What we anxiously fear in the influenza virus – a cross between two strains, resulting in a new variant we have no resistance against – has occurred in another pathogen, the Leishmania parasite. This was uncovered by researchers of the Institute of Tropical Medicine (ITG). The new hybrid species might not be more dangerous than their parents, but it’s too early to know. Kenian scientist Samwel Odiwuor receives for his discovery a PhD at ITG and Antwerp University.
Leishmania mexicana parasitic protozoans. Each protozoan has a long flagellum (thread-like structure) that is used for locomotion. The Leishmania protozoans are the cause of the tropical disease leishmaniasis, which is transmitted by bites from infected sandflies. There are two forms of the disease. Cutaneous leishmaniasis affects the skin and mucus membranes, giving rise to an ulcer at the site of the sandfly bite. This mainly heals naturally, although scarring may occur. The more serious kala-azar causes fever and liver damage, and can be fatal. Treatment is with anti-protozoal drugs.
Credit: Wikipedia
After malaria, leishmaniasis is the most deadly parasitic disease in developing countries. It is caused by unicellular organisms, Leishmania, transmitted by small mosquitoes (sand flies) while bloodsucking. Yearly the parasite hits two million people worldwide, of which four thousand in Southern Europe. Most victims are poor. Which means not much research is put into it: developing medicines or diagnostics costs more than it ever could bring in.
Credit: Wikipedia
Biologically spoken, Leishmania is a remarkable organism. It is one of a few disease-causing organisms to adapt in millions of years of evolution to quite diverse environments, without making use of the normal motor of genetic innovation, sex.
During an innovative genetic analysis of Leishmania parasites from Africa and South America, Samwel Odiwuor discovered vestiges of sex between different species of Leishmania, resulting in new, hybrid varieties of the organism. It still has to be sorted out if the newcomers are ‘better’ at causing disease, as often is the case with hybrids.
If we want to understand how these parasites operate, how they can hide in animals, what they do to a human, which techniques and strategies they use to keep up against our immune system and our medicines (and it looks like they have a few tricks never before seen in biology) – then we will have to understand how they themselves are built and how they work. This research is a considerable step on that long road.
Leishmaniasis is transmitted by the bite of female phlebotomine sandflies. The sandflies inject the infective stage, promastigotes, during blood meals. Promastigotes that reach the puncture wound are phagocytized by macrophages and transform into amastigotes. Amastigotes multiply in infected cells and affect different tissues, depending in part on the Leishmania species. This originates the clinical manifestations of leishmaniasis. Sandflies become infected during blood meals on an infected host when they ingest macrophages infected with amastigotes. In the sandfly's midgut, the parasites differentiate into promastigotes, which multiply and migrate to the proboscis.
Credit: Wikipedia
Source: Institute of Tropical Medicine Antwerp
Leishmania mexicana parasitic protozoans. Each protozoan has a long flagellum (thread-like structure) that is used for locomotion. The Leishmania protozoans are the cause of the tropical disease leishmaniasis, which is transmitted by bites from infected sandflies. There are two forms of the disease. Cutaneous leishmaniasis affects the skin and mucus membranes, giving rise to an ulcer at the site of the sandfly bite. This mainly heals naturally, although scarring may occur. The more serious kala-azar causes fever and liver damage, and can be fatal. Treatment is with anti-protozoal drugs.
After malaria, leishmaniasis is the most deadly parasitic disease in developing countries. It is caused by unicellular organisms, Leishmania, transmitted by small mosquitoes (sand flies) while bloodsucking. Yearly the parasite hits two million people worldwide, of which four thousand in Southern Europe. Most victims are poor. Which means not much research is put into it: developing medicines or diagnostics costs more than it ever could bring in.
Biologically spoken, Leishmania is a remarkable organism. It is one of a few disease-causing organisms to adapt in millions of years of evolution to quite diverse environments, without making use of the normal motor of genetic innovation, sex.
During an innovative genetic analysis of Leishmania parasites from Africa and South America, Samwel Odiwuor discovered vestiges of sex between different species of Leishmania, resulting in new, hybrid varieties of the organism. It still has to be sorted out if the newcomers are ‘better’ at causing disease, as often is the case with hybrids.
If we want to understand how these parasites operate, how they can hide in animals, what they do to a human, which techniques and strategies they use to keep up against our immune system and our medicines (and it looks like they have a few tricks never before seen in biology) – then we will have to understand how they themselves are built and how they work. This research is a considerable step on that long road.
Leishmaniasis is transmitted by the bite of female phlebotomine sandflies. The sandflies inject the infective stage, promastigotes, during blood meals. Promastigotes that reach the puncture wound are phagocytized by macrophages and transform into amastigotes. Amastigotes multiply in infected cells and affect different tissues, depending in part on the Leishmania species. This originates the clinical manifestations of leishmaniasis. Sandflies become infected during blood meals on an infected host when they ingest macrophages infected with amastigotes. In the sandfly's midgut, the parasites differentiate into promastigotes, which multiply and migrate to the proboscis.
Source: Institute of Tropical Medicine Antwerp
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