Research Article Association between Accessory Gene Regulator Polymorphism and Mortality among Critically Ill Patients Receiving Vancomycin for Nosocomial MRSA Bacteremia: A Cohort Study Angélica Cechinel, 1 Denise P. Machado, 1 Eduardo Turra, 1 Dariane Pereira, 1 Rodrigo P. dos Santos, 2 Regis G. Rosa, 1 and Luciano Z. Goldani 1 1 Infectious Diseases Unit, Hospital de Cl´ ınicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, 90035-903 Porto Alegre, RS, Brazil 2 Hospital Infection Control Section, Hospital de Cl´ ınicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, 90035-903 Porto Alegre, RS, Brazil Correspondence should be addressed to Luciano Z. Goldani; lgoldani@ufrgs.br Received 19 March 2015; Accepted 23 September 2015 Copyright © 2016 Ang´ elica Cechinel et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background. Polymorphism of the accessory gene regulator group II (agr) in methicillin-resistant Staphylococcus aureus (MRSA) is predictive of vancomycin failure therapy. Nevertheless, the impact of group II agr expression on mortality of patients with severe MRSA infections is not well established. Objective. Te goal of our study was to evaluate the association between agr polymorphism and all-cause in-hospital mortality among critically ill patients receiving vancomycin for nosocomial MRSA bacteremia. Methods. All patients with documented bacteremia by MRSA requiring treatment in the ICU between May 2009 and November 2011 were included in the study. Cox proportional hazards regression was performed to evaluate whether agr polymorphism was associated with all-cause in-hospital mortality. Covariates included age, APACHE II score, initial C-reactive protein plasma levels, initial serum creatinine levels, vancomycin minimum inhibitory concentration, vancomycin serum levels, and time to efective antibiotic administration. Results. Te prevalence of group I and group II agr expression was 52.4% and 47.6%, respectively. Bacteremia by MRSA group III or group IV agr was not documented in our patients. Te mean APACHE II of the study population was 24.3 (standard deviation 8.5). Te overall cohort mortality was 66.6% (14 patients). Afer multivariate analysis, initial plasma C-reactive protein levels ( = 0.01), initial serum creatinine levels ( = 0.008), and expression of group II agr ( = 0.006) were positively associated with all-cause in-hospital mortality. Patients with bacteremia by MRSA with group II agr expression had their risk of death increased by 12.6 times when compared with those with bacteremia by MRSA with group I agr expression. Conclusion. Group II agr polymorphism is associated with an increase in mortality in critically ill patients with bacteremia by MRSA treated with vancomycin. 1. Introduction Methicillin-resistant Staphylococcus aureus (MRSA) is well recognized as a major cause of nosocomial infection world- wide. Its strong adaptive power to antibiotics has resulted in the emergence of methicillin-resistant S. aureus (MRSA) [1, 2]. Resistance to methicillin and other -lactam antibiotics is caused by the mecA gene, which is situated on a mobile genetic element, the staphylococcal cassette chromosome mec (SCCmec) [3]. Although the origin of MRSA is not fully understood, it is suspected that methicillin-susceptible S. aureus (MSSA) acquired the mecA gene through horizon- tal transfer from coagulase-negative staphylococci. Recent studies have shown that overall in-hospital mortality rates for patients with bloodstream infections due to MRSA are in the range of 30% but can be as high as 65% in some centers [4, 5]. A thorough knowledge of the epidemiology and the molecular epidemiology of MRSA strains is required to develop efective strategies to prevent the spread of MRSA. Te aim of the present study was to evaluate the associ- ation between agr polymorphism and all-cause in-hospital Hindawi Publishing Corporation Canadian Journal of Infectious Diseases and Medical Microbiology Volume 2016, Article ID 8163456, 5 pages http://dx.doi.org/10.1155/2016/8163456