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1.
Mechanisms of bacterial biocide and antibiotic resistance 总被引:2,自引:0,他引:2
K. Poole 《Journal of applied microbiology》2002,92(S1):55S-64S
2.
McBain AJ Rickard AH Gilbert P 《Journal of industrial microbiology & biotechnology》2002,29(6):326-330
The lethality of biocides depends upon their interaction with a number of distinct biochemical targets. This often reflects
reactive chemistry for any given agent, such as thiol oxidation. Susceptibility may vary markedly between different target
organisms, and changes within the more sensitive targets can alter the inhibitory effect. The multiplicity of potential targets,
however, usually dictates against the development of overt resistance to concentrations used for hygienic applications. Similarly,
although changes in cellular permeability toward such agents, mediated either by envelope modification or the induction of
efflux-pumps may reduce susceptibility, they rarely influence the outcome of treatments at use-concentration. It has recently
been proposed that chronic exposure of the environment to biocides used in a variety of commercial products might expose some
microbial communities to subeffective concentrations causing emergence of resistant clones. Such resistance might relate to
mutational changes in the most susceptible target or to regulatory mutants that cause the constitutive expression of certain
efflux pumps. Although selection of organisms with such modifications is unlikely to influence the effectiveness of the biocides,
changes in their susceptibility to third-party antibiotics can be postulated. This is particularly the case where a cellular
target is shared between a biocide and an antibiotic, or where induction of efflux is sufficient to confer antibiotic resistance
in the clinic. Although such linkage has been demonstrated in the laboratory in pure culture, it has not been documented in
environments commonly exposed to biocides. In nature, the effects of chronic stressing with biocides are complicated by competition
between microbial community members that may result in clonal expansion of naturally insusceptible clones.
Received 11 March 2002/ Accepted in revised form 16 August 2002 相似文献
3.
S.B. Levy 《Journal of applied microbiology》2002,92(S1):65S-71S
4.
Levy SB 《Symposium series (Society for Applied Microbiology)》2002,(31):65S-71S
Energy-driven drug efflux systems are increasingly recognized as mechanisms of antibiotic resistance. Chromosomally located or acquired by bacteria, they can either be activated by environmental signals or by a mutation in a regulatory gene. Two major categories exist: those systems energized by proton motive force and those dependent on ATP. The pumps may have limited or broad substrates, the so-called multiple drug resistance pumps, which themselves form a number of related families. The multiple antibiotic resistance (mar) locus and mar regulon in Escherichia coli and other members of the Enterobacteriaceae is a paradigm for a generalized response locus leading to increased expression of efflux pumps. One such pump, the AcrAB pump extrudes biocides such as triclosan, chlorhexidine and quaternary ammonium compounds as well as multiple antibiotics. In Pseudomonas aeruginosa, a number of multidrug efflux pumps export a broad range of substrates. Since bacteria expressing these pumps thwart the efficacy of both kinds of therapeutic agents which control infectious diseases--biocides which prevent transmission of infectious disease agents and antibiotics which treat and cure infectious diseases--they are of particular concern. The prudent use of antibiotics and biocides will guard against the selection and propagation of drug-resistant mutants and preserve the efficacy of these valuable anti-infective agents. 相似文献
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Progress in DNA technology, analytical methods and computational tools is leading to new developments in synthetic biology and metabolic engineering, enabling new ways to produce molecules of industrial and therapeutic interest. Here, we review recent progress in both antibiotic production and strategies to counteract bacterial resistance to antibiotics. Advances in sequencing and cloning are increasingly enabling the characterization of antibiotic biosynthesis pathways, and new systematic methods for de novo biosynthetic pathway prediction are allowing the exploration of the metabolic chemical space beyond metabolic engineering. Moreover, we survey the computer-assisted design of modular assembly lines in polyketide synthases and non-ribosomal peptide synthases for the development of tailor-made antibiotics. Nowadays, production of novel antibiotic can be tranferred into any chosen chassis by optimizing a host factory through specific strain modifications. These advances in metabolic engineering and synthetic biology are leading to novel strategies for engineering antimicrobial agents with desired specificities. 相似文献
7.
Mechanisms of antibiotic resistance in Staphylococcus aureus 总被引:1,自引:0,他引:1
8.
