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Kiang, Risaku Fukumoto and Nikolai V. Gorbunov",authors:[{id:"157452",title:"Dr.",name:"Juliann",middleName:null,surname:"Kiang",fullName:"Juliann Kiang",slug:"juliann-kiang"},{id:"158709",title:"Dr.",name:"Risaku",middleName:null,surname:"Fukumoto",fullName:"Risaku Fukumoto",slug:"risaku-fukumoto"},{id:"158710",title:"Dr.",name:"Nikolai",middleName:null,surname:"Gorbunov",fullName:"Nikolai Gorbunov",slug:"nikolai-gorbunov"}]},{id:"38467",title:"Tissue Occurrence of Carbonyl Products of Lipid Peroxidation and Their Role in Inflammatory Disease",slug:"tissue-occurrence-of-carbonyl-products-of-lipid-peroxidation-and-their-role-in-inflammatory-disease",signatures:"Maria Armida Rossi",authors:[{id:"148504",title:"Prof.",name:"Maria",middleName:null,surname:"Rossi",fullName:"Maria Rossi",slug:"maria-rossi"}]},{id:"38465",title:"The Role of Physical Exercise on Lipid Peroxidation in Diabetic Complications",slug:"the-role-of-physical-exercise-on-lipid-peroxidation-in-diabetic-complications",signatures:"Yaşar Gül Özkaya",authors:[{id:"142843",title:"Dr.",name:"Y. Gul",middleName:null,surname:"Ozkaya",fullName:"Y. Gul Ozkaya",slug:"y.-gul-ozkaya"}]},{id:"38466",title:"Reactive Oxygen Species Act as Signaling Molecules in Liver Carcinogenesis",slug:"reactive-oxygen-species-act-as-signaling-molecules-in-liver-carcinogenesis",signatures:"María Cristina Carrillo, María de Luján Alvarez, Juan Pablo Parody, Ariel Darío Quiroga and María Paula Ceballos",authors:[{id:"142215",title:"PhD.",name:"Maria Cristina",middleName:null,surname:"Carrillo",fullName:"Maria Cristina Carrillo",slug:"maria-cristina-carrillo"},{id:"142855",title:"Dr.",name:"Maria De Luján",middleName:null,surname:"Alvarez",fullName:"Maria De Luján Alvarez",slug:"maria-de-lujan-alvarez"},{id:"142858",title:"BSc.",name:"Juan Pablo",middleName:null,surname:"Parody",fullName:"Juan Pablo Parody",slug:"juan-pablo-parody"},{id:"142859",title:"Dr.",name:"Ariel Darío",middleName:null,surname:"Quiroga",fullName:"Ariel Darío Quiroga",slug:"ariel-dario-quiroga"},{id:"142861",title:"BSc.",name:"Maria Paula",middleName:null,surname:"Ceballos",fullName:"Maria Paula Ceballos",slug:"maria-paula-ceballos"}]},{id:"38459",title:"Lipid Peroxidation and Antioxidants in Arterial Hypertension",slug:"lipid-peroxidation-and-antioxidants-in-arterial-hypertension",signatures:"Teresa Sousa, Joana Afonso, António Albino-Teixeira and Félix Carvalho",authors:[{id:"131252",title:"Prof.",name:"Félix",middleName:null,surname:"Carvalho",fullName:"Félix Carvalho",slug:"felix-carvalho"},{id:"140800",title:"Prof.",name:"António",middleName:null,surname:"Albino-Teixeira",fullName:"António Albino-Teixeira",slug:"antonio-albino-teixeira"},{id:"142410",title:"Prof.",name:"Teresa",middleName:null,surname:"Sousa",fullName:"Teresa Sousa",slug:"teresa-sousa"},{id:"142411",title:"MSc.",name:"Joana",middleName:null,surname:"Afonso",fullName:"Joana Afonso",slug:"joana-afonso"}]},{id:"38476",title:"Lipid Peroxidation and Reperfusion Injury in Hypertrophied Hearts",slug:"lipid-peroxidation-and-reperfusion-injury-in-hypertrophied-hearts",signatures:"Juliana C. Fantinelli, Ignacio A. Pérez Núñez, Luisa F. González Arbeláez and Susana M. Mosca",authors:[{id:"98613",title:"Dr.",name:"Susana",middleName:null,surname:"Mosca",fullName:"Susana Mosca",slug:"susana-mosca"}]},{id:"38455",title:"Lipid Peroxidation by-Products and the Metabolic Syndrome",slug:"lipid-peroxidation-by-products-and-the-metabolic-syndrome",signatures:"Nicolas J. Pillon and Christophe O. Soulage",authors:[{id:"139163",title:"Dr.",name:"Nicolas",middleName:"Jean",surname:"Pillon",fullName:"Nicolas Pillon",slug:"nicolas-pillon"},{id:"139829",title:"Dr.",name:"Christophe",middleName:null,surname:"Soulage",fullName:"Christophe