Abstract
Riboflavin deficiency, even in a relatively early stage, greatly lowers the resistance of the rat to endemic typhus, thereby resulting in a fatal disease. Not only the serosal cells, but also the endothelial cells in several organs, notably the Kupfer cells of the liver, become greatly distended with rickettsiae under these conditions. Preliminary experiments strongly suggest that advanced vitamin A deficiency, even when making animals markedly cachetic, does not have a comparable effect. Riboflavin deficient animals remain alive for several weeks with an abnormal intracellular metabolism. This type of deficiency is worthy of further study as a possible method of approach in the investigation of other intracellular parasites and filtrable viruses. Speculation regarding the mechanism concerned also suggests the desirability of a study of the effects of this deficiency upon the production of immune bodies in general.
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