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Antibiotics, bacterial resistance

Raman spectra, 6,652 kinetic studies, 6,699 Rhus vemicifera spectra, 6,652 type 2-depleted, 6,699 (3-Lactam antibiotics bacterial resistance, 6,462 (3-Lactamases zinc, 6, 612 Lactams hydrolysis... [Pg.154]

The mechanisms of resistance to biocides are relatively poorly understood in comparison with antibiotics. Bacterial resistance to antibiotics is normally considered to be of two types (a) intrinsic (innate, natural), a natural property of the organism, or (b) acquired, either by chromosomal mutation or by the acquisition of extraneous DNA, usually acquired as plasmids or transposons [53, 236, 237]. [Pg.176]

Resistance to antimicrobial agents is of concern as it is well known that bacterial resistance to antibiotics can develop. Many bacteria already derive some nonspecific resistance to biocides through morphological features such as thek cell wall. Bacterial populations present as part of a biofilm have achieved additional resistance owkig to the more complex and thicker nature of the biofilm. A system contaminated with a biofilm population can requke several orders of magnitude more chlorine to achieve control than unassociated bacteria of the same species. A second type of resistance is attributed to chemical deactivation of the biocide. This deactivation resistance to the strong oxidising biocides probably will not occur