Today i am going to write about Leishmania, a protozoa found to be infectious and causing Visceral Leishmaniasis (VL).
The leishmaniases are a complex of diseases, caused by kinetoplastid flagellates of the genus Leishmania, which include visceral leishmaniasis (VL), the most severe form of the disease, lethal if left untreated, and several forms of cutaneous leishmaniasis (CL), which may be mutilating, disfiguring, or disabling when lesions are multiple. Three hundred fifty million people in 88 countries are at risk. The yearly incidence is 0.5 million cases of VL and 1.5 million cases of CL. The number of people suffering from these diseases has increased during the last decade.
Leishmaniasis is transmitted by the bite of female phlebotomine sandflies belonging to some 30 species, different throughout the world. Twenty Leishmaniaspecies are pathogenic for humans. The causative agents of VL are members of the Leishmania donovani complex, classified into four species: Leishmania archibaldi, Leishmania chagasi, Leishmania donovani, and Leishmania infantum, distinguished by their vectors and reservoir hosts and in pathology.
In the Indian subcontinent 200 million people are estimated to be at risk of developing Visceral Leishmaniasis (VL). VL, also known as kala-azar is a fatal parasitic disease caused by Leishmania donovani, an intracellular parasite transmitted in the Indian continent by Phlebotomus argentipes. The reported number of cases in the region was 100,000 per year in 2005, but the actual figure may be 5 to 8 times higher.
Life cycle of Leishmania is promastigote-amastigote-promastigote. In the life cycle, the parasite organism is engulfed by reticuloendothelial cells in which it multiplies by binary fission and then parasitizes macrophages.
The sandfly vector becomes infected when feeding on the blood of an infected individual or an animal reservoir host. The leishmania parasites live in the macrophages as round, non-motile amastigotes (3-7 micrometers in diameter). The macrophages are ingested by the fly during the blood- meal and the amastigotes are relesed into the stomach of insect. Almost immediately the amastigotes transform in to the motile, elongated (10-20 micrometers), flagellate promastigote form. The promastigotes then migrate to the alimentary tract of the fly, where they live extracellularly and multiply by binary fission. Four to five days after feeding the promastigotes move forward to the oesophagus and the salivary glands of the insect. When the sandlfy next feeds on a mammalian host, it's proboscis pierces the skin and saliva containing anti-coagulant is injected into the wound to prevent the blood from clotting, the leishmania promastigotes are transferred to the host along with the saliva. Once in the host the promastigotes are taken up by the macrophages where they rapidly revert to the amastigote form. The leishmania are able to resist the microbiocidal action of the acid hydrolases release form the lysozymes and so survive and multiply inside the macrophages, eventually leading to the lysis of the macrophages. The released amastigotes are taken up by additional macrophages and so the cycle continues. Ultimately all the organs containing macrophages and phagocytes are infected, especially the spleen, liver and bone marrow
Refer this - http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=5661 for its taxonomical classification.
Note - The content is taken from different research papers - 1) Incidence of Symptomatic and Asymptomatic Leishmania donovani Infections in High-Endemic Foci in India and Nepal: A Prospective Study, 2) Evolutionary and geographical history of the Leishmania donovani complex with a revision of current taxonomy, and some other web material.
The leishmaniases are a complex of diseases, caused by kinetoplastid flagellates of the genus Leishmania, which include visceral leishmaniasis (VL), the most severe form of the disease, lethal if left untreated, and several forms of cutaneous leishmaniasis (CL), which may be mutilating, disfiguring, or disabling when lesions are multiple. Three hundred fifty million people in 88 countries are at risk. The yearly incidence is 0.5 million cases of VL and 1.5 million cases of CL. The number of people suffering from these diseases has increased during the last decade.
Leishmaniasis is transmitted by the bite of female phlebotomine sandflies belonging to some 30 species, different throughout the world. Twenty Leishmaniaspecies are pathogenic for humans. The causative agents of VL are members of the Leishmania donovani complex, classified into four species: Leishmania archibaldi, Leishmania chagasi, Leishmania donovani, and Leishmania infantum, distinguished by their vectors and reservoir hosts and in pathology.
In the Indian subcontinent 200 million people are estimated to be at risk of developing Visceral Leishmaniasis (VL). VL, also known as kala-azar is a fatal parasitic disease caused by Leishmania donovani, an intracellular parasite transmitted in the Indian continent by Phlebotomus argentipes. The reported number of cases in the region was 100,000 per year in 2005, but the actual figure may be 5 to 8 times higher.
Life cycle of Leishmania is promastigote-amastigote-promastigote. In the life cycle, the parasite organism is engulfed by reticuloendothelial cells in which it multiplies by binary fission and then parasitizes macrophages.
The sandfly vector becomes infected when feeding on the blood of an infected individual or an animal reservoir host. The leishmania parasites live in the macrophages as round, non-motile amastigotes (3-7 micrometers in diameter). The macrophages are ingested by the fly during the blood- meal and the amastigotes are relesed into the stomach of insect. Almost immediately the amastigotes transform in to the motile, elongated (10-20 micrometers), flagellate promastigote form. The promastigotes then migrate to the alimentary tract of the fly, where they live extracellularly and multiply by binary fission. Four to five days after feeding the promastigotes move forward to the oesophagus and the salivary glands of the insect. When the sandlfy next feeds on a mammalian host, it's proboscis pierces the skin and saliva containing anti-coagulant is injected into the wound to prevent the blood from clotting, the leishmania promastigotes are transferred to the host along with the saliva. Once in the host the promastigotes are taken up by the macrophages where they rapidly revert to the amastigote form. The leishmania are able to resist the microbiocidal action of the acid hydrolases release form the lysozymes and so survive and multiply inside the macrophages, eventually leading to the lysis of the macrophages. The released amastigotes are taken up by additional macrophages and so the cycle continues. Ultimately all the organs containing macrophages and phagocytes are infected, especially the spleen, liver and bone marrow
Refer this - http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=5661 for its taxonomical classification.
Note - The content is taken from different research papers - 1) Incidence of Symptomatic and Asymptomatic Leishmania donovani Infections in High-Endemic Foci in India and Nepal: A Prospective Study, 2) Evolutionary and geographical history of the Leishmania donovani complex with a revision of current taxonomy, and some other web material.
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