Lysostaphin-coated mesh prevents staphylococcal infection and significantly improves survival in a contaminated surgical field.

Mesh and wound infections during hernia repair are predominantly caused by Staphylococcus aureus. Human acellular dermis (HAD) is known to lose its integrity in the face of large bacterial loads. The goal of this study was to determine if lysostaphin (LS), a naturally occurring anti-Staphylococcal protein, can protect HAD mesh from S. aureus infection. HAD samples, 3 cm × 3 cm, were implanted in the onlay fashion on the anterior abdominal wall of rats (n = 75). Subjects were grouped based on presence of antimicrobial bound to HAD (none or LS) and presence of S. aureus inoculum (sterile, 10⁶, 10⁸ CFU). At 60 days, meshes were explanted, and bacterial growth, histology, and mesh tensile strength were examined. None of the controls receiving bacterial inoculation without LS survived to 60 days. All LS-HAD sterile and LS-10⁶ animals survived to explantation. The LS-HAD 10⁸ group had a mortality rate of 50 per cent. All surviving LS-treated animals (n = 25) had negative wound and mesh cultures. Blinded gross and histologic evaluation and measured tensile strengths between all LS groups were comparable. Animals implanted with LS-HAD had a dramatically improved rate of survival. All animals surviving to 60 days had completely cleared S. aureus from their wounds with maintenance of mesh integrity and tensile strength. These findings strongly suggest the clinical use of LS-treated mesh in contaminated fields may translate into a more durable hernia repair.