Soulage",slug:"christophe-soulage"}]},{id:"38475",title:"Region Specific Vulnerability to Lipid Peroxidation in the Human Central Nervous System",slug:"region-specific-vulnerability-to-lipid-peroxidation-in-the-human-central-nervous-system",signatures:"Alba Naudí, Mariona Jové, Victòria Ayala, Omar Ramírez, Rosanna Cabré, Joan Prat, Manuel Portero-Otin, Isidre Ferrer and Reinald Pamplona",authors:[{id:"139955",title:"Prof.",name:"Reinald",middleName:null,surname:"Pamplona",fullName:"Reinald Pamplona",slug:"reinald-pamplona"}]},{id:"38474",title:"Role of Lipid Peroxidation in the Pathogenesis of Age-Related Cataract",slug:"role-of-lipid-peroxidation-in-the-pathogenesis-of-age-related-cataract",signatures:"Bojana Kisic, Dijana Miric, Lepsa Zoric and Aleksandra Ilic",authors:[{id:"139383",title:"Prof.",name:"Bojana",middleName:null,surname:"Kisic",fullName:"Bojana Kisic",slug:"bojana-kisic"},{id:"150937",title:"Prof.",name:"Dijana",middleName:null,surname:"Miric",fullName:"Dijana Miric",slug:"dijana-miric"},{id:"150938",title:"Prof.",name:"Lepsa",middleName:null,surname:"Zoric",fullName:"Lepsa Zoric",slug:"lepsa-zoric"},{id:"150939",title:"Dr.",name:"Aleksandra",middleName:null,surname:"Ilic",fullName:"Aleksandra Ilic",slug:"aleksandra-ilic"}]},{id:"38462",title:"Lipid Peroxidation in Hepatic Fibrosis",slug:"lipid-peroxidation-in-hepatic-fibrosis",signatures:"Ichiro Shimizu, Noriko Shimamoto, Katsumi Saiki, Mai Furujo and Keiko Osawa",authors:[{id:"142420",title:"Dr.",name:"Ichiro",middleName:null,surname:"Shimizu",fullName:"Ichiro Shimizu",slug:"ichiro-shimizu"}]},{id:"38463",title:"Use of CoA Biosynthesis Modulators and Selenoprotein Model Substance in Correction of Brain Ischemic and Reperfusion Injuries",slug:"use-of-coa-biosynthesis-modulators-and-selenoprotein-model-substance-in-correction-of-brain-ischemic",signatures:"Nina P. Kanunnikova, Natalya Z. Bashun and Andrey G. Moiseenok",authors:[{id:"142487",title:"Prof.",name:"Nina",middleName:null,surname:"Kanunnikova",fullName:"Nina Kanunnikova",slug:"nina-kanunnikova"},{id:"142491",title:"Dr.",name:"Natalya",middleName:null,surname:"Bashun",fullName:"Natalya Bashun",slug:"natalya-bashun"},{id:"142503",title:"Prof.",name:"Andrey",middleName:null,surname:"Moiseenok",fullName:"Andrey Moiseenok",slug:"andrey-moiseenok"}]},{id:"38464",title:"Lipid Peroxidation and Polybrominated Diphenyl Ethers – A Toxicological Perspective",slug:"lipid-peroxidation-and-polybrominated-diphenyl-ethers-a-toxicological-perspective",signatures:"Mary C. Vagula and Elisa M. Konieczko",authors:[{id:"141806",title:"Dr.",name:"Mary",middleName:null,surname:"Vagula",fullName:"Mary Vagula",slug:"mary-vagula"},{id:"150947",title:"Prof.",name:"Elisa",middleName:null,surname:"Konieczko",fullName:"Elisa Konieczko",slug:"elisa-konieczko"}]}]}]},onlineFirst:{chapter:{type:"chapter",id:"72508",title:"Strategic Role Players of Important Antimicrobial-Resistant Pathogens",doi:"10.5772/intechopen.92742",slug:"strategic-role-players-of-important-antimicrobial-resistant-pathogens",body:'\nBacterial infections have been threatening human population since time immemorial. Being one of the leading causes of morbidity and mortality (Figure 1), the latest global rise in antibiotic resistance threatens to undo decades of progress in treating such bacterial infectious diseases caused by the pathogens. In fact, multidrug resistance (MDR) conferred by Gram-positive and -negative bacteria is difficult to treat and may even be, untreatable with conventional antibiotics. The case has turned out to be so serious that many of these microorganisms are at least resistant to a single drug regimen while several are moving from developing MDR to extensively and total drug resistance, referred to as XDR and TDR, respectively.
