OBJECTIVE:To establish the risk factors for joint infection by oxacillin-resistant Staphylococcus aureus (MRSA) using clinical and epidemiological data.METHODS:All septic arthritis cases of the knee and hip diagnosed and treated in our institution from 2006 to 2012 were evaluated retrospectively. Only patients with cultures identified as microbial agents were included in the study. The clinical and epidemiological characteristics of the patients were analyzed, seeking the differences between populations affected by MRSA and oxacillin-sensitive Staphylococcus aureus (MSSA).RESULTS:S. aureus was isolated in thirty-five patients (46.0%) in our total sample, 25 in the knee and 10 in the hip. Of these 35 patients, 22 presented with MSSA and 13 presented with MRSA. Provenance from a health service-related environment, as described by the Centers for Disease Control and Prevention, was the only variable associated with oxacillin-resistant strains of this bacterium (p = 0.001).CONCLUSION:Provenance from a health service-related environment was associated with a higher incidence of MRSA-related septic arthritis, suggesting that this agent should be considered in the initial choice of antibiotic treatment. Previous surgeries of the knee or affected limb and the absence of leukocytes might also be related to infection with this agent.

Pigment epithelium derived factor (PEDF) exerts trophic actions to motoneurons and modulates nonneuronal restorative events, but its effects on neuroplasticity responses after spinal cord (SC) injury are unknown. Rats received a low thoracic SC photothrombotic ischemia and local injection of PEDF and were evaluated behaviorally six weeks later. PEDF actions were detailed in SC ventral horn (motor) in the levels of the lumbar central pattern generator (CPG), far from the injury site. Molecules related to neuroplasticity (MAP-2), those that are able to modulate such event, for instance, neurotrophic factors (NT-3, GDNF, BDNF, and FGF-2), chondroitin sulfate proteoglycans (CSPG), and those associated with angiogenesis and antiapoptosis (laminin and Bcl-2) and Eph (receptor)/ephrin system were evaluated at cellular or molecular levels. PEDF injection improved motor behavioral performance and increased MAP-2 levels and dendritic processes in the region of lumbar CPG. Treatment also elevated GDNF and decreased NT-3, laminin, and CSPG. Injury elevated EphA4 and ephrin-B1 levels, and PEDF treatment increased ephrin A2 and ephrins B1, B2, and B3. Eph receptors and ephrins were found in specific populations of neurons and astrocytes. PEDF treatment to SC injury triggered neuroplasticity in lumbar CPG and regulation of neurotrophic factors, extracellular matrix molecules, and ephrins.