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Resistance in bacteria

Li X-Z, Nikaido H (2004) Efflux-mediated drug resistance in bacteria. Drugs 64 159-204... [Pg.106]

Russell A.D. Day M.J. (1996) Antibiotic and biocide resistance in bacteria. Microbios, 85, 45-65. Russell A.D. Furr J.R. (1996) Biocides mechanisms of antifimgal action and tluigal resistance. Sci... [Pg.277]

Biochemical tests are usually performed after pure cultures have been obtained. The standard indole, methyl red, Voges-Proskauer, citrate, and litmus milk tests may be used to show important physiological characteristics. To study the functional diversity of bacteria, the utilization of carbohydrates, amines, amides, carboxylic acids, amino acids, polymers, and other carbon and nitrogen sources can be tested.28 Dilution-based most-probable number (MPN) techniques with phospholipid fatty acids as biomarkers have been employed for studying different bacterial species in lakes.40 The patterns of antibiotic resistance in bacteria isolated from natural waters have been useful for identifying sources of water pollution.34... [Pg.5]

NRDC also noted that the frequency of antibiotic resistance In bacteria that cause disease Increases when animals are fed subtherapeutlc levels of these drugs. Thus, when animals become 111 with one of these resistant organisms, treatment with therapeutic levels of the antibiotic of choice may not be effective. [Pg.109]

Aminoglycoside efflux is a significant mechanism of aminoglycoside resistance in bacteria of the genera Pseudomonas, Burkholderia, and Stenotrophomonas. There are five classes of transmembrane efflux systems associated with antibiotic resistance however, the resistance nodulation division (RND) family is the predominant class (Table 3.1). ... [Pg.124]

Antibiotic resistance in bacteria is not a fixed property, and the degree of resistance detectable in the laboratory probably bears litde relationship to the resistance of the organism when growing in the intestinal tract of animals. The types of resistance that bacteria may develop to the action of antibiotics involve two distinct mechanisms mutation and inheritance. The former mechanism affects DNA sequence and results in the synthesis of a protein or macromolecule by the bacterial chromosome that differs from the original chemical entity, with the ability to interfere with the antibiotic activity. Because an antibiotic hinders a bacterium only after it has entered or crossed the cell wall and has bound to a target site, resistance can develop directly if the mutation has so altered the characteristics of the protein or macromolecule that the cell wall, receptor site, or transport mechanism is no longer friendly to the antibiotic. [Pg.257]

Inherited resistance in bacteria is accepted as the most important type from the standpoint of the community and the environment. Studies of isolated microorganisms of animal and human origin have demonstrated that plasmids from both sorts of isolates were practically identical. In terms of the dissemination of resistance determinants of R-plasmids, one must regard the problem as involving both humans and animals as vectors. Presence of a large reservoir of antibiotic-resistant organisms in animals has been demonstrated in the United States. [Pg.259]

Rani, D. B. R. Mahadevan, A. (1989). Plasmid-encoded metal resistance in bacteria. Journal of Scientific Industrial Research, 48, 338-45. [Pg.338]

Chopra, I. 1998. Overexpression of target genes as a mechanism of antibiotic resistance in bacteria. J. Antimicrob. Chemother. 41, 584—588. [Pg.138]

Antibiotic resistance in bacteria is likely a result of horizontal gene transfer, and also of nnhnked point mutations in the pathogen s genome, at a rate of abont 1 in 10 per chromosomal replication. [Pg.309]

Clavulanic acid (Figure 20.2) is a 8-lactamase inhibitor used to overcome resistance in bacteria that secrete /3-lactamase. It is usually combined with amoxicillin (Figure 20.2). [Pg.311]

Li XZ, Nikaido H. Efflux-mediated drug resistance in bacteria. [Pg.101]

Resistance—In bacteria, the acquisition of genetic mutations that render the bacteria invulnerable to the action of antibiotics. [Pg.107]

Lubelski, J., Konings, W.N., and Driessen, A.J. (2007) Distribution and physiology of ABC-type transporters contributing to multidrug resistance in bacteria. Microbiology and Molecular Biology Reviews, 71 (3), 463—476. [Pg.148]

Lomovskaya, O. and Watkins, W. (2001) Inhibition of efflux pumps as a novel approach to combat drug resistance in bacteria. Journal of Molecular Microbiology and Biotechnology, 3 (2), 225—236. [Pg.153]

Area, P, Rico, M., Brana, A.E, Villar, C.J., Hardisson, C., and Suarez, J.E., Formation of an adduct between fosfomycin and glutathione. A new mechanism of antibiotic resistance in bacteria, Antimicrob. Agents Chemother, 32, 1552, 1988. [Pg.195]

PJL Daniels. Aminoglycoside Antibiotics, Drug Action and Drug Resistance in Bacteria, vol. 2. Baltimore University Park Press, 1975, pp 77-111. [Pg.348]

Crowder MW, Spencer J, Vila AJ (2006) Metallo-beta-lactamases novel weaponry for antibiotic resistance in bacteria. Acc Chem Res 39 721-728... [Pg.150]

E. coli, Shig. sonnei, and Shig. Jlexneri to panfuran hydrochloride decreased by 500, 400 and 15 times respectively. The results of numerous studies demonstrate that the development of nitrofuran resistance in bacteria represents the survival and multiplication of a few inherently resistant organisms rather than an induced change in all individuals. The evidence indicates also that cell permeability might be one of the reasons but not the only factor in nitrofuran resistance. [Pg.345]


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