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• W2046358093 abstract "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 parasitæmia 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 parasitæmia 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 parasites. It may also explain why host species naturally resistant 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 parasitæmia required to produce illness." @default.
• W2046358093 created "2016-06-24" @default.
• W2046358093 creator A5084713074 @default.
• W2046358093 date "1978-07-01" @default.
• W2046358093 modified "2023-09-23" @default.
• W2046358093 title "DOES ENDOTOXIN CAUSE BOTH THE DISEASE AND PARASITE DEATH IN ACUTE MALARIA AND BABESIOSIS?" @default.
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• W2046358093 doi "https://doi.org/10.1016/s0140-6736(78)91386-7" @default.
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