Does endotoxin cause both the disease and parasite death in acute malaria and babesiosis?
When mice are infected with either of several species of Plasmodium or Babesia the amount of Escherichia coli lipopolysaccharide (L.P.S.) required to kill them is decreased several hundred fold. The higher their parasitaemia the greater their susceptibility. There is indirect evidence that more L.P.S. than usual is present during infection with these parasites. In a very susceptible host this may be sufficient to produce endotoxin shock. Non-antibody mediators able to kill rapidly dividing cells, which are released during endotoxin shock, may then control the parasitaemia of acute primary attacks. This may explain why agents such as B.C.G., which produce responsiveness to abnormally low concentrations of L.P.S., protect against infection with certain of these parasities. It may also explain why host species naturally resistance to L.P.S. become ill only at high parasite concentrations, and why others with a naturally high susceptibility to L.P.S. become ill when infected with relatively few parasites. In the individual host convalescence from certain bacterial infections or concomitant infection with L.P.S.-producing organisms may vary the parasitaemia required to produce illness.[1]References
- Does endotoxin cause both the disease and parasite death in acute malaria and babesiosis? Clark, I.A. Lancet (1978) [Pubmed]
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