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Treatment of visceral leishmaniasis

Author
Caryn Bern, MD, MPH
Section Editor
Peter F Weller, MD, FACP
Deputy Editor
Elinor L Baron, MD, DTMH

INTRODUCTION

Visceral leishmaniasis (VL; also known as kala-azar) is caused by parasites of the Leishmania donovani complex. These parasites may be divided taxonomically and geographically into two groups: L. donovani (South Asia and East Africa) and L. infantum (Mediterranean basin, western Asia from the Middle East to Pakistan, Brazil, and other parts of the New World) (table 1) [1,2]. L. chagasi is synonymous with L. infantum [2].

Issues related to treatment of VL will be reviewed here. Issues related to epidemiology, clinical manifestations, and prevention of visceral leishmaniasis are discussed separately, as are issues related to cutaneous leishmaniasis. (See related topics.)

GENERAL PRINCIPLES

In the absence of treatment, the case fatality rate of fully manifest clinical visceral leishmaniasis (VL, kala-azar) without treatment is >90 percent [3,4]. Mortality is often due to hemorrhagic or infectious complications. Treatment consists of antileishmanial therapy; the main constraints on the choice of antileishmanial drug are cost and availability. Drug resistance must also be considered, especially for VL originating in the Indian subcontinent. Supportive therapy to address nutritional status, concomitant anemia, hemorrhagic complications, and secondary infections is also essential to optimize treatment outcomes [1,5]. (See 'Therapeutic approaches' below.)

Patients with VL should be evaluated for HIV coinfection; if found, HIV should be treated aggressively. In the absence of effective immune reconstitution, treatment response is poor in HIV-VL-coinfected patients [6-8]. (See 'HIV coinfection' below.)

THERAPEUTIC APPROACHES

Agents with efficacy against visceral leishmaniasis (VL) include amphotericin B, pentavalent antimonial drugs, paromomycin (a parenteral aminoglycoside), and miltefosine (the first oral drug for treatment of VL) (table 2).

              

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