hepatotoxicity occur in up to 50% of patients (and are usually reversible). Pancreatitis and abnormalities of cardiac repolarization also occur; the latter is generally unassociated with arrhythmia and resolves within two months after completion of treatment. At least one case of laryngeal edema has been reported to be associated with antimony therapy. Oral miltefosine has also been used for treatment for VL and CL. None of these drugs appears to be associated with long-term toxicity.
VL is estimated to be the third-most common opportunistic infection in HIV-infected persons in southern Europe (Choi and Lerner 2002). The association emphasizes immune control of the organism and reactivation of quiescent infection in the setting of reduced cell-mediated immune response. Indeed, Leishmania infection might reactivate in patients with CD4 counts below 200/µL (Choi and Lerner 2002). The World Health Organization (WHO) estimates that 25-70% of adult VL cases in southern Europe now occur in HIV-infected patients and that AIDS increases the risk of VL by a factor of 100-1,000 (Choi and Lerner 2002). Clinically, leishmaniasis in HIV-infected persons is characterized by atypical presentations (including pulmonary disease, lingual and esophageal ulcerations, and fever of unknown origin), reduced rates of treatment response, progression from cutaneous to visceral disease, higher rates of death, and reduced sensitivity of serologic tests.
Infections with L. major have not led to viscerotropic infection, parenteral or vertical transmission, or presentation as an opportunistic infection associated with HIV. Old World CL as a rule resolves spontaneously and rarely causes chronic scarring. All of the numerous cases of CL that have occurred in soldiers involved in OIF (CDC 2003b; CDC 2004b) have reportedly responded to relatively short courses of sodium stibogluconate (Weina et al. 2004; Willard et al. 2005). However, some cases have been associated with large lesions and long duration. Given the difficulty in diagnosis, unrecognized CL has the potential to cause substantial cosmetic problems.
DCL is not as responsive to therapy as CL and can cause progressive disfiguration and destruction of skin and soft tissue.
The organisms responsible for VL also infect monocytes and macrophages; however, in contrast with L. major, they may establish latency in these cells. This phenomenon results in a demonstrable risk of recurrence in the setting of immunosuppression induced by chemotherapy, transplantation-related processes, or HIV infection (Basset et al. 2005). As discussed above, immune control of VL involves primarily CD4+ T-cell activity (Th1-type response). Conversely, VL promotes formation of Th2-type cytokines, which can inhibit control of the disease. VL is itself an immunosuppressive disease, partly because of infiltration of reticuloendothelium of liver, spleen, and bone marrow and because it has been associated with polyclonal B-cell activation and increased production of numerous autoantibodies. One case report of GBS that predated the clinical appearance of VL by about a month has been reported;