Differential arthritogenicity of Staphylococcus aureus strains isolated from biological samples

BACKGROUND: Staphylococcus aureus is the most common agent of septic arthritis that is a severe, rapidly progressive and destructive joint disease. Superantigens produced by S. aureus are considered the major arthritogenic factors. In this study, we compared the arthritogenic potential of five superantigen-producing staphylococcal strains. METHODS: Male C57BL/6 mice were intravenously infected with ATCC 19095 SEC(+), N315 ST5 TSST-1(+), S-70 TSST-1(+), ATCC 51650 TSST-1(+) and ATCC 13565 SEA(+) strains. Clinical parameters as body weight, arthritis incidence and clinical score were daily evaluated. Joint histopathological analysis and spleen cytokine production were evaluated at the 14th day after infection. RESULTS: Weight loss was observed in all infected mice. ATCC 19095 SEC(+), N315 ST5 TSST-1(+) and S-70 TSST-1(+) were arthritogenic, being the highest scores observed in ATCC 19095 SEC(+) infected mice. Intermediate and lower clinical scores were observed in N315 ST5 TSST-1(+) and S-70 TSST-1(+) infected mice, respectively. The ATCC 13565 SEA(+) strain caused death of 85% of the animals after 48 h. Arthritis triggered by the ATCC 19095 SEC(+) strain was characterized by accentuated synovial hyperplasia, inflammation, pannus formation, cartilage destruction and bone erosion. Similar joint alterations were found in N315 ST5 TSST-1(+) infected mice, however they were strikingly more discrete. Only minor synovial proliferation and inflammation were triggered by the S-70 TSST-1(+) strain. The lowest levels of TNF-α, IL-6 and IL-17 production in response to S. aureus stimulation were found in cultures from mice infected with the less arthritogenic strains (S-70 TSST-1(+) and ATCC 51650 TSST-1(+)). The highest production of IL-17 was detected in mice infected with the most arthritogenic strains (ATCC 19095 SEC(+) and N315 ST5 TSST-1(+)). CONCLUSIONS: Together these results demonstrated that S. aureus strains, isolated from biological samples, were able to induce a typical septic arthritis in mice. These results also suggest that the variable arthritogenicity of these strains was, at least in part, related to their differential ability to induce IL-17 production.