《International Biodeterioration》1990,26(2-4):101-110
Bacterial resistance to biocides is basically of two types: (i) intrinsic, a natural chromosomally-controlled property of an organism, (ii) acquired, resulting from genetic changes in a cell and arising either by mutation or by the acquisition of genetic material. Both types of resistance are discussed together with the underlying biochemical mechanisms where known. Specific examples of organisms are provided by reference to bacterial spores, mycobacteria, other Gram-positive bacteria and Gram-negative bacteria. The stability of resistance to biocides is considered, as is the possible linkage between biocide and antibiotic resistance. 相似文献
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Unfortunately for mankind, it is very likely that the antibiotic resistance problem we have generated during the last 60 years due to the extensive use and misuse of antibiotics is here to stay for the foreseeable future. This view is based on theoretical arguments, mathematical modeling, experiments and clinical interventions, suggesting that even if we could reduce antibiotic use, resistant clones would remain persistent and only slowly (if at all) be outcompeted by their susceptible relatives. In this review, we discuss the multitude of mechanisms and processes that are involved in causing the persistence of chromosomal and plasmid-borne resistance determinants and how we might use them to our advantage to increase the likelihood of reversing the problem. Of particular interest is the recent demonstration that a very low antibiotic concentration can be enriching for resistant bacteria and the implication that antibiotic release into the environment could contribute to the selection for resistance. Several mechanisms are contributing to the stability of antibiotic resistance in bacterial populations and even if antibiotic use is reduced it is likely that most resistance mechanisms will persist for considerable times. 相似文献
11.
Multiple drug resistance can form in bacteria by functioning the membrane transport systems, responsible for release of antibacterial compounds from the cell into the environment. These transport mechanisms activated in the majority of cases by energy of proton transmembrane gradient are presented by solitary membrane transporting proteins and by functionally related transporter groups, periplasma proteins, and external membrane porines. Many bacterial drug transporters can bind and transfer a number of structurally heterogeneous substrates. Drug transporters known today have different origin and primary physiological functions. The genetic system of transporter type drug resistance is as a rule characterized by a cluster structure and related to mobile genetic elements. Transport mechanisms of drug resistance create an extra adaptation potential of microorganisms under conditions of selective pressure. 相似文献
12.
Streptococcus pneumoniae is a major pathogen causing potentially life-threatening community-acquired diseases in both the developed and developing world. Since 1967, there has been a dramatic increase in the incidence of penicillin-resistant and multiply antibiotic-resistant pneumococci worldwide. Prevention of access of the antibiotic to the target, inactivation of the antibiotic and alteration of the target are mechanisms that S. pneumoniae has developed to resist antibiotics. Recent studies on antibiotic-tolerant pneumococcal mutants permitted development of a novel model for the control of bacterial cell death. 相似文献
13.
Gunn JS 《Microbes and infection / Institut Pasteur》2000,2(8):907-913
Enteric bacteria are resistant to the bactericidal effects of intestinal bile, but these resistance mechanisms are not completely understood. It is becoming increasingly apparent that enteric bacteria have evolved to utilize bile as a signal for the temporal production of virulence factors and other adaptive mechanisms. A greater understanding of the resistance and response of bacteria to bile may assist the development of novel therapeutic, prevention, and diagnostic strategies to treat enteric and extraintestinal infections. 相似文献
14.
Unowsky, Joel (Northwestern University Medical School, Chicago, Ill.), and Martin Rachmeler. Mechanisms of antibiotic resistance determined by resistance-transfer factors. J. Bacteriol. 92:358-365. 1966.-This study was concerned with the mechanism of expression of drug resistance carried by resistance-transfer (R) factors of two types: fi(-) (negative fertility inhibition) and fi(+) (positive fertility inhibition). The levels of drug resistance determined by R factors used in this study were similar to those reported by other investigators. A new finding was that Escherichia coli carrying the fi(-) episome was resistant to 150 to 200 mug/ml of streptomycin. The growth kinetics of R factor-containing cells were similar in the presence or absence of streptomycin, chloramphenicol, and tetracycline, but a period of adaptation was necessary before cells began exponential growth in the presence of tetracycline. By use of radioactive antibiotics, it was shown that cells containing the fi(-) episome were impermeable to tetracycline and streptomycin, whereas cells containing the fi(+) episome were impermeable only to chloramphenicol. Cell-free extracts from fi(+) and fi(-) cells were sensitive to the antibiotics tested in the polyuridylic acid-stimulated incorporation of phenylalanine into protein. 相似文献
15.
持留菌是细菌群体中一小部分具有表型耐药的细菌。自1944年被发现后,近几十年来因其在慢性持续性感染和生物膜感染中的重要作用而得到越来越多的重视。已有的研究结果表明,细菌持留的机理复杂,涉及的相关信号通路有毒素-抗毒素系统、细胞能量代谢及蛋白核酸合成等生理状态的降低、DNA保护修复系统、蛋白酶系统、反式翻译、外排泵系统等。虽然不同细菌的持留机理有一定的相似性和保守性,但不同细菌的持留机制也存在差异,如毒素-抗毒素系统在大肠埃希菌(Escherichia coli)中的过度激活可导致持留菌增加,但在金黄色葡萄球菌(Staphylococcus aureus)中却并无相同作用。本文从持留菌的研究历史出发,综述了当前对革兰氏阴性菌和阳性菌的持留机制方面的研究进展,同时探讨了在持留菌相关感染疾病方面的治疗策略,以期为更好地解决持留菌带来的问题,缩短治疗时间提供新的思路。 相似文献
16.
