Leishmaniasis

Lancet. 1999 Oct 2;354(9185):1191-9. doi: 10.1016/S0140-6736(98)10178-2.

Abstract

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.

PIP: This paper discusses the pathogenesis and clinical management of leishmaniasis. Leishmaniasis is a vector-borne disease caused by obligate intramacrophage protozoa, characterized by diversity and complexity. It is endemic in areas of the tropics, subtropics, and southern Europe, in settings ranging from rain forests in Americas to deserts in western Asia, and from rural to periurban areas. Several clinical syndromes are categorized under the term leishmaniasis: most notably visceral, cutaneous, and mucosal leishmaniasis, which result from replication of the parasite in macrophages of the mononuclear phagocyte system, dermis, and naso-oro-pharyngeal mucosa, respectively. These syndromes are caused by a total of about 21 leishmanial species, which are transmitted by about 30 species of phlebotomine sandflies. Clinical manifestation of the disease depends on the type of leishmaniasis, which could be life-threatening systemic infection (visceral), chronic skin sores (cutaneous), or dreaded metastatic complications, which causes facial disfigurement (mucosal). Clinical management is directed to prevent death from visceral leishmaniasis and morbidity from cutaneous and mucosal leishmaniasis. Also included in its management is the ongoing research on immunoregulation of leishmaniasis in the understanding of the immune response to intracellular pathogens and rationalizing vaccine development. General principles on the disease diagnosis and treatment are outlined in this paper.

Publication types

  • Review

MeSH terms

  • Amphotericin B / therapeutic use
  • Animals
  • Antimony / therapeutic use
  • Antiprotozoal Agents / therapeutic use*
  • Drug Administration Schedule
  • Female
  • HIV Infections / complications
  • Humans
  • Leishmania / isolation & purification
  • Leishmaniasis / diagnosis
  • Leishmaniasis / drug therapy*
  • Leishmaniasis / immunology
  • Leishmaniasis / transmission
  • Leishmaniasis, Cutaneous / diagnosis
  • Leishmaniasis, Cutaneous / drug therapy
  • Leishmaniasis, Mucocutaneous / diagnosis
  • Leishmaniasis, Mucocutaneous / drug therapy
  • Leishmaniasis, Visceral / complications
  • Leishmaniasis, Visceral / diagnosis
  • Leishmaniasis, Visceral / drug therapy
  • Male

Substances

  • Antiprotozoal Agents
  • Amphotericin B
  • Antimony