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.

We used transposon (Tn) mutagenesis to study the role of capsular polysaccharide/adhesin (PS/A) and slime in adherence of Staphylococcus epidermidis to catheters. pLTV1, containing Tn917-LTV1, was transformed into S. epidermidis M187 by protoplast fusion with S. aureus RN4220(pLTV1), creating M187(pLTV1). Tn mutants were isolated following growth at 42 degrees C; mutants deficient in PS/A and slime production were selected. PS/A- and slime-deficient Tn mutants had a 10-fold decrease in vitro in the initial phase of adherence to catheters, comparable to levels of strains that do not produce PS/A. Introduction of Tn917-LTV1-interrupted DNA from PS/A-deficient mutant M187sn3 into the parental strain via transformation of protoplasts yielded recipients with inserts identical to those of the Tn mutant that were PS/A and slime deficient. Chromosomal DNA flanking the Tn in mutant M187sn3 was cloned into Escherichia coli. The cloned DNA was found to hybridize to approximately 5-kb EcoRI fragments from the parental strain and from control Tn mutants that express parental levels of PS/A and to either approximately 9- or approximately 14-kb EcoRI fragments from other highly adherent, PS/A-producing strains. Mapping studies demonstrated that in the eight PS/A-deficient mutants that have been isolated, the Tn insertions all occur within a region of approximately 11.6 kb that is defined by three EcoRI sites. These results support previous findings indicating that in S. epidermidis PS/A is involved with in vitro adherence to plastic biomaterials and elaboration of PS/A is closely associated with slime production.