Temperature-dependent expression of virulence genes in Shigella species

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Abstract
The pathogenicity of Shigella spp. involves the ability of the bacteria to penetrate and replicate within the epithelial cells of the large intestine. Model systems for examining the virulence of shigellae employ Henle [human embryonic] intestinal epithelial cells in tissue culture and an in vivo assay for virulence in guinea pig eyes (Sereny test). Using these systems, the genetic and physiological bases for the ability of shigellae to invade epithelial cells were studied. Expression of virulence in Shigella spp. was dependent on the temperature at which the bacteria were grown. When grown at 37.degree. C, strains of S. flexneri 2a, S. sonnei and S. dysenteriae 1 were fully virulent and invaded Henle cells. They also produced keratoconjunctivitis in guinea pigs. When grown at 30.degree. C, the bacteria neither penetrated Henle cells nor produced conjunctivitis in the Sereny test and were phenotypically avirulent. Strains grown at 33.degree. C were only partially invasive in the Henle assay; strains grown at 35.degree. C were as invasive as strains grown at 37.degree. C. Using the Henle cell assay, the loss of ability to penetrate epithelial cells was determined to be completely reversed by shifting the growth temperature from 30.degree. to 37.degree. C. The percentage of Henle cells invaded by bacteria increased with increasing time of growth at 37.degree. C. Restoration of invasiveness after growth at 30.degree. C required protein synthesis. When shigellae were grown at 30.degree. C and shifted to 37.degree. C for 2 h in the presence of chloramphenicol, the bacteria remained noninvasive. Similarly treated bacteria grown at 37.degree. C were still invasive. Evidently, expression of one or more genes required for virulence of Shigella spp. are subject to regulation by growth temperature.

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