Abstract
Gelatinase and serine protease were found to contribute in concert to pathogenesis in a rabbit model of endophthalmitis. However, a mutant defective in the fsr regulator was observed to be more attenuated than a mutant rendered defective in the expression of gelatinase and serine protease as the result of a polar transposon insertion into the former. This increased attenuation suggests that there are possible additional pleiotropic effects of the defect in fsr on expression of traits contributing to the pathogenesis of enterococcal infection.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Bacterial Proteins / genetics
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Bacterial Proteins / metabolism*
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Endophthalmitis / microbiology
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Endophthalmitis / pathology*
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Enterococcus faecalis / enzymology
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Enterococcus faecalis / genetics
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Enterococcus faecalis / pathogenicity*
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Eye / microbiology
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Eye / pathology
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Female
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Gelatinases / metabolism*
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Gram-Positive Bacterial Infections / microbiology
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Gram-Positive Bacterial Infections / pathology
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Mutation
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Rabbits
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Serine Endopeptidases / metabolism*
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Virulence
Substances
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Bacterial Proteins
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Serine Endopeptidases
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Gelatinases