\nRates of infection (left) vs. mortality (right) statistics as per National Center for Health Statistics (CDC), 2017.
All the aforementioned classes of resistance, namely MDR, XDR and TDR, commonly referred to as antimicrobial resistance (AMR), has been conferred the main cause for the second leading global disease burden of bacterial infection in the twenty-first century, as reported by WHO [1]. Importantly, the development of antibiotics has directly influenced the initial resistance caused by using newer agents. Moreover, the discovery of new antibiotic classes is reported to be void since 1987, when lipopeptides was the last class introduced (Figure 2) [2]. Thus, it has become increasingly difficult to find therapeutic options to treat organisms developing AMR, such as
The timeline of the development of different antibiotic classes.
The rise of AMR development has become a serious concern more than what can be even perceived. This is potentiated by different facts ranging from adverse effects of existing antibiotics and consequent re-purposing and/or chemical modification or their withdrawal leading to the sparing usage of new ones due to resistance concerns and ultimately a shortage in the development of new antibiotics [3, 4, 5]. Moreover, environments of hospitals and other health care systems as well as social communities and advanced transport systems have enabled the spread of AMR easier and faster [6]. This is evidenced by a recent increase in the carbapenem resistance (e.g. meropenem) due to the presence of carbapenemase, a.k.a. New Delhi metallo-β-lactamase-1 (NDM-1) in various Enterobacterales isolates [7]. Initially reported to have found in a patient in Sweden in 2008 who had originated from India, such cases were found later in UK patients having either travel or ancestral history from the Indian subcontinent [6]. A variation of no such travel or hospital contacts, for patients harboring NDM-1, was also reported by 2011 [8], along with drinking water and sewage samples containing a range of NDM-1 harboring bacteria (e.g.
Antibiotic vs. vaccine-resistant phenomenon. HGT represents horizontal gene transfer, green and red colored cells denote antibiotic-sensitive and -resistant bacteria, respectively.
AMR is exhibited when a microorganism survives in the presence of an antibiotic concentration that is generally adequate to prevent or stop its growth. Thus, in clinical terms “prone” and “resistant” are generally used to infer the efficacy or failure of medical therapy, respectively [10]. Moreover, the microbes can either be inherently resistant to an antibiotic or develop resistance after their exposure to incorrect and/or insufficient dosage prescription. This is commonly the case for patients routinely communicating with hospital settings thereby having gradually increased resistance to frequently used antibiotics. For these cases of hospital-acquired infections (HAI), certain bacteria develop drug-resistant strains through natural selection mechanism which promotes the persistence of bacterial strains having acquired some mutation [11]. However, the increased profile of these pathogens with AMR varies, even though they arise from similar causes.
\nAMR resistance may evolve as a mechanistic consequence of gene mutation or direct gene transfer, the latter being also known as horizontal gene transfer (HGT). Of these two, HGT helps to acquire new resistance genes and virulence determinants through a multitude of mechanisms including conjugation, transduction or transformation among related and/or non-related species [10]. This phenomenon is commonly associated with bacterial adaptation to new niches or lifestyles and has an impact on the development of its genomic content. Again, HGT, with the help of mobile genetic elements (MGEs) like transposons, has been reported to have conferred resistance to a broad range of antibiotics, particularly toward new ones. Moreover, transmissible plasmids and phages often bear genes that confer antibiotic resistance to one or more distinct antibiotics and facilitate their transfer across different genera. Such evolution essentially underpins the survival of the developing MDR strains and may be a major reason for the global outbreaks.
