Leishmania are vector‐borne parasitic protozoa that cause the human tropical disease leishmaniasis. Over 30 species have been described, with 11 of these being important pathogens. The disease has three main forms: cutaneous, mucocutaneous and visceral leishmaniasis. The parasites undergo a complex developmental cycle in their phlebotomine sand fly vectors leading to the differentiation of infectious metacyclic promastigote forms, and are transmitted by bite. Many species are zoonotic, being maintained in domestic or wild animal reservoir hosts, and the others are anthroponotic and transmitted from human to human. In their mammalian hosts they live as intracellular amastigote forms inside macrophages. There are relatively few drugs available to treat leishmaniasis, and control of the sand fly vectors or reservoir hosts is difficult. The best long‐term solution to the public health challenge of leishmaniasis will be vaccines, and progress is being made, but an effective vaccine for human usage has not been developed yet.

Key Concepts

  • Leishmania are intracellular parasites that live in the phagolysosomes of macrophages, a unique location for a eukaryotic pathogen.
  • The different forms of leishmaniasis result from infection of differently located populations of macrophages and the human response to infection.
  • Leishmaniasis is a chronic infection that can be treated, but limited drugs are available and no prophylactic vaccine is yet available for human use.
  • There are many species of Leishmania but all share a common set of molecular, biochemical and cell biological features along with species‐specific properties.
  • There are more sand fly vectors than Leishmania species, but they exist in specific pairs, each parasite being transmitted by one or more particular species of sand fly.

Keywords: parasitic protozoa; phlebotomine sand fly; tropical medicine; anthroponotic; zoonotic; promastigote; amastigote; Viannia; Sauroleishmania

Figure 1. The geographical distribution of leishmaniasis. The distribution of individual Leishmania species and the diseases they cause is given in Table . Some 350 million people in over 100 countries are at risk of infection. The main areas are indicated, but within these transmission varies from sporadic to intense, and may be continuous, seasonal or epidemic in nature. Risk of transmission is localised, with each individual focus of transmission separated from others by geographical or ecological barriers.
Figure 2. Phylogeny of Leishmania. Analysis of 21 species of Leishmania is shown, including the 11 species described in Table . In addition to these are shown: L. turanica and L. gerbilli, two nonpathogenic species closely related to L. major, and both in subgenus Leishmania (A); four species in the subgenus Sauroleishmania (B), L. adleri, L. gymnodactyli, L. hoogstraali and L. tarentolae, none of which are pathogenic to humans; two additional species in subgenus Viannia (C), L. naiffi and L. lainsoni both human pathogens; and two members of the L. enriettii species complex, L. enriettii (nonpathogen) and L. martiniquensis (pathogen). Crithidia fasciculata was used as the outgroup.
Figure 3. The life cycle of Leishmania. The parasites alternate between a female sand fly and mammalian host. In addition to humans, the medically important species can also be transmitted to a variety of animal reservoir hosts (for details see Table ). In most endemic regions it is these reservoir hosts that are responsible for long‐term maintenance of the parasite life cycle. This is because human infections, although serious for the individual, are not easily acquired by sand flies and, therefore, represent a dead end for the parasite in such cases. However, important exceptions are L. donovani and L. tropica, where sand flies can acquire infection from human hosts. The progress of human infection is quite variable, but follows two general patterns: a skin lesion developing into cutaneous leishmaniasis or absence of a skin lesion followed by development of visceral leishmaniasis. Parasites are acquired by female sand flies during blood feeding, and initially multiply in the blood meal within the abdominal midgut of the sand fly. Two patterns of development are seen: in members of the subgenus Leishmania the infection spreads directly to the anterior midgut; in members of the subgenus Viannia there is a phase in the hindgut first. In both cases the parasites accumulate at the stomodeal valve, which separates the midgut from the foregut. From this position they can be transmitted when the sand fly inserts her proboscis to take another blood meal.
Figure 4. Developmental forms of Leishmania. Each cell contains a central nucleus (n) and kinetoplast (k) in the single mitochondrion (mt). The flagellum (f) arises from the flagellar pocket (fp). Amastigote forms are intracellular, nonmotile and found in the mammalian host. Promastigote forms are extracellular, motile and found in the sand fly host.
Figure 5. The leishmaniasis spectrum: the range of potential events and outcomes following inoculation of a human host by Leishmania parasites. Individual Leishmania species have different potentials: letters by arrows indicate parasites with potential to cause cutaneous (C), mucocutaneous (MC) or visceral (V) disease (Table ). The final outcomes are boxed in blue. ‘Subclinical infection’ is where the parasite is present but there are no overt signs of disease; ‘metastasis’ indicates spread from the initial site of inoculation to other locations and ‘intractable lesions’ are persistent lesions that do not respond to treatment and do not resolve naturally. Only the most common outcomes are shown. For example, chemotherapy could be used to treat all infections, but is commonly applied only to visceral disease.


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Further Reading

Adak S and Datta R (eds) (2015) Leishmania: Current Biology and Control. Poole, UK: Caister Academic Press.

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Molyneux DH and Ashford RW (1983) The Biology of Trypanosoma and Leishmania, Parasites of Man and Domestic Animals. London: Taylor & Francis.

Myler PJ and Fasel N (eds) (2008) Leishmania: After the Genome. Poole, UK: Caister Academic Press.

Peters W and Killick‐Kendrick R (eds) (1987) The Leishmaniases in Biology and Medicine. London: Academic Press.

Smith DF and Parsons M (eds) (1996) Molecular Biology of Parasitic Protozoa. Oxford: Oxford University Press.

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Bates, Paul A(Nov 2015) Leishmania. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0001968.pub3]