helper 1 cells; TNF-α, tumor necrosis factor alpha; tsDMARDs, targeted synthetic disease-modifying antirheumatic drugs; VL, visceral leishmaniasis.