Elsevier

The Lancet

Volume 354, Issue 9185, 2 October 1999, Pages 1191-1199
The Lancet

Seminar
Leishmaniasis

https://doi.org/10.1016/S0140-6736(98)10178-2Get rights and content

Summary

In 1903, Leishman and Donovan separately described the protozoan now called Leishmania donovani in splenic tissue from patients in India with the life-threatening disease now called visceral leishmaniasis. Almost a century later, many features of leishmaniasis and its major syndromes (ie, visceral, cutaneous, and mucosal) have remained the same; but also much has changed. As before, epidemics of this sandfly-borne disease occur periodically in India and elsewhere; but leishmaniasis has also emerged in new regions and settings, for example, as an AIDS-associated opportunistic infection. Diagnosis still typically relies on classic microbiological methods, but molecular-based approaches are being tested. Pentavalent antimony compounds have been the mainstay of antileishmanial therapy for half a century, but lipid formulations of amphotericin B (though expensive and administered parenterally) represent a major advance for treating visceral leishmaniasis. A pressing need is for the technological advances in the understanding of the immune response to leishmania and the pathogenesis of leishmaniasis to be translated into field-applicable and affordable methods for diagnosis, treatment, and prevention of this disease.

Section snippets

Immunology

Scientists are studying the immunoregulation of leishmaniasis to improve understanding of the immune response to intracellular pathogens in general and leishmania in particular, to find out whether manipulations of the immune system could be therapeutic, and to rationalise vaccine development. Many insights about immunoregulation have been gained through murine models of leishmaniasis,11 but the complexities of clinical leishmaniasis require further study. The use of cytokine and other types of

General principles about diagnosis

Ideally, all cases of leishmaniasis should be confirmed by demonstration of the parasite, which is straightforward (except for needing an invasive procedure) if parasites are plentiful (eg, in kala-azar) but otherwise can be difficult (eg, for viscerotropic leishmaniasis, mucosal disease, and chronic skin lesions [panel 2]). Examination of giemsa-stained slides of the relevant tissue is still the technique most commonly used to visualise the parasite. The sample should be examined by light

General principles about treatment

The good news is that leishmaniasis is treatable. However, antileishmanial therapy is a bewildering subject, largely because of the complexities of the disease and the inadequacies of published information. The plethora of published reports based on anecdotal or otherwise suboptimal data creates the illusion that many good treatment options exist. The harsh realities are that few of the touted agents have been assessed adequately in clinical trials; few of the many combinations of syndromes,

Clinical manifestations

Visceral leishmaniasis encompasses a broad range of manifestations of infection. Infection remains asymptomatic or subclinical in many cases, or can follow an acute, subacute, or chronic course. The classic kala-azar syndrome is exemplified by patients such as those in Sudan15 who are heavily infected throughout the mononuclear phagocyte system; develop life-threatening disease after an incubation period of weeks to months; and have fever, severe cachexia (figure 1), hepatosplenomegaly

Clinical manifestations

Like visceral leishmaniasis, both old-world and new-world cutaneous leishmaniasis encompass a broad range of severity and manifestations of infection. Travellers can become infected even after short stays in leishmaniasis-endemic areas. Cutaneous infection can remain subclinical or become clinically apparent after a variable incubation period that averages several weeks. Stereotypically, lesions evolve from papules, to nodules, to ulcerative lesions, with a central depression and raised,

Mucosal leishmaniasis

Mucosal leishmaniasis, a dreaded sequela of new-world cutaneous leishmaniasis, is caused by parasites of the Viannia subgenus (panel 1) in most cases and results from haematogenous or lymphatic dissemination of amastigotes from the skin to the naso-oropharyngeal mucosa. In most cases it becomes evident within several years of resolution of the original cutaneous lesions, but it can ensue while the lesions are present or decades after they heal. Adequate systemic treatment of cutaneous

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