Protective immunization against Staphylococcus aureus infection in a novel experimental wound model in mice.

A novel murine experimental wound infection model was used to assess the efficacy of multi-component immunization against Staphylococcus aureus infection. Necrotic lesions were induced in mice with venom from Bothrops asper and infected with a low inoculum, 1 × 10(2) CFU. The wound infection model therefore more resembles a clinical case of S.

Lack of the extracellular 19-kilodalton fibrinogen-binding protein from Staphylococcus aureus decreases virulence in experimental wound infection.

A mutant deficient for the 19-kDa extracellular fibrinogen-binding protein (Fib) from Staphylococcus aureus has been constructed. The gene was inactivated by allele replacement. A 2.

Streptococcus mutans major adhesion surface protein, P1 (I/II), does not contribute to attachment to valvular vegetations or to the development of endocarditis in a rat model.

Streptococcus mutans P1 antigen functions as an adhesion factor for binding to salivary pellicle on tooth surfaces. It induces increased antibody titres in patients with Strep. mutans endocarditis.

Collagen binding of Staphylococcus aureus is a virulence factor in experimental endocarditis.

The role of Staphylococcus aureus collagen binding in the development of experimental endocarditis was studied. Two isogenic strains of S. aureus, 1 carrying an insertional inactivation of the gene encoding collagen-binding protein, were compared in a rat model of catheter-induced infective endocarditis (i.

Reconsideration of the role of fibronectin binding in endocarditis caused by Staphylococcus aureus.

The adherence characteristics in vivo and virulence of two isogenic strains of Staphylococcus aureus differing in fibronectin binding were compared in a rat model of catheter-induced infective endocarditis. No differences were found between the two strains. The results strongly point to the multifactorial nature of bacterial adherence to damaged heart valves and suggest that other binding functions can compensate for the lack of fibronectin binding in S.

Effect of low level energy laser irradiation on wound healing. An experimental study in rats.

In this randomized experimental study the wound healing process in rats was investigated after treatment with low level energy laser. In the caudal area of the back of 38 rats, standardized full thickness wounds were punched out bilaterally. The animals were randomly divided into two groups, A and B with 19 rats in each group.

Immunization with fibronectin binding protein from Staphylococcus aureus protects against experimental endocarditis in rats.

Rats were immunized with a fusion protein (gal-FnBP) encompassing beta-galactosidase and the domains of fibronectin binding protein from Staphylococcus aureus responsible for binding to fibronectin. Antibodies against gal-FnBP were shown to block the binding of S. aureus to immobilized fibronectin in vitro.