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According to the World Health Organisation (WHO) Schistosomiasis infects more than 200 million people, with 120 million of those showing symptoms of the disease. It is endemic in 74 developing countries and the usual route of infection is by contact with infested surface water that contains certain species of snails which are carrying the parasite. There are five known water-borne flatworm species that cause the disease. Although schistosomiasis has a low mortality rate, these human parasites are capable of causing chronic pain.
Parasite larvae known as cercariae latch onto and penetrate the skin of a human host. Enzymes produced by the human parasites break down proteins in the skin to allow them to get inside. Over the course of several days and developmental stages, the parasite travels to the lungs and then to the liver. Female worms which live inside male worms can release thousands of eggs everyday which trigger an immune response.
Schistosomiasis symptoms include;
- Severe anaemia
- Chronic abdominal pain
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Schistosomiasis Prevention and Parasite Removal
Praziquantel is the only available drug treatment, and it is effective, but there is a risk that the parasites might build up a resistance to it, and it does not prevent re-infection. So there is a need to stock up and replenish our therapeutic arsenal with new and improved drugs.
An important first step in the drug development process is finding out just how the human parasite ticks, so that any underlying weaknesses can be exploited for our benefit. To this end researchers have been sequencing the parasitic genome of two flatworm species to uncover new targets for schistosomiasis treatment, and the genetic blueprints of Schistosoma mansoni and Schistosoma japonicum were revealed in two papers in Nature in July 2009.
S. mansoni has 11,809 genes and a number of genes have been identified which code for the enzymes that break down the skin. These could be target by new drugs to stop the worms from boring into tissue. The scientists have identified a number of drugs already on the market that might be able to achieve this. It also turns out that the human parasite relies on its host for essential fats, because it lacks an enzyme to make them. This is a chink in the parasitic armour that can be exploited by new drug treatments.
Schistosoma japonicum has even more genes than S. mansoni. This will not only reveal how these parasites function when they exploit host nutrients, hormones and signalling pathways, but will provide an even more stunning array of opportunities to combat the cause of the debilitating, and sometimes fatal disease.
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Berriman M. et al (2009). The genome of the blood fluke Schistosoma mansoni. Nature.