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Ciprofloxacin
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Jason Kwong, M. Lindsay Grayson
Diagnostic laboratory detection of transmissible quinolone resistance has previously proved problematic. Cavaco and Aarestrup (2009a) assessed various methods for their accuracy in detecting quinolone resistance, particularly low-level fluoroquinolone resistance conferred by the transferable plasmid-mediated genes qnrA, qnrB, and qnrS, as well as the aac(6¢)-Ib-cr gene. Although screening for nalidixic acid resistance by MIC testing or disk diffusion was efficient for detection of mutants (gyrase, topoisomerase, and efflux), direct testing using ciprofloxacin or norfloxacin was required for detection of qnr and aac(6¢)-Ib-cr. (Cavaco and Aarestrup, 2009a). Furthermore, the complexity of the resistance mechanisms may produce substantial variation in susceptibility testing results, particularly if they are in combination (Rodriguez-Martinez et al., 2015a; Rodriguez-Martinez et al., 2015b). In the current era, these plasmid-mediated resistance genes may be more readily detected through high-throughput whole genome sequencing (Guillard et al., 2010; Zankari et al., 2012).
Plazomicin: an intravenous aminoglycoside antibacterial for the treatment of complicated urinary tract infections
Published in Expert Review of Anti-infective Therapy, 2020
Anastasia Bilinskaya, Kristin E. Linder, Joseph L. Kuti
As a result of plasmid-mediated resistance affecting multiple antibiotic classes, treatment options for MDR Enterobacterales are limited. For the management of ESBL infections, carbapenems have traditionally been considered the treatment of choice because of improved survival outcomes when compared with non-carbapenem alternatives [32]. Given the rapid rise in resistance, carbapenem-sparing strategies have been suggested to preserve the class’s activity. Potentially useful alternatives include new ß-lactam/ß-lactamase inhibitor combinations (ceftazidime/avibactam, ceftolozane/tazobactam, meropenem/vaborbactam, imipenem/cilastatin/relebactam), conventional ß-lactams (cefepime, piperacillin/tazobactam), and non-ß-lactam antibiotics (fluoroquinolones, aminoglycosides, nitrofurantoin, fosfomycin, trimethoprim-sulfamethoxazole, tigecycline) [33]. Each alternative may have variable activity and should be carefully selected based on the source of the ESBL-infection, pharmacokinetic properties, and individual susceptibility results. For CREs, treatment options include eravacycline, cefiderocol, ceftazidime/avibactam, meropenem/vaborbactam, aztreonam/avibactam, or imipenem/cilastatin/relebactam, or combination therapy with carbapenems, polymyxins, tigecycline, older aminoglycosides, or fosfomycin [33,34]. Although a variety of alternative antibiotics are available, many have limited pharmacokinetic properties or safety concerns. For example, polymyxin antibiotics carry a substantial risk of nephrotoxicity and neurotoxicity, in addition to highly varied concentrations with current dosing strategies. Furthermore, tigecycline is limited due to inadequate drug concentrations at certain infection sites and tolerability concerns secondary to gastrointestinal adverse effects [33]. As a result, there is an urgent need for novel antibiotics with increased activity against these MDR Enterobacterales.
Progress towards the development of Klebsiella vaccines
Published in Expert Review of Vaccines, 2019
Myeongjin Choi, Sharon M Tennant, Raphael Simon, Alan S Cross
In the last two decades, there has been a dramatic increase in the resistance of KP to beta-lactam antibiotics, including third-generation cephalosporins, commonly employed to treat KP infections. This extended-spectrum beta lactamases (ESBL) resistance, first identified in the US in 1989, forced clinicians to rely on carbapenem antibiotics, but perhaps due to the pressure of treating ESBL-producing strains with carbapenems, carbapenem-resistant Enterobacteriaceae (CRE) emerged in the US in 1996, with carbapenemase-producing KP (KP-C) the most common [10]. In data submitted to the U.S. Centers for Disease Control and Prevention (CDC) databases (National Healthcare Safety Network [NHSN], National Nosocomial Infections Surveillance [NNIS] systems) over the last decade, CRE strains increased from 1.2% to 4.2% of isolates in 2011, with KP becoming the most resistant (1.6% to 10.4%) [11]. KP-C now represents 8% of KP in the United States [12] and up to 28% of KP in the Mid-Atlantic States [13]. Patients infected in the bloodstream with CRE have a higher mortality (20% vs 10%), increased length of stay (LOS) in the hospital and intensive care unit (ICU) and are less likely to be discharged home [14]. Each year KP-C are responsible for 85% of CRE infections in the United States and 520 deaths. Moreover, ESBL-producing KP strains account for ~17,000 nosocomial infections and 1100 deaths annually [15]. In 2011 additional carbapenemases, such as plasmid-encoded New Delhi metallo-beta-lactamase (NDM-1) and MBL and VIM soon followed. The emergence of MDR KP over the last two decades along with its rapid spread and high mortality led the CDC to declare MDR KP one of three most urgent threats in the US in its landmark 2013 report [15]. MDR KPs necessitate the use of toxic, less effective, ‘last resort’ antibiotics such as polymixin/colistin. Ominously, in 2015, plasmid-mediated resistance to colistin was discovered in an E. coli isolate in China conferred by the mcr-1 gene [16]. Nearly 20% of livestock in China harbor this gene. Aided by air travel, it has now spread globally. Patients from developed countries who travel to less developed countries for less-expensive medical procedures (‘medical tourism’) have returned with extensively resistant bacteria in wound infections [17].