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Visceral leishmaniasis: Epidemiology and control

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


Leishmaniasis consists of a complex of vector-borne diseases caused by more than 20 species of the protozoan genus Leishmania and is transmitted by sand fly vectors (table 1) [1,2]. Clinical manifestations range from cutaneous ulcers to systemic multiorgan disease. Visceral leishmaniasis (VL) is caused primarily by the two related species Leishmania donovani and Leishmania infantum (synonym Leishmania chagasi).

An estimated 200,000 to 400,000 new VL cases and 20,000 to 40,000 deaths from VL occur each year [3,4]. Among tropical diseases, leishmaniasis ranks second in mortality and fourth in loss of disability-adjusted life years (DALYs) [5]. Leishmaniasis is considered one of the "most neglected diseases" given its strong association with poverty and the limited resources invested in new tools for diagnosis, treatment, and control [6,7].

Issues related to epidemiology and control are discussed here. Issues related to clinical manifestations, diagnosis, and treatment are discussed separately. (See "Visceral leishmaniasis: Clinical manifestations and diagnosis" and "Visceral leishmaniasis: Treatment".)


The epidemiology and ecology of visceral leishmaniasis (VL) in a particular region are determined by characteristics of the parasite species, sand fly species, and mammalian reservoir host(s) (figure 1). In all major endemic areas, asymptomatic infections (measured by seroconversion and/or leishmanin skin testing) outnumber clinically manifest disease [8-11]. Seroconversion reflects newly acquired infection but may precede onset of clinical VL by months [9,10].

The best measure of protective immunity is the leishmanin skin test (LST), which reflects durable but probably not permanent cell-mediated immunity. Individuals with positive LST have more than 95 percent reduced risk of VL compared with those with negative LST, and the age-related rise in positive LST prevalence in a community parallels the age-related decrease in disease risk [11-14]. A parallel fall in the average age of VL patients may be observed as an epidemic matures [15]. Factors that increase the likelihood an individual will progress from leishmanial infection to clinical VL include poor nutritional status, age <5 years (for L. infantum infection), HIV coinfection, and host immunogenetic factors [13,16-20].

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Literature review current through: Dec 2017. | This topic last updated: Jul 25, 2017.
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