REVIEW Praziquantel works by causing severe spasms and paralysis of the worms' muscles. This paralysis is accompanied - and probably caused - by a rapid Ca 2+ influx inside the schistosome. Morphological alterations are another early effect of praziquantel. These morphological alterations are accompanied by an increased exposure of schistosome antigens at the parasite surface. The worms are then either completely destroyed in the intestine or passed in the stool. An interesting quirk of praziquantel is that it is relatively ineffective against juvenile schistosomes. While initially effective, effectiveness against schistosomes decreases until it reaches a minimum at 3-4 weeks. Effectiveness then increases again until it is once again fully effective at 6-7 weeks. Glutathione S-transferase (GST), an essential detoxification enzyme in parasitic helminths, is a major vaccine target and a drug target against schistosomiasis. Schistosome calcium ion channels are currently the only known target of praziquantel.
REFERENCES
[1]
Opposing Roles of Voltage-Gated Ca2+ Channels in Neuronal Control of Regenerative Patterning Dan Zhang, John D. Chan, et al. J. Neurosci. 31, 15983-15995, (2011)
[2]
Cytochalasin D abolishes the schistosomicidal activity of praziquantel. Pica-Mattoccia, L., et al. Exp. Parasitol. 115, 344-351, (2007)
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Doenhoff MJ, Cioli D, Utzinger J: Praziquantel: mechanisms of action, resistance and new derivatives for schistosomiasis. Curr Opin Infect Dis. 2008 Dec;21(6):659-67.
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McManus DP, Loukas A: Current status of vaccines for schistosomiasis. Clin Microbiol Rev. 2008 Jan;21(1):225-42.
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