Plasmids drug resistance

Careful empirical selection of the expression platform for carotenogenesis has included selection of the best strains for stability and degree of accumulation and the selection of compatible drug-resistance combinations and low copy number polycistronic plasmids to enhance product accumulation by decrease of metabolic burden." 5 Matthews and Wurtzel discussed culture and induction conditions - that have been explored in most studies. Most efforts to engineer carotenoid biosynthesis in E. coli focused on the genes and enzymes of the pathway and had a modest effect on improved accumulation. For example, substitution and over-expression of a GGPPS that uses IPP directly (discussed in... 

Development of resistance to rifaximin is primarily due to a chromosomal one-step alteration in the drug target, DNA-dependent RNA polymerase. This differs from the plasmid-mediated resistance commonly acquired by bacteria to aminoglycoside antibiotics such as neomycin... 

Analogues of the umuDC genes can be found in locations other than the bacterial chromosome, for example, plasmid pKMIOl (Walker and Dobson, 1979), a derivative of the drug resistance plasmid R46 (Mortelmans and Stocker, 1979), which carried mucAB genes (Shanabruch and Walker, 1980) (see pp. 879-880). 

Schluter A, Szczepanowsld R, Puhler A et al (2007) Genomics of IncP-1 antibiotic resistance plasmids isolated from waste water treatment plants provides evidence for a widely accessible drug resistance gene pool. KEMS Microbiol Rev 31(4) 449-477... 

E Coli strains bearing R-plasmids can be transferred from animal to man. Under the proper circumstances, organisms of animal origin can colonize in the human gut. However, colonization is not considered necessary for transfer of drug resistance to strains that inhabit the human gut. 

Use of penicillin and the tetracyclines also causes selection for pathogenicity factors, that is, disease-causing factors. These factors and drug resistance have been shown to be linked on the same plasmid. Pathogenicity and antibiotic resistance can therefore be transferred simultaneously to other organisms. 

R-plasmids can be transferred from normally nonpathogenic E. coli to certain pathogenic strains of bacteria with which they may come in contact in man or animals. Since R-plasmids carry drug resistance, this transfer can result in the creation of pathogenic strains of bacteria which are resistant to antibiotic therapy. 

B. Overproduction (A) of PABA is one of the resistance mechanisms of sulfonamides. Changes in the synthesis of DNA gyrases (B) is a well-described mechanism for quinolone resistance. Plasmid-mediated resistance (C) does not occur with quinolones. An active efflux system for transport of drug out of the cell has been described for quinolone resistance, but it is not plasmid mediated. Inhibition of structural blocks (D) in bacterial cell wall synthesis is a basic mechanism of action of p-lactam antibiotics. Inhibition of folic acid synthesis (E) by blocking different steps is the basic mechanism of action of sulfonamides. 

Foster, T.J. (1983). Plasmid-determined resistance to antimicrobial drugs and toxic metal ions in bacteria. Microbiological Reviews, 47, 361-409-... 

Plasmids carry a variety of genes which are often useful to bacteria. Some proteins encoded by plasmid genes confer drug resistance to a bacterium. Some are antibiotics. For example, a protein encoded by a gene in plasmid ColEl is toxic to other strains of E. coli. Some plasmids carry genes for enzymes needed for the oxidation of hydrocarbons. Some plasmids contain... 

Plasma amine oxidase 886 Plasma antithrombin III 177 Plasma membrane 12, 379 Plasmalemma. See Plasma membrane Plasmalogens 383s, 384 Plasmids 5, 248249 ColEl 248 drug resistance 248 Plasmin 634 Plasminogen 634 Plasmodesmata 10... 

DNA transfer of drug resistance Of particular clinical concern is resistance acquired due to DNA transfer from one organism to another. Resistance properties are usually encoded in extrachro-mosomal R factors (plasmids). These may enter cells by processes such as transduction (phage-mediated), transformation or, most importantly, bacterial conjugation. 

Plasmid-mediated resistance to sulphonamides results from the duplication of dihydropteroate synthetase (DHPS). The normal DHPS remains sensitive but the plasmid-encoded DHPS, two types (I and II) of which have been found in Gram-negative bacteria, binds considerably less of these drugs [203]. 

Exposure to antibiotics does not, in itself, cause bacteria to become drug resistant. Changes in bacteria that fecilitate resistance occur naturally as a result of mutation (i.e., change in the chromosomal DNA) or as a result of the bacteria receiving extrachromosomal DNA in the form of a plasmid from other bacteria. Exposure to an antibiotic simply selects for strains of the organism that have become resistant through these natural processes. Misuse of antibiotics (e.g., prescribing them for nonbacte-rial infections) increases the rate at which this selection occurs. 

The solid nutrient medium in the petri dish contains the antibacterial drug ampiciliin This drug kills . coli however, the cells that harbor the plasmid readily grow in the presence of the drug because part of the plasmid contains a gene that codes for a drug resistance factor. A bacterium that has accepted a plasmid is said to have acquired ampidllin resistance. 

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