Abstract
The mechanism of enteropathogenicity of human enteropathogenic Escherichia coli (EEC) was studied by ligated gut loop tests in rabbits, keratoconjunctival tests in guinea pig eyes and feeding tests on human volunteers, and by examining for their ability to penetrate into HeLa cells.Strains of invasive EEC (Shigella-like) serotypes produced inflammatory changes and fluid accumulation in the ligated rabbit gut loop, keratoconjunctivitis in guinea pig eyes, and penetration into HeLa cells. With few exceptions, no enterotoxic activity was demonstrated with cell-free filtrates of broth cultures. It was considered that EEC strains of this group may probably cause disease in man by a mechanism similar to that of Shigella organisms, and that enterotoxin production may not be concerned with the pathogenicity of these organisms.When strains of noninvasive EEC including 27 OK group serotypes were studied, 46 of 67 cultures employed produced fluid accumulation and histopathological changes in ligated gut loop tests in rabbits, whereas none of them induced keratoconjunctivitis in guinea pig eyes nor penetration into HeLa cells. In addition, cell-free filtrates from broth cultures of 12 out of 20 strains produced alterations similar to those caused by living culture in the gut loop tests. When R-state cultures derived from three strains of noninvasive EEC serotypes were tested for their activity in rabbit gut loops, it was demonstrated that the mutants no longer had the ability to produce positive gut loop reactions, although filtrates of the R cultures were still able to cause pathological alterations in the loops. Cell cultures killed by acetone, chloroform, or heat failed to give positive gut loop reactions.Positive gut loop reactions were also induced by some strains not belonging to the recognized EEC serotypes originating from sources other than gastroenteritis patients.Nine strains consisting of four of noninvasive EEC and five enterotoxigenic strains not belonging to the recognized EEC serotypes were tested with human volunteers. All the former strains caused acute gastroenteritis in the volunteers, while the latter elicited on response.These results suggest that enterotoxin production is not concerned in the mechanism of enteropathogenicity of noninvasive EEC. On the other hand, it seemed that the ability to multiply in the intestine is essential in the enteropathogenicity of noninvasive EEC strains, although an enterotoxic substance demonstrated in cell-free filtrates may play a role in the development of gastroenteritis.
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