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ShareOct. 4, 2006 — The most dangerous form of malaria is difficult to treat and claims two million lives a year. Now, researchers at Karolinska Institutet in Sweden have developed a powerful new weapon against the disease.
Severe anaemia, respiratory problems and encephalopathy are common and life-threatening consequences of serious malaria infection. The diseases are caused when the malaria bacteria P.falciparium infects the red blood cells, which then accumulate in large amounts, blocking the flow of blood in the capillaries of the brain and other organs.
The reason that the blood cells conglomerate and lodge in the blood vessels is that once in the blood cell the parasite produces proteins that project from the surface of the cell and bind with receptors on other blood cells and on the vessel wall, and thus act like a glue. The challenge facing scientists has been to break these bonds so that the infected blood cells can be transported by the blood stream into the spleen and destroyed.
The research group, which is headed by Professor Mats Wahlgren, has now developed a substance that prevents infected blood cells from binding in this way. The substance also releases blood cells already bound. Using this method, scientists have been able to treat severe malaria in rats and primates effectively; it now remains to be seen whether these results can be replicated in people.
"There's often a lack of ability to treat people suffering from severe malaria," says Professor Wahlgren. "We've developed a substance that might be able to help these patients."
Previously, an anti-coagulant called heparin was used in the treatment of severe malaria. Heparin was able to release the blood cells, but it was soon withdrawn when it was shown that the substance caused internal bleeding. The new substance is a development of heparin, and has the important difference of having no effect on normal blood coagulation.
The study, which is jointly financed by Swedish International Development Cooperation Agency and Dilafor AB, is to be presented on 29 September in PLoS Pathogens.
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