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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Shiro, H. et al.

Transposon mutants of Staphylococcus epidermidis deficient in elaboration of capsular polysaccharide/adhesin and slime are avirulent in a rabbit model of endocarditis.

Virulence comparisons were made in a rabbit model of endocarditis between wild-type and transposon mutants of Staphylococcus epidermidis deficient in elaboration of the capsular polysaccharide/adhesin (PS/A) and slime. The parental phenotype grew from 36 (61%) of 59 cultures of blood. The PS/A-negative phenotype grew in 1 (1%) of 98 cultures of blood (P < .001). No animals infected with PS/A-negative strains developed endocarditis compared with 75% of rabbits infected with PS/A-positive strains. PS/A-producing strains survived better than did PS/A-deficient strains in intact, absorbed rabbit or human serum plus human leukocytes. There was also greater deposition of C3 onto the PS/A-deficient strains than with the PS/A-producing isogenic strains. PS/A functions as an antiphagocytic bacterial capsule preventing C3 deposition and phagocytosis; loss of this structure increases the strain's susceptibility to opsonic killing and decreases its virulence.[1]

References

Transposon mutants of Staphylococcus epidermidis deficient in elaboration of capsular polysaccharide/adhesin and slime are avirulent in a rabbit model of endocarditis. Shiro, H., Muller, E., Gutierrez, N., Boisot, S., Grout, M., Tosteson, T.D., Goldmann, D., Pier, G.B. J. Infect. Dis. (1994) [Pubmed]

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