\nBesides the emerging species of bacteria exhibiting MDR, namely
Human infections due to
The initial AMR acquired by
\n
\n
\n
\n
Tuberculosis (TB) poses serious global health crisis as an important chronic infectious disease caused by strains of
\n
Generally associated with HAI in immunocompromised patients,
\n
Several health interventions have been proposed as alternatives to current antibiotic therapy and prevent the resistant mechanisms of which, the development of new drug classes, use of vaccines or other therapeutic strategies are noteworthy (Figure 4) [59]. In fact, using computational approaches, certain proteins and/or phenotypes, having plausible involvement in antibiotic resistance, are proposed [60, 61, 62, 63, 64] as discussed below.
\nAlternative strategies to combat antimicrobial resistance and their mechanisms of action.
Bacterial chaperones like DnaK, belonging to the heat shock proteins (Hsp)70 family, are produced by cells in response to exposure to stressful conditions [65]. The interaction between the two domains of such Hsp70, namely ATPase and the substrate-binding domain, triggers the chaperone-based activity of DnaK which are also enhanced by the co-chaperone such as DnaJ (Hsp40 family) and chaperone GroE (Hsp60 family) [66]. DnaK acts on unfolded and partially folded protein chains by binding and controlling their configuration [67].
\nBesides stress response, DnaK plays a significant housekeeping role in maintaining normal bacterial cellular growth and homeostasis [68]. Thus, any alterations in the
Antibiotic resistance can be triggered, in MDR bacteria, by four discrete mechanisms viz. target modification, reduced permeability and improved efflux, drug inactivation and drug extrusion by the multidrug efflux pumps (EP) [73]. Due to their poly-substrate specificity, besides having the potential to expel a broad variety of antibiotics, these EP also manage the development of other resistance mechanisms by decreasing intracellular antibiotics concentration and stimulating mutation accumulation [73]. Consequently, over-expression of multidrug EP is involved with clinically related antibiotic resistance. Thus, there has been increasing evidence of EP having biochemical functions in bacteria along with their appearance under strict regulations in response to some physiological and environmental signals [73]. Hence, a systematic knowledge of EP is important for the development of EP inhibitors as promising AMR intervention strategies.
\nEP are present in almost all bacterial species involved in AMR. They can be located on plasmids or chromosomes that encode this class of proteins. The five families of bacterial EP, found to be involved in MDR, are the major facilitator superfamily (MFS), the multidrug and toxic compound extrusion (MATE) family, the ATP-binding cassette (ABC) superfamily, the small multidrug resistance (SMR) family, and the resistance-nodulation-division (RND) family, based on their composition, energy sources and substrates used [73]. Importantly, only RND superfamily is found in Gram-negative bacteria due to its structure containing tripartite complex and the efflux systems of the other four families are widely distributed in both Gram-positive and -negative bacteria. These EP can be either single or multiple-component transporters depending on their specific classes. They comprise both an inner and an outer membrane transporter, like the RND type. It has been found that RND family pumps are frequently associated with therapeutically important bacterial resistance such as AcrB in
In fact, antibiotics such as fluoroquinolone, tetracycline, rifampin, novobiocin, chloramphenicol and B-lactams were used to analyze the substrate profile of housekeeping efflux system AcrAB-TolC in
Efflux pump | \nPump type | \nRegulator | \nRegulator family | \nInducible signal | \n
---|---|---|---|---|
AdeABC | \nRND | \nAdeRS | \nTCS | \n∼ | \n
MexXY | \nRND | \nMexZ | \nTetR | \nTetracycline, erythromycin, gentamicin | \n
MexAB | \nRND | \nMexR | \nMarR | \nSuperoxide stress | \n
\n | \n | NalD | \nTetR | \n∼ | \n
MexCD | \nRND | \nNfxB | \nLacI/GalR | \nBiocide chlorhexidine | \n
MexEF | \nRND | \nMetT | \nLysR | \nChloramphenicol, GSNO | \n
AcrAB | \nRND | \nMarA | \nAraC | \n∼ | \n
\n | \n | RamA | \nAraC | \nIndole, bile salts | \n
\n | \n | RamR | \nTetR | \n∼ | \n
\n | \n | SoxS | \nAraC | \n∼ | \n
\n | \n | AcrR | \nTetR | \n∼ | \n
AcrD | \nRND | \nBaeSR | \nTCS | \nIndole, zinc, copper | \n
\n | \n | CpxAR | \nTCS | \nIndole, zinc, copper | \n
AcrEF | \nRND | \nAcrS | \nTetR | \n∼ | \n
MdtABC | \nRND | \nBaeSR | \nTCS | \nIndole, zinc, copper | \n
\n | \n | CpxAR | \nTCS | \nIndole, zinc, copper | \n
MacAB | \nABC | \nPhoQP | \nTCS | \nMagnesium | \n
MdsABC | \nRND | \nGolS | \nMerR | \nGold | \n
MepA | \nMFS | \nQacR | \nTetR | \nRhodamine 6G, TPP | \n
QacA | \nMATE | \nMepR | \n\n | Chlorhexidine, cetrimide, dequalinium | \n
Two component systems (TCS) are commonly found in bacteria, allowing them to respond to various fluctuations in the environment. Canonically, TCS are composed of a response regulator (RR) and a histidine kinase (HK) [78]. The membrane associated HKs can detect and transform various environmental sensations by autophosphorylation. The HKs can then transphosphorylate their cognate partners, the RRs, which then influence the expression of downstream genes to affect the concerned phenotype [78].
