SUMMARY : Studies on the pathogenicity of Shigella have been conducted, employing various experimental models and acid agglutination test with S. flexneri 2a strain 5503 and its variants. The parent strain 5503 isolated from a dysentery monkey behaved as a virulent one with respect to oral infectivity for monkeys, keratoconjunctival infectivity for guinea pigs, and penetration and multiplication within cultured monolayer cells, whereas variants 5503-I and 5503-II derived from strain 5503 were avirulent. Neither parenteral virulence for mice nor acid agglutinability gave consistent relation. The results obtained agreed well with those established by LaBrec et al.(1964).Localization of the dysentery bacilli and inflammatory reactions induced were followed by examining keratoconjunctivitis in guinea pigs by the fluorescent antibody and histopathological techniques.The significance in the pathogenesis of bacillary dysentery of epithelial cell penetration and intracellular multiplication of the bacilli is discussed in connection with oral infectivity for monkeys.
SUMMARY:HeLa S3 and Henle's intestinal epithelial cells infected with virulent and avirulent strains of Shigella flexneri bacilli were studied by phase contrast, time-lapse cinemicrography.Virulent Shigella bacilli were found to attach to the surface of the cells evoking vigorous ruffling movement of the cell membrane.This was followed by the formation of pinocytotic vesicles and incorporation of bacilli into cells. In contrast, avirulent bacilli never became attached to cultured cells.Intracellular Shigella bacilli moved conspicuously independent of the movement of cellular organella and were seen within microfibrillar protrusions from the surface of the host cell. The bacilli exhibited polarity while moving and this movement was inhibited or halted by tetracycline.The nature of the movement of intracellular Shigella bacilli is discussed.
The experimental system utilized in investigating the correlation between the chemical structures of muramyl peptides and their protective activities in the sepsis type of systemic infections caused by Escherichia coli was applied in evaluating the enhancement of resistance to infection induced by 32 synthetic glycopeptide analogs, including 6-O-acyl derivatives and 1-alpha-O-benzyl derivatives of muramyl dipeptide (N-acetyl muramyl-L-alanyl-D-isoglutamine). In assessing the 6-O-acyl derivatives of muramyl dipeptide, we found that the degree of protective activity was attributable to the kinds of fatty acids introduced. Acylation of the 6-hydroxy group on the muramic acid moiety in muramyl dipeptide with natural mycolic acid or a synthetic fatty acid possessing either an alpha-branched or an alpha-branched, beta-hydroxylated group resulted in a decrease in or a disappearance of the protective activity of muramyl dipeptide. Acylation with a normal fatty acid or an iso fatty acid resulted in a retention or enhancement of muramyl dipeptide activity. The activity of acylated derivatives containing linear fatty acids was stimulated by increasing the chain length up to 18 carbon atoms. The highest degree of protective activity occurred with the derivatives acylated with straight-chain fatty acids, particularly with the derivatives acylated with palmitic acid and arachidic acid. Benzylation of the 1-hydroxy group of muramyl dipeptide resulted in a decrease in or a loss of protective activity.
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