Figure 1. The geographical distribution of leishmaniasis. The distribution of individual Leishmania species and the diseases they cause is given in Table 1. Some 350 million people in 88 countries are at risk of infection. Within the areas outlined, transmission varies from sporadic to intense, and may be continuous, seasonal or epidemic in nature. Risk of transmission is localized, with each individual focus of transmission separated from others by geographical or ecological barriers.

Figure 2. The life cycle of Leishmania. The parasites alternate between a female sandfly 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 1). 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 sandflies and, therefore, represent a dead end for the parasite. Important exceptions are L. donovani and L. tropica, where sandflies 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 sandflies during bloodfeeding, and initially multiply in the bloodmeal within the abdominal midgut of the sandfly. Two patterns of development are seen: in members of the subgenus Leishmania the infection speads 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 sandfly inserts her proboscis to take another bloodmeal.

Figure 3. 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 sandfly host.

Figure 4. 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 1). 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.