Decolonisation of MRSA and its effect on surgical site infections--a study in a tertiary care institute.

BACKGROUND: Two-thirds of surgical site infections (SSI) because of Staphylococcus aureus are caused by Methicillin resistant Staphylococcus aureus (MRSA). This study was done to assess the efficacy of topical 2% mupirocin with 2% chlorhexidine gluconate body wash in decolonizing MRSA and its impact in preventing SSI because of MRSA. The various risk factors associated with MRSA carriers and SSI were also studied because of paucity of data in the developing world. METHODS: We did a non-randomised interventional trial in 602 patients undergoing elective general surgical operations. All patients in case (297) group were screened for MRSA and those positive were decolonised with topical 2% mupirocin calcium ointment and daily baths with 2% chlorhexidine antiseptic solution for 5 days. Control (305) group patients underwent surgery without decolonisation. Postoperatively, all patients were followed up for SSI for 30 days. RESULTS: Prevalence of MRSA carriers was 7.5% with decolonisation rate of 95.2%. The SSI incidence was 21.3%. The significant risk factors for SSI were type of anaesthesia (p = 0.002), duration of surgery (p = 0.001) and preoperative hospital stay (p = 0.001). There was a significant association between MRSA carrier positivity at the time of surgery and SSI (p = 0.041). CONCLUSIONS: There was no reduction in rate of SSI or other nosocomial infections in patients undergoing elective general surgical operations following preoperative MRSA decolonisation with 2% mupirocin and 2% chlorhexidine gluconate in MRSA carriers. MRSA carrier status was a significant risk factor for SSI but not for other nosocomial infections.

Breaking the 'harmony' of TNF-α signaling for cancer treatment.

Tumor necrosis factor-alpha (TNF-α) binds to two distinct receptors, TNFR1/p55 and TNFR2/p75. TNF-α is implicated in the processes of tumor growth, survival, differentiation, invasion, metastases, secretion of cytokines and pro-angiogenic factors. We have shown that TNFR2/p75 signaling promotes ischemia-induced angiogenesis via modulation of several angiogenic growth factors. We hypothesized that TNFR2/p75 may promote tumor growth and angiogenesis. Growth of mouse Lewis lung carcinoma (LLC1) and/or mouse melanoma B16 cell was evaluated in wild type (WT), p75 knockout (KO) and double p55KO/p75KO mouse tumor xenograft models. Compared with WT and p55KO/p75KO mice, growth of tumors in p75KO mice was significantly decreased (twofold) in both LLC and B16 tumors. Tumor growth inhibition was correlated with decreases in vascular endothelial growth factor (VEGF) expression and capillary density, as well as bone marrow-derived endothelial progenitor cells incorporation into the functional capillary network, and an increase in apoptotic cells in LLC xenografts. Gene array analysis of tumor tissues showed a decrease in gene expression in pathways that promote tumor angiogenesis and cell survival. Blocking p75 by short-hairpin RNA in cultured LLCs led to increases in TNF-mediated apoptosis, as well as decreases in the constitutive and TNF-mediated expression of angiogenic growth factors (VEGF, HGF, PLGF), and SDF-1α receptor CXCR4. In summary, p75 is essential for tumor angiogenesis and survival in highly vascularized murine lung tumor xenografts. Blocking p75 expression may lead to tumor regression. This may represent new and effective therapy against lung neoplasms and potentially tumors of other origin.