CDC twenty four seven. (SBQ13BS.31.1) Real-time PCR and statistical analyses of acrAB and ramA expression in clinical isolates of. The more replications a cell undergoes, the higher the chance it has to mutate. 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After an overnight fast, a baseline hydrogen sample is collected and then 10 g of lactulose, or 5080 g of glucose, is administered in 120200 mL of water. Nutritional consequences of intestinal bacterial overgrowth. The .gov means its official. 2014a. Chen Q, Li X, Zhou H, Jiang Y, Chen Y, Hua X, Yu Y. Bacteria, not humans, become antibiotic resistant. Structural basis for TetM-mediated tetracycline resistance. Fifth, proper interpretation of results in the setting of rapid or delayed gastric emptying has not been validated. However, antibiotics, and particularly the improper use of these drugs, provide selective pressure to bacterial colonies, whereby the most sensitive organisms are killed quickly, and the most resistant organisms are able to survive and replicate. Interestingly, the AdeABC pump appears to show some selectivity among the tetracyclines, as minocycline is reported to be a weaker substrate than other tetracyclines (Coyne et al. Chemical structures of clinically used tetracyclines and development candidates. government site. 2015), steric interference by the bulk of the C-9 side chain is also a significant factor in maintaining ribosome binding in the presence of RPPs. 2001; Al-Hamad et al. Briefly, in Gram-negative cells such as E. coli, tetracycline passively diffuses through the outer membrane porins OmpF and OmpC (Mortimer and Piddock 1993; Thanassi et al. Transduction occurs when a bacterial virus, called a bacteriophage, detaches from one bacterial cell, carrying with it some of that bacteriums genome, and then infects another cell. Comparison of the, Stotzer PO, Kilander AF. For example, the antibiotics chloramphenicol and tetracyclin inhibit the bacterial and encodes a xanthine-guanine phosphoribosyltransferase capable of conferring resistance to oxytetracycline (Nonaka and Suzuki 2002). Pimentel M, Chow EJ, Lin HC. Molecular evidence for the ancient origin of the ribosomal protection protein that mediates tetracycline resistance in bacteria. Bem AE, Velikova N, Pellicer MT, Baarlen P, Marina A, Wells JM. Mechanisms of Antibiotic Resistance Microbiol Spectr. Ruzin A, Visalli MA, Keeney D, Bradford PA. 2005b. [35] Therefore, ABCB1 levels can be monitored. When an organism is resistant to more than one drug, it is said to be multidrug-resistant. Which of the following species of bacteria are known to produce mecA? 2015), in clinical isolates of Gram-negative bacteria Neisseria gonorrhoeae and K. pneumoniae (Hu et al. Functions of tetracycline efflux proteins that do not involve tetracycline. Improvements in diagnostic equipment to facilitate the isolation and detection of resistant bacteria such as MRSA in hospital settings have enabled rapid identification of these organisms within hours rather than days or weeks. Antibiotic Resistance Mechanisms: Bacteria develop ability to hydrolyze these drugs using lactamase. Germs restrict access by changing the entryways or limiting the number of entryways. 2004. Effects of efflux transporter genes on susceptibility of. 2014. Linking to a non-federal website does not constitute an endorsement by CDC or any of its employees of the sponsors or the information and products presented on the website. 2012) and Germany (Werner et al. 2011). Small intestinal motility disturbances and bacterial overgrowth in patients with liver cirrhosis and portal hypertension. 2004b; Ruzin et al. McDermott L, Jacobus NV, Snydman DR, Kerstein K, Grossman TH, Sutcliffe JA. Accessibility 11 Some authors advocate for the empiric treatment of suspected SIBO without diagnostic testing. Sixth, special populations of patients (eg, postgastrectomy, obesity surgery, advanced age) may require different standards.79,80 Seventh, recent antibiotic use may alter the results, although the ideal antibiotic-free interval prior to testing is not known.2 Lastly, the effects of H2RAs and PPIs on breath test results remain controversial.81. 2014). Antibiotic resistance can be either plasmid mediated or maintained on the bacterial chromosome. 2006), have been reported to recognize tetracycline, but their clinical significance remains to be shown. 1988; Kobayashi et al. Hoban DJ, Reinert RR, Bouchillon SK, Dowzicky MJ. A bedside I&D is performed and he is started on broad-spectrum IV antibiotics. Our editors will review what youve submitted and determine whether to revise the article. 