\nA thorough investigation of the correlation between efflux pumps and TCSs in
Again, PhoPQ TCS, the core virulence regulator in
Bacteria | \nInhibitors | \nTCS | \nMechanisms | \nReference | \n
---|---|---|---|---|
\n | \nXR770 | \nBaeSR OmpR/ EnvZ | \nInhibition of key interacting residues of DHp domain of HK | \n[89] | \n
\n | NSC9608 (8 compounds, NCI library) | \nPhoP-Q | \nInhibition of formation of the PhoP-DNA complex | \n[90] | \n
\n | \nThiazole derivatives | \nAlgr1-2 | \nInhibition of phosphorylation/dephosphorylation of Algr2 Inhibition of DNA-binding activity of Algr1 | \n[90] | \n
\n | \nThiazole derivatives | \nVanR-S | \nInhibition of autophosphorylation | \n[90] | \n
\n | \nWalkmycin B and Waldiomycin | \nWalK-R | \nBinds to the HK cytoplasmic domain for the inhibition of autophosphorylation | \n[90] | \n
Salicylanilide | \nKinA/Spo0F | \nAffects membrane fluidity, disturbing signal transduction | \n[90] | \n|
\n | \nBis-phenol | \nVanR-S | \n— | \n[90] | \n
Representative TCS targets with their known inhibitors.
TCS can play an important role in drug discovery. There are several ways to target TCS proteins. Of these, the structure-based virtual screening (SBVS) analysis is carried out using compound databases containing a broad range of prospective inhibitors, including structures known to be antibacterial [93].
\nBiofilms, in both single and multi-species groups, communicate and cooperate to perform complex processes with each other and their environment [94]. With the scientists aiming to understand the intercellular interactions that encourage the development of biofilms, they are presently a serious health issue, playing a major role in abiotic device-related diseases such as catheters, prosthetic valves and contact lenses [95].
\nBiofilm formation can be explored in different stages comprising (a) distinctive adhesion of the planktonic bacteria (PB) to a solid surface [96], (b) micro-colonies (MC) formation surrounded by protective secreted molecules known as the matrix of extra polymeric substances (EPS) having up to 97% water as the main component [97] and (c) dispersal including shedding of PB or MC from the mature biofilm [97]. The last phase can encourage further biofilm colonization of the host which can eventually benefit the bacteria with a limited supply of nutrients and waste accumulation [97]. Importantly, the transition from planktonic growth to surface life is triggered by several environmental signals known as various stresses for the bacteria based on their ecological niche [98]. These include UV radiation, pH changes, oxygen tension, osmolarity, iron availability, temperature, nutrient supply and desiccation [98], which may disrupt their fundamental functions such as growth and survival capability. The environmental indications, however, vary significantly between organisms. Thus,
Recent advances in biofilm research have proven its connection to various pathways and proteins [61]. For instance, defects in MDR EP activity reduced the biofilm formation and thus, EP inhibitors have been employed as a promising biofilm inhibition approach for strains of
The constant increase in AMR is a significant public health concern that needs to be addressed now. This review starts with an introduction to AMR followed by the threats from the clinically important MDR pathogens and their rise. With the existing management strategies for MDR by the scientists still ongoing, we have taken up this study to propose an integrated approach to deal with MDR threats. Thus, the review ends with new connections of important bacterial components with MDR.
\nThe authors acknowledge the support of Sunway University, Selangor, Malaysia for providing the computational facilities and wishes to thank Hend Salah for the valuable contribution in developing the artwork for the concept provided.
\nThe authors declare no conflict of interest.
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