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Leishmaniasis is caused by species of the intracellular protozoan parasite belonging to the genus Leishmania. There are three main categories of leishmaniasis: cutaneous leishmaniasis (oriental sore), mucocutaneous leishmaniasis (espundia) and visceral leishmaniasis (kala azar). An incidence rate of 400 000 new cases per year has been reported, and the world wide prevalence of leishmaniasis is estimated to be 12 million cases (MODABBER 1987). Visceral leishmaniasis is fatal if not treated. The last epidemic of leishmaniasis that occurred in India in 1977-1978 caused an estimated 20 000 deaths. Most forms of leishmaniasis are zoonotic, and humans are infected only secondarily. Animal reservoirs of species pathogenic to man include the sloth, dog and rodent. The parasites are transmitted by female sandflies, and the flagellated promastigotes develop in the gut of the sandfly and in cell-free cultures. Transformation into the amastigote stage occurs within the mammalian macrophage. Primary drug treatment is based on antimony compounds, notably the pentavalent antimonials sodium stibogluconate and N-methylglucamine antimonate. These must be given in daily intramuscular doses for several weeks; they entail unpleasant side effects and are not very effective against cutaneous leishmaniasis. The only immunisation strategy against leishmaniasis used so far with any success in man has been restricted to the cutaneous diseases. It is based on convalescent immunity following controlled induction of a lesion with viable L. major (GREENBLATT 1980). The feasibility of vaccination with killed vaccines is currently being evaluated. |
