What are the evolutionary constraints that determine the life cycle of a pathogen like plasmodium?
I didnt quite get your answer. Do you mean that the feeding hour of mosquito is different between the rodent and human mosquito? or Is the lenght of life cycle stages of these parasites different in the mosquito stages (sexual stages), which gets reflected in the vertebrate host?
There are usually problems answering 'why' questions, especially when the basis was natural. My contribution here is that there are species specific differences in the erythrocytic cycles of human infective Plasmodium species. For P. falciparum, P. ovale, P. vivax it lasts 40-48 hours of the tertian frequency of bouts of fever, chills and pains. For P. malariae and P. knowlesi, the cycle lasts 72 hours of the quartan frequency. These differences could be due to the size of the schizont merozoite load within the red blood cells and the ability of the cell membrane to resist internal pressure to lyse. For the P. berghei in a relatively smaller rodent host with a supposedly smaller red blood cell size, the pressure to lyse under internal merozoite challenge could yield faster hence the 24 hours cycle. This is on the assumption that more merozoites are not produced by the schizont of P. berghei and that the schizogony was not naturally faster for the species. These are research provoking areas for comparative parasitology.
Thanks for the answer David. That was a very good explanation for the differences we see. I understand that "why" questions are difficult to answer but these are the questions that gives us a complete understanding of the system. Are there any relationship between the size of the RBC and mechanical stability of the membrane?
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