Bacteria antibiotic resistance

Cloning procedure (in bacteria) Recombinant plasmids transfected into bacteria Antibiotic resistance used to select bacteria with recombinant plasmids Blot growth plate and probe with P-DNA for gene, or with Tantibody for protein... 

Alkaliphilic bacteria Antibiotic resistance Antimicrobial compounds... 

Tolypomycin Y (48) shows strong antibacterial activity against gram-positive bacteria and Neisseriagonorrheae. When adininistered by subcutaneous, intraperitoneal, and intravenous routes, tolypomycin Y is effective in mice infected with Staphylococcus aureus Streptococcuspyrogenes and Diplococcuspneumoniae. Cross-resistance is observed with rifampicia but not with other antibiotics. Resistance to tolypomycin Y develops rapidly. The bioactivity of tolypomycin R... 

Bacteria produce chromosomady and R-plasmid (resistance factor) mediated P-lactamases. The plasmid-mediated enzymes can cross interspecific and intergeneric boundaries. This transfer of resistance via plasmid transfer between strains and even species has enhanced the problems of P-lactam antibiotic resistance. Many species previously controded by P-lactam antibiotics are now resistant. The chromosomal P-lactamases are species specific, but can be broadly classified by substrate profile, sensitivity to inhibitors, analytical isoelectric focusing, immunological studies, and molecular weight deterrnination. Individual enzymes may inactivate primarily penicillins, cephalosporins, or both, and the substrate specificity predeterrnines the antibiotic resistance of the producing strain. Some P-lactamases are produced only in the presence of the P-lactam antibiotic (inducible) and others are produced continuously (constitutive). 

One approach to combating antibiotic resistance caused by P-lactamase is to inhibit the enzyme (see Enzyme inhibition). Effective combinations of enzyme inhibitors with P-lactam antibiotics such as penicillins or cephalosporins, result in a synergistic response, lowering the minimal inhibitory concentration (MIC) by a factor of four or more for each component. However, inhibition of P-lactamases alone is not sufficient. Pharmacokinetics, stability, ability to penetrate bacteria, cost, and other factors are also important in determining whether an inhibitor is suitable for therapeutic use. Almost any class of P-lactam is capable of producing P-lactamase inhibitors. Several reviews have been pubUshed on P-lactamase inhibitors, detection, and properties (8—15). 

For many years, it was thought that binary fission was the only method of reproduction in bacteria, but it is now known that there are three methods of reproduction in which genetic exchange can occur between pairs of cells, and thus a form of sexual reproduction is exhibited. These processes are transformation, conjugation and transduction. Further details ofthese processes as they affect antibiotic resistance will be found in Chapter 9. 

Bacterial resistance to antibiotics has been recognized since the first drugs were introduced for clinical use. The sulphonamides were introduced in 1935 and approximately 10 years later 20% of clinical isolates of Neisseria gonorrhoeae had become resistant. Similar increases in sulphonamide resistance were found in streptococci, coliforms and other bacteria. Penicillin was first used in 1941, when less than 1 % of Staphylococcus aureus strains were resistant to its action. By 1947,3 8% of hospital strains had acquired resistance and currently over 90% of Staph, aureus isolates are resistant to penicillin. Increasing resistance to antibiotics is a consequence of selective pressure, but the actual incidence of resistance varies between different bacterial species. For example, ampicillin resistance inEscherichia coli, presumably under similar selective pressure as Staph, aureus with penicillin, has remained at a level of 30-40% for mai years with a slow rate of increase. Streptococcus pyogenes, another major pathogen, has remained susceptible to penicillin since its introduction, with no reports of resistance in the scientific literature. Equally, it is well recognized that certain bacteria are unaffected by specific antibiotics. In other words, these bacteria have always been antibiotic-resistant. 

Acquired resistance. This occurs when bacteria which were previously susceptible become resistant, usually, but not always, after exposure to the antibiotic concerned. Intrirrsic resistance is always chromosomally mediated, whereas acquired resistance may occirr by mutations in the chromosome or by the acquisition of genes coding for resistance ftom an external source normally via a plasmid or transposon. Both types are clinically important and can result in treatment failure, although acquired resistance is more of a threat in the spread of antibiotic resistance (Russell Chopra 1996). 

Plasmids have the ability to transfer within and between species and can therefore be acquired from other bacteria as well as a consequence of cell division. This property makes plasmid-acquired resistance much more threatening in terms ofthe spread of antibiotic resistance than resistance acquired due to chromosomal mutation. Plasmids also harbour transposons (section 2.1.3), which enhances their ability to transfer antibiotic resistance genes. 

Unless risk factors for infection owing to potentially antibiotic-resistant bacteria ° Late-onset hospital-acquired pneumonia... 

From the foregoing, it seems likely that apart from a small number of specialist medical applications, the efficacy of surface coated devices may be compromised by antibiotic-resistant bacteria, together with the barrier effect provided by conditioning films that will rapidly coat biomaterials in situ.43... 

Wireman, J., Liebert, C., Smith, T., and Summers, A., Association of mercury resistance with antibiotic resistance in the gram-negative fecal bacteria of primates, Appl Environ Microbiol, 63 (11), 4494-4503, 1997. 

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