Mechanisms of Shigella pathogenesis

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Abstract
The disease-provoking capacity of a wildtype strain of Shigella dysenteriae 1, capable both of penetrating intestinal epithelial cells and of producing toxin, was compared with that of three mutants derived from it that were altered in both or either of these cell properties. The results of studies on several animal models (rabbit ileal loop, fasted guinea pigs, and monkeys) indicate that the disease caused by a nontoxigenic, penetrating mutant was not easily distinguishable from that of the original toxin-producing parent strain. A nonpenetrating mutant that had retained the toxin-producing ability and a double mutant lacking penetrating and toxin production did not cause clinical disease. These findings do not exclude a function for toxin in the pathogenesis of dysentery by S. dysenteriae, but indicate that the more important property for causing disease is the ability to penetrate and multiply in the colonic mucosa.