2). [14] A similar asexual method is used by fungi and is called "parasexuality". Gastrointestinal transit through esophagus, stomach, small and large intestine in patients with progressive systemic sclerosis. The substrate most commonly used is a readily metabolized carbohydrate, such as lactulose, glucose, sucrose, or xylose. Antibiotics are divided into classes based on how they enter cell walls and destroy bacteria. A study by Bratu et al. 2010), Spain (Rodriguez-Avial et al. Falagas ME, Vardakas KZ, Kapaskelis A, Triarides NA, Roussos NS. Medications should be reviewed to determine if they are playing a role in the development of symptoms. Antibiotics reduce or eliminate the bacterial overload and reverse the mucosal inflammation associated with overgrowth and malabsorption. Antibiotics and bacterial resistance in the 21st century. [26] The chemicals contained in these preparations, besides harming beneficial organisms, may intentionally or inadvertently target organisms that have the potential to develop resistance. 2008. However, in the presence of antibiotics, the survival advantage conferred off-sets the high metabolic cost and allows resistant strains to proliferate. Eradication of small intestinal bacterial overgrowth reduces symptoms in irritable bowel syndrome. Shindo K, Fukumura M. Effect of H2-receptor antagonists on bile acid metabolism. Damier-Piolle L, Magnet S, Bremont S, Lambert T, Courvalin P. 2008. In vitro activity of tigecycline: MICs, MBCs, time-kill curves and post-antibiotic effect. The crystal structure of multidrug-resistance regulator RamR with multiple drugs. However, in the same study, K. pneumoniae mutants selected in vitro for reduced tigecycline susceptibility showed increases in marA and acrB expression, but not soxS and ramA, so the interplay of regulators appears complicated. Several studies have demonstrated that abnormalities in the MMC may predispose to the development of SIBO.1921 Postprandial peristalsis includes irregular, high-amplitude contractions in the stomach (to assist with trituration and gastric emptying).22 Gastroparesis, a chronic disorder of delayed gastric emptying, can develop secondary to long-standing diabetes, connective tissue disorders, a prior viral infection, and ischemia.23 Impaired gastric peristalsis can lead to SIBO due to stasis of food and bacteria in the upper GI tract. aPoorer substrates for AdeABC as compared with other tetracycline drugs. Dean CR, Visalli MA, Projan SJ, Sum PE, Bradford PA. 2003. Drug resistance is the reduction in effectiveness of a medication such as an antimicrobial or an antineoplastic in treating a disease or condition. 2012. Hirata T, Saito A, Nishino K, Tamura N, Yamaguchi A. Hentschke M, Wolters M, Sobottka I, Rohde H, Aepfelbacher M. 2010. 2001). Differential contribution of AcrAB and OqxAB efflux pumps to multidrug resistance and virulence in. Connell SR, Trieber CA, Dinos GP, Einfeldt E, Taylor DE, Nierhaus KH. Patients should always be promptly treated with antibiotics/antifungals when the drugs are needed for infections and to treat sepsis. pyogenes (Grp.A)**Step. Folate synthesized by bacteria in the human upper small intestine is assimilated by the host. High-level chromosomally mediated tetracycline resistance in, Activity of minocycline against R factor-carrying Enterobacteriaceae. 2004a. 1987; Sanchez-Pescador et al. All of the following are recommended for long-term management EXCEPT: (OBQ04.190) In H. pylori, a triple mutation AGA 965-967 TTC in the h31 loop, and a deletion of G942 (E. coli numbering), each conferred tetracycline resistance (Trieber and Taylor 2002). During periods of fasting, a migrating motor complex (MMC) develops approximately every 90-120 minutes to sweep residual debris through the GI tract. 2008; Martin and Rosner 2011); for instance, MarA regulates more than 60 genes collectively referred to as the mar regulon, for multiple antibiotic resistance (Barbosa and Levy 2000). The roles of MarC and MarB in multidrug resistance are less well defined; MarC has been shown to encode a periplasmic protein, which appears to indirectly affect the transcription of marA (Vinue et al. Green arrows indicate interactions in which tetracycline resistance is increased, and red arrows indicate interactions in which tetracycline resistance is reduced. See the text for details. Many other bacterial pathogens lack vaccines as a preventive measure, but infection by these bacteria can often be treated or prevented with antibiotics. Regulation of expression of Gram-negative intrinsic multidrug-resistance mechanisms affecting tetracyclines. 