Discovery of a Fluoroquinolone-Resistant Serratia marcescens Clinical Isolate without Quinolone Resistance-Determining Region Mutations

Sir, Serratia marcescens, once considered to be an innocuous and non-pathogenic organism, is now an important cause of hospitalacquired infections. This organism is associated with respiratory tract infections, urinary tract infections, septicemia, meningitis, and wound infections [1, 2]. S. marcescens infections are difficult to treat because of high resistance to a wide variety of antibiotics, including cephalosporins, fluoroquinolones, and aztreonam [2]. Fluoroquinolones are broad-spectrum bactericidal antimicrobial agents that are used to treat various bacterial infections. Although S. marcescens infections are frequently treated with fluoroquinolones, the incidence of fluoroquinolone resistance continues to increase in clinical settings in China [2]. Fluoroquinolone resistance is mainly caused by chromosomal mutations affecting the quinolone resistance-determining region (QRDR) of gyrA and gyrB, which encode DNA gyrase subunits, and parC and parE, which encode topoisomerase IV subunits [3]. Moreover, plasmid-mediated quinolone resistance (PMQR) genes have been reported in gram-negative bacteria, including S. marcescens, and include the qnr, qep, and oqx systems [4]. The major cause of fluoroquinolone resistance is chromosomal mutation. The acquisition of PMQR genes alone results in a low level of fluoroquinolone resistance and does not lead to minimum inhibitory concentrations (MICs) exceeding the threshold of these agents [3]. We isolated a S. marcescens strain, designated as GN0780, from the wound drainage fluid of a 66-yr-old male patient who had femoral fractures and was admitted to the Department of Orthopedics at the People’s Hospital of Huangshan (Huangshan, China) in 2011. The MICs of ciprofloxacin (CIP), levofloxacin (LVX), gatifloxacin (GAT), and nalidixic acid (NAL) exceeded the resistance thresholds proposed by the Clinical and Laboratory Standards Institute (2012) (Table 1) [5]. Surprisingly, direct DNA sequencing of the QRDRs did not reveal any mutations in