Mechanisms of bacterial resistance to chromium compounds 总被引:1,自引:0,他引:1
Martha I. Ramírez-Díaz César Díaz-Pérez Eréndira Vargas Héctor Riveros-Rosas Jesús Campos-García Carlos Cervantes 《Biometals》2008,21(3):321-332
Chromium is a non-essential and well-known toxic metal for microorganisms and plants. The widespread industrial use of this
heavy metal has caused it to be considered as a serious environmental pollutant. Chromium exists in nature as two main species,
the trivalent form, Cr(III), which is relatively innocuous, and the hexavalent form, Cr(VI), considered a more toxic species.
At the intracellular level, however, Cr(III) seems to be responsible for most toxic effects of chromium. Cr(VI) is usually
present as the oxyanion chromate. Inhibition of sulfate membrane transport and oxidative damage to biomolecules are associated
with the toxic effects of chromate in bacteria. Several bacterial mechanisms of resistance to chromate have been reported.
The best characterized mechanisms comprise efflux of chromate ions from the cell cytoplasm and reduction of Cr(VI) to Cr(III).
Chromate efflux by the ChrA transporter has been established in Pseudomonas aeruginosa and Cupriavidus
metallidurans (formerly Alcaligenes eutrophus) and consists of an energy-dependent process driven by the membrane potential. The CHR protein family, which includes putative
ChrA orthologs, currently contains about 135 sequences from all three domains of life. Chromate reduction is carried out by
chromate reductases from diverse bacterial species generating Cr(III) that may be detoxified by other mechanisms. Most characterized
enzymes belong to the widespread NAD(P)H-dependent flavoprotein family of reductases. Several examples of bacterial systems
protecting from the oxidative stress caused by chromate have been described. Other mechanisms of bacterial resistance to chromate
involve the expression of components of the machinery for repair of DNA damage, and systems related to the homeostasis of
iron and sulfur. 相似文献
17.
K Brønstad K Drønen L Øvreås V Torsvik 《Journal of industrial microbiology & biotechnology》1996,17(3-4):253-259
The community structure in two different agricultural soils has been investigated. Phenotypic diversity was assessed by applying BIOLOG-profiles on a total of 208 bacterial isolates. Diversity indices were calculated from cluster analysis of the BIOLOG data. The bacterial isolates were also evaluated for resistance towards six different antibiotics, mercury resistance and the presence of plasmids. The presence of tetracycline-resistant determinants class A to E among Gram-negative bacteria was analysed with DNA probes. The distribution of tetracycline resistance markers among colonies growing on non-selective and tetracycline-selective plates were compared. The phenotypic approach demonstrated some difference in the diversity within the two soils. The frequency of antibiotic resistance isolates was high in both soils, whereas the frequency of mercury resistance differed significantly. We found no correlation between plasmid profiles and antibiotic resistance patterns. We found all the tetracycline resistance determinants except class B, indicating that the diversity of the tetracycline resistance determinants was complex in populations of resident soil bacteria under no apparent selective pressure for the genes in question. 相似文献
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de Figueiredo P Terra B Anand JK Hikita T Sadilek M Monks DE Lenskiy A Hakomori S Nester EW 《Extremophiles : life under extreme conditions》2007,11(1):133-143
Penicillins are widespread in nature and lethal to growing bacteria. Because of the severe threat posed by these antibiotics,
bacteria have evolved a wide variety of strategies for combating them. Here, we describe one unusual strategy that involves
the activity of a catalytic carbohydrate. We show that the cyclic oligosaccharide, β-cyclodextrin (βCD), can hydrolyze, and
thereby inactivate, penicillin in vivo. Moreover, we demonstrate that this catalytic activity contributes to the antibiotic
resistance of a bacterium that synthesizes this oligosaccharide in the laboratory. Taken together, these data not only expand
our understanding of the biochemistry of penicillin resistance, but also provide the first demonstration of natural carbohydrate-mediated
catalysis in a living system.
Paul de Figueiredo, Becky Terra and Jasbir Kaur Anand have contributed equally to this work. 相似文献
20.
Antibiotic treatment by humans generates strong viability selection for antibiotic-resistant bacterial strains. The frequency of host antibiotic use often determines the strength of this selection, and changing patterns of antibiotic use can generate many types of behaviors in the population dynamics of resistant and sensitive bacterial populations. In this paper, we present a simple model of hosts dimorphic for their tendency to use/avoid antibiotics and bacterial pathogens dimorphic in their resistance/sensitivity to antibiotic treatment. When a constant fraction of hosts uses antibiotics, the two bacterial strain populations can coexist unless host use-frequency is above a critical value; this critical value is derived as the ratio of the fitness cost of resistance to the fitness cost of undergoing treatment. When strain frequencies can affect host behavior, the dynamics may be analyzed in the light of niche construction. We consider three models underlying changing host behavior: conformism, the avoidance of long infections, and adherence to the advice of public health officials. In the latter two, we find that the pathogen can have quite a strong effect on host behavior. In particular, if antibiotic use is discouraged when resistance levels are high, we observe a classic niche-construction phenomenon of maintaining strain polymorphism even in parameter regions where it would not be expected. 相似文献