5K11 AI00865/AI/NIAID NIH HHS/United States. Spanu T, De Angelis G, Cipriani M, Pedruzzi B, DInzeo T, Cataldo MA, Sganga G, Tacconelli E. 2012. 2012. 2012. Nielsen LE, Snesrud EC, Onmus-Leone F, Kwak YI, Aviles R, Steele ED, Sutter DE, Waterman PE, Lesho EP. Tursi A, Brandimarte G, Giorgetti GM. A large component of the intrinsic antibiotic-resistance response in bacteria is due to increased expression of intrinsic efflux pumps (Piddock 2006; Li et al. Phylogeny of efflux-mediated tetracycline resistance genes and related proteins revisited, marA, a regulated locus which controls expression of chromosomal multiple antibiotic resistance in. 2). More recently, a fully synthetic chemistry approach has led to the discovery of eravacycline, which shows promise in the treatment of serious infections caused by a broad range of bacterial pathogens. 2009), and in B. fragilis, BmeABC (Pumbwe et al. epidermidis, S aureus**S epidermis**E.Coli**Klebsiella**, RickettsiaMycoplasmaSpirochetes(Lyme's disease), Bacteroides fragilisS aureusCoagulase-negative Staph & StrepExcellent Bone Penetration, Pseudomembranous colitisHypersensitivity Reaction, PhototoxicityAchilles tendon ruptureImpaired fracture healing, ThrombocytopeniaAvoid in third trimester of pregnancy, Bacillus anthracisBacillus cereusClostridium tetaniClostridium botulinumClostridium perfringensClostridium difficile. The immune system is a network of biological processes that protects an organism from diseases.It detects and responds to a wide variety of pathogens, from viruses to parasitic worms, as well as cancer cells and objects such as wood splinters, distinguishing them from the organism's own healthy tissue.Many species have two major subsystems of the immune system. Lupien A, Gingras H, Leprohon P, Ouellette M. 2015. Some evidence from the spread of meticillin-resistant S aureus and meticillin-susceptible S aureus suggests that drug-resistant infections do not simply replace drug-susceptible infections, 63, 64 but this finding might not generalise to all other pathogens and other mechanisms of resistance. Dey A, Yadav M, Kumar D, Dey AK, Samal S, Tanwar S, Sarkar D, Pramanik SK, Chaudhuri S, Das A. Chem Sci. The group 2 pumps possess 14 transmembrane segments and include Tet(K) and Tet(L), the most common tetracycline-specific efflux pumps in Gram-positive clinical isolates. (OBQ11.70) [9] Chemotherapy causes fibroblasts near tumors to produce large amounts of the protein WNT16B. 2014. Chang CS, Chen GH, Lien HC, et al. The decision is made to proceed with irrigation and debridement, nail removal with exchange for a polymethylmethacrylate intramedullary nail with vancomycin and tobramycin. tenocytes in the Achilles tendon have exhibited degenerative changes when viewed microscopically after fluoroquinolone administration. The interdigestive motor complex of normal subjects and patients with bacterial overgrowth of the small intestine. 2013). 2009, Chen et al. , with special predilection for the Achilles tendon. These mechanisms give rise to resistance because they result in biochemical modifications that alter certain bacterial cell properties that normally render the cell sensitive to an antibiotic. In viruses, an equivalent "cost" is genomic complexity. 2013. Effect of octreotide on gastric and small bowel motility in patients with gastroparesis. Teo M, Chung S, Chitti L, et al. For antibiotic resistance, which represents a widespread problem nowadays, drugs designed to block the mechanisms of bacterial antibiotic resistance are used. Both IV and oral formulations are in development. 2006). 2008; Coyne et al. Mechanisms of tigecycline resistance among. Uptake into the cytoplasm is partially energy dependent, involving passive diffusion, proton motive force, and phosphate bond hydrolysis (McMurry and Levy 1978; Smith and Chopra 1984; Yamaguchi et al. Before Antimicrobial resistance and antineoplastic resistance challenge clinical care and drive research. Unable to load your collection due to an error, Unable to load your delegates due to an error. Some evidence from the spread of meticillin-resistant S aureus and meticillin-susceptible S aureus suggests that drug-resistant infections do not simply replace drug-susceptible infections, 63, 64 but this finding might not generalise to all other pathogens and other mechanisms of resistance. 