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Surgical site infections (SSIs) are defined as superficial infections, deep incisional infections, and organ/organ space infections that occur within 30 days of the surgical procedure or up to 90 days if a prosthetic implant has been used. Incidence of SSI is highest in recipients of small bowel transplant, followed by liver, pancreas, and kidney transplant. These are diagnosed by the presence of at least one of the following: purulent discharge from the wound, organism identified from the specimen obtained from the site with culture/nonculture-based methods, evidence of infection on gross/histopathological examination or on imaging, or a clinical diagnosis of SSI by a physician. The spectrum of organisms implicated in SSIs in solid organ transplant recipients is more diverse due to underlying end-stage organ failure, need for immunosuppression, prolonged hospitalization, colonization or active infection in the deceased organ donor, contamination during organ transportation/preservation. SSI in solid organ transplant can be prevented leading to hospital stay and cost of transplantation. Minimizing surgical operative time, sterile and appropriate surgical technique and antimicrobial prophylaxis, management of patient comorbidities as well as glucose and temperature regulation are important for prevention of SSI. This article discusses useful preventive strategies for preventing SSI such as preoperative bathing, use of appropriate preoperative antibiotic prophylaxis, surgical site and hand preparation, use of wound protectors, drapes and gowns, incisional wound irrigation, adequate nutritional support, and use of perioperative oxygenation. [ABSTRACT FROM AUTHOR]

Background Complement 3 glomerulopathy (C3G) results from dysfunction of the alternative complement pathway (ACP). No data are available on post-transplant C3G in South Asia. Methods In this study, renal allograft biopsies of C3G patients performed from 2012 to 2017 were analysed for ACP functional assay (APFA), serum complement levels, complement factor H (CFH), complement factor B (CFB) and autoantibodies to CFH and CFB. Limited genetic screening for CFH / CFHR5 genes was carried out. All study patients were also followed up. Results A total of 21 cases of C3G were included, of which 11 had native C3G disease (that is, recurrent C3G). Of these 11 recurrent cases, 7 presented with allograft dysfunction and 4 with proteinuria and renal dysfunction. Early post-transplant recurrence (<1 month) was noted in six patients, whereas recurrence in five patients occurred within 8–17 months of transplant. Biopsies showed mild focal mesangial expansion with or without endocapillary proliferation and thrombotic microangiopathy. Rejection was also noted in six patients. APFA/C3 levels were low in all cases. Serum CFH levels were low [dense deposit disease (DDD), 44%; C3 glomerulonephritis (C3GN), 25%], whereas CFB levels were normal. Autoantibodies to CFH, CFB and C3 nephritic factor were present in 11, 0 and 44% of DDD cases, respectively, and in 17, 17 and 33% of C3GN cases, respectively. Genetic analysis revealed only non-pathogenic CFH gene variants (93%). No novel mutation was found. At follow-up (140 months), stable graft was noted in 28% of cases, progressive renal failure in 19%, graft loss in 34%, and 19% of patients died. Conclusion Post-transplant C3G can present with graft dysfunction and/or proteinuria. Subtle histological findings demand careful interpretation of immunofluorescence results. Autoantibodies to complement pathway regulatory proteins are common, and no novel mutation has been found from limited genetic workup. Clinical outcome is poor. [ABSTRACT FROM AUTHOR]