“…The latter can result, for example, from HIV infections, antitumour and immune-ablative chemotherapies or immunosuppressive treatments with glucocorticoids, azathioprine, methotrexate, cyclophosphamide, the calcineurin inhibitors ciclosporin and tacrolimus, the mTOR inhibitors rapamycin (sirolimus) and everolimus, or with biological agents directed against TNF (anti-TNF-antibodies, soluble TNF receptor) or T cell costimulatory molecules. Consequently, immunosuppressed patients with AIDS,11 93 organ transplantations,2 94 haematopoietic malignancies (eg, leukaemia, lymphomas, Hodgkin's disease), autoimmune diseases (eg, systemic lupus erythematosus, rheumatoid arthritis, sarcoidosis, polyarteritis nodosa, Wegener's granulomatosis, Behçet's disease, myasthenia gravis), chronic inflammatory bowel diseases (Crohn's disease, ulcerative colitis) or allergic disorders (eg, asthma, atopic dermatitis) have all been shown to develop severe CL, VL or systemic leishmaniasis, either after primary infection or as a result of reactivation of persistent parasites 95–107. CL, mucosal leishmaniasis or VL can also develop in HIV-infected patients as a manifestation of an immune reconstitution inflammatory syndrome following highly active antiretroviral therapy 108…”