2013. (OBQ04.58) Rifaximin (Xifaxan, Salix; a nonabsorbed rifamycin derivative) proved better than chlortetracycline at improving hydrogen breath testing and symptoms of SIBO.95 However, a recent randomized crossover trial comparing rifaximin and metronidazole demonstrated superiority of metronidazole at improving hydrogen breath test results and symptoms of SIBO.94 In a group of patients with Crohn's disease and abnormal breath hydrogen tests, both metronidazole and ciprofloxacin normalized breath tests and improved bloating, loose stools, and abdominal pain.96 A randomized controlled trial comparing norfloxacin and amoxicillin/clavulanate demonstrated similar efficacy at improving hydrogen breath analysis and diarrhea output compared to Sacchromyces boulardii and placebo; however, there was no improvement in other abdominal symptoms including bloating, flatus, abdominal pain, and borborygmi.97. This review will focus on recent developments in the understanding of tetracycline-resistance mechanisms and their potential impact on the clinical utility of tetracycline-class antibiotics. 1982; Nelson and Levy 2011). Antibiotics work by binding to bacterial cells and penetrating their cells walls. Strictures of the small intestine, which can develop after surgery, after radiation, in association with Crohn's disease, or secondary to medication use, also predispose to the development of SIBO.31 Finally, resection of the ileocecal valve increases the risk of developing SIBO, because retrograde movement of bacteria from the colon into the small intestine can now readily occur. The development of inexpensive, commercially available gas chromatographs to measure exhaled hydrogen and/or methane has led to the widespread use of breath testing for the diagnosis of bacterial overgrowth. Plasmid encode an enzyme that acetylate the drug, thereby inactivating it. a bacterial gene encoding a penicillin-binding protein (PBP2a). Parkman HP, Hasler WL, Fisher RS. Nigo M, Cevallos CS, Woods K, Flores VM, Francis G, Perlman DC, Revuelta M, Mildvan D, Waldron M, Gomez T, et al. Several TCSs have been implicated in modulating susceptibility to tetracycline-class antibiotics in Gram-negative and -positive bacteria, presumably by affecting permeability and/or expression of intrinsic multidrug efflux systems. Recent animal studies have demonstrated that acute pancreatitis can alter the MMC57 and that acute necrotizing pancreatitis disturbs the jejunal MMC leading to SIBO.58 A study of 35 patients with chronic pancreatitis and pancreatic insufficiency found that 34% had SIBO, as determined by a glucose breath test.59. Consistent with this recent finding, earlier work by Bauer et al. The tetracycline destructases: A novel family of tetracycline-inactivating enzymes, Susceptibility of tetracyclines to Tet(A) resistance is independent of interdomain loop sequence. All identified articles were then manually searched for other relevant studies. Bad bugs need old drugs: A stewardship programs evaluation of minocycline for multidrug-resistant, Regulation of bacterial drug export systems. 1950. Protein-losing enteropathy in the human and experimental rat blind-loop syndrome. Example: Klebsiella pneumoniaebacteria produce enzymes called carbapenemases, which break down carbapenem drugs and most other beta-lactam drugs. Because Bacteroides species are obligate aerobes, it is not surprising that the oxidoreductases encoded by tet(X) and its orthologs tetX1 and tetX2 do not confer resistance in the isolates in which they were originally found (Whittle et al. The Centers for Disease Control and Prevention (CDC) cannot attest to the accuracy of a non-federal website. 2012, 2014b) reported that tigecycline resistance (MIC 8 g/mL) correlated with overexpression of AdeABC in the majority of isolates, likely resulting from mutations in adeR and adeS encoding changes in conserved amino acid residues, or an insertion sequence (IS) in adeS producing a truncated constituitively on form of AdeS. A novel MATE family efflux pump contributes to the reduced susceptibility of laboratory-derived. In A. baumannii, the AdeRS TCS controls expression of the major multidrug efflux pump AdeABC (Marchand et al. 1993). Germs get rid of antibiotics using pumps in their cell walls to remove antibiotic drugs that enter the cell. Daurel C, Fiant AL, Bremont S, Courvalin P, Leclercq R. 2009. Based on meta-analyses of clinical trial data, the FDA issued a safety alert in 2010 and a black box warning in 2013 because of an observed increase in mortality risk in patients treated with tigecycline, as compared with other drugs (U.S. Food and Drug Administration 2010, 2013). 2000; Pioletti et al. Tursi A. Gastrointestinal motility disturbances in celiac disease. 2006. Haboubi NY, Lee GS, Montgomery RD. All of the following antibiotics function by interfering with cell wall synthesis EXCEPT, 7th Annual Interdisciplinary Conference on Orthopedic Value-Based Care, Type in at least one full word to see suggestions list, Orthopaedic Summit Evolving Techniques 2020, Evolving Technique Update: Antibiotic Powders & Irrigations - Burt Yaszay, MD, Basic ScienceAntibiotic Classification & Mechanism. Expression of the RND-type efflux pump AdeABC in, Binding of purified multiple antibiotic-resistance repressor protein (MarR) to mar operator sequences, Promoter discrimination at class I MarA regulon promoters mediated by glutamic acid 89 of the MarA transcriptional activator of. You will be subject to the destination website's privacy policy when you follow the link. Iivonen MK, Ahola TO, Matikainen MJ. 2015). 1950). Please enable it to take advantage of the complete set of features! 2015. The skin is the body's largest mechanical barrier against the external environment and invasion by microorganisms. Linkevicius M, Sandegren L, Andersson DI. 2012; Jenner et al. Substrate specificities of MexAB-OprM, MexCD-OprJ, and MexXY-oprM efflux pumps in. Ross JI, Eady EA, Cove JH, Cunliffe WJ. Thus, the genetic material of bacteria is free-floating within the cell, making it open to gene transfer (the movement of a segment of genetic material from one bacterial cell to another), which often involves the transmission of plasmids. The original source of the genes for these enzymes is not known with certainty; however, mobile genetic elements, called transposons (jumping genes), may have played a role in their appearance and may facilitate their transfer to other bacterial species. Mechanisms of Antibiotic Resistance Microbiol Spectr. National Library of Medicine HGT is an important factor in the evolution of many organisms. 2015). 2004). The most successful examples of this approach include minocycline, doxycycline, tigecycline, and omadacycline. 2015). RamA, which controls expression of the MDR efflux pump AcrAB-TolC, is regulated by the Lon protease, A review of intravenous minocycline for treatment of multidrug-resistant, Update on acquired tetracycline resistance genes, Mechanisms of bacterial antibiotic resistance and lessons learned from environmental tetracycline-resistant bacteria, Antimicrobial Resistance in the Environment. a double-blind, randomized, placebo-controlled study. 2002; De Majumdar et al. Patients with normal intestinal enteric flora rely on gastric intrinsic factor to bind to vitamin B12 to permit absorption in the ileum. When the bacteriophage inserts its genetic content into the genome of the next bacterium, the previous bacteriums DNA also is incorporated into the genome. Change the targets for the antibiotic or antifungal. Corrazza GR, Menozzi MG, Strocchi A, et al. Blind loop syndrome and small bowel bacterial contamination. Therefore, other measures have been undertaken, including educating the public about the proper use of antibiotics and the importance of completing a full regimen as prescribed. 1995). Decreased susceptibility to tigecycline in. Normalization of lactulose breath testing correlates with symptom improvement in irritable bowel syndrome. 2009. Kobayashi T, Nonaka L, Maruyama F, Suzuki S. 2007. 2: Optimization of the C-9 side-chain for antibacterial activity and oral efficacy, marA locus causes decreased expression of OmpF porin in multiple-antibiotic-resistant (Mar) mutants of, A multidrug resistance regulatory chromosomal locus is widespread among enteric bacteria. Ramirez J, Dartois N, Gandjini H, Yan JL, Korth-Bradley J, McGovern PC. 2015a,b,c). Copper alloy surfaces have intrinsic properties to destroy a wide range of microorganisms.In the interest of protecting public health, especially in healthcare environments with their susceptible patient populations, an abundance of peer-reviewed antimicrobial efficacy studies have been conducted in the past ten years regarding copper's efficacy to destroy E. coli O157:H7, Example: Some Candida species produce pumps that get rid of azoles such as fluconazole. 2014) or arose during treatment with another antibiotic (Hornsey et al. Guidelines for the evaluation and management of chronic diarrhea. The antibiotic has no target to attack in a virus. 2000; Morita et al. 2011; Zhong et al. When a resistant strain of bacteria is the dominant strain in an infection, the infection may be untreatable and life-threatening. The actual process of resistance mechanism can be very complex. 2001). 2014), and in in vitro studies with E. coli and Acinetobacter baumannii (Beabout et al. Clipboard, Search History, and several other advanced features are temporarily unavailable. RamA is an alternate activator of the multidrug resistance cascade in, Tetracycline antibiotics: Mode of action, applications, molecular biology, and epidemiology of bacterial resistance. confers resistance to penicillin; e.g. 1995; Ruzin et al. This process appears to be the most common mechanism by which resistance develops; it is facilitated by the fact that bacteria are prokaryotic organisms (which means that they do not have a nucleus protecting the genome) and by the presence of small pieces of DNA called plasmids that exist in a bacterial cell separate from the chromosome. 2005; Sutcliffe et al. Because the drug is so specific, any mutation in these molecules will interfere with or negate its destructive effect, resulting in antibiotic resistance. 2015). What is the mechanism of action of vancomycin? 2004). Surgically induced obstructive jaundice can lead to bacterial overgrowth and increased bacterial translocation from the GI tract in laboratory animals.50 Clinical studies have shown that patients with advanced liver disease are more likely to have abnormalities in gut motility compared to those with lower Child-Pugh scores.24,51,52 These include abnormalities in the MMC and an increase in the frequency of clustered contractionsboth of which may promote bacterial stasis and the development of SIBOin 3168% of patients.5356 SIBO does not appear to be an independent risk factor for liver injury, however. Small bowel motility disorders also predispose to the development of SIBO, because bacteria may not be effectively swept from the proximal bowel into the colon. 2015. The challenges of directly measuring small bowel bacterial contamination led to the development of several indirect tests to diagnose SIBO.71 Breath testing is now the predominant method to evaluate patients for potential overgrowth because of its simplicity, safety, and lack of invasiveness. Philadelphia[PA]: Lippincott Williams & Wilkins; 2005. p 265. The 9-t-butylglycylamido moiety at the C-9 position in tigecycline was shown to improve binding affinity and translational inhibition by >100-fold and 20-fold, respectively, over that of tetracycline; however, the mechanism of RPP evasion could not be fully explained (Olson et al. Ribosome-targeting antibiotics and mechanisms of bacterial resistance. 2012. Keeney D, Ruzin A, McAleese F, Murphy E, Bradford PA. 2008. 2014b; Abdallah et al. Sun JR, Perng CL, Lin JC, Yang YS, Chan MC, Chang TY, Lin FM, Chiueh TS. Perman JA, Modler S, Barr RG, et al. Riordan SM, McIver CJ, Wakefield D, et al. In recent surveillance studies, the prevalence of tetracycline resistance in selected European countries was found to be 66.9% and 44.9% for extended-spectrum -lactamase (ESBL)-producing Escherichia coli and Klebsiella species (spp. Assessment of Eravacycline against a recent global collection of 4,462 Enterobacteriaceae clinical isolates (20132014). Crystallographic studies with the Thermus thermophilus 30S ribosomal subunit have revealed at least one high-occupancy tetracycline-binding site (Tet-1) and five other minor binding sites in 16S rRNA (Brodersen et al. First, the small bowel must be intubated. Production of antibiotic-modifying enzymes and synthesis of antibiotic-insensitive bacterial targets are the primary resistance mechanisms for the other classes of antibiotics, including trimethoprim, the sulfonamides, the aminoglycosides, chloramphenicol, and the quinolone drugs. This in turn either kills the bacteria or stops them from multiplying. This consists of an initial hydrogen peak prior to 90 minutes, followed by a fall of more than 5 ppm over two consecutive samples, and then a second peak in breath hydrogen as the substrate enters the cecum.37. 2015a). Srinivasan VB, Venkataramaiah M, Mondal A, Vaidyanathan V, Govil T, Rajamohan G. 2012. Yoon EJ, Courvalin P, Grillot-Courvalin C. 2013. (2012). In a study by Linkevicius et al. Hospitals that have adopted these methods have lost fewer patients to complications caused by bacterial infections. MarA is a key activator of stress-responsive genes, and its role in promoting overexpression of the major multidrug efflux pump, AcrAB (Li and Nikaido 2009), is central to conferring an MDR phentoype in enteric bacteria (Gambino et al.
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