Here is an interesting article I found researching protozoa behavior. It is a good article on how these parasites modify our erythrocytes (red blood cells).
Many of us consider endothelial infection to be more of a bartonella phenomena. But this explains that plasmodium use this tissue as a safe haven as well. They can avoid the spleen this way. The protozoans don't infect the endothelium directly, but cause their host (the red blood cells) to attach to the endothelium tissue. This could cause blockage in the capillaries and result in greatly decreased circulation to the extremities.
From the text:
"Antigenic Variation- The malarial parasite modifies the erythrocyte by exporting proteins into the host cell. One such modification is the expression of PfEMP1 on the erythrocyte surface which functions as the cytoadherent ligand. The binding of this ligand to receptors on host endothelial cells promotes sequestration and allows the infected erythrocyte to avoid the spleen. Numerous PfEMP1 genes (i.e., the var gene family) provide the parasite with a means to vary the antigen expressed on the erythrocyte surface. This antigenic variation also correlates with different cytoadherent phenotypes."
I'm not sure what this next sentence means, but perhaps Chondroitin supplementation might impact cytoadherence.
The sentence: "Chondroitin sulfate A (CSA) has been implicated in the cytoadherence within the placenta and may contribute to the adverse affects of P. falciparum during pregnancy."
Someone else will have to give commentary on what this is saying. Could it be that supplementing may inhibit cytoadherence of the infected RBCs?
[ 06-27-2015, 04:33 PM: Message edited by: TNT ]
Posted by TNT (Member # 42349) on :
A quote from the above (text)book I linked to-Ultrastructural Pathology:The Comparative Cellular Basis of Disease, by Norman F. Cheville- really stood out to me.
It is a well-known fact that bacteria cause bone infections. In trying to sort my symptoms, I have wondered at times if protozoans ever cause bone infections. I had looked a couple times on PubMed, but did not find any literature supporting bone infections with protozoa. Perhaps a more exhaustive search would have brought something up.
But, here it is in this book on page 545:
"The erythrocytic phase is facilitated and prolonged in some species of Plasmodium by concentration of infected erythrocytes in the bone marrow. Here they attach to venular endothelium and move to have access to developing reticular cells. Merozoites can thereby infect new cells without exposure to antibodies and other anti-plasmodial substances that circulate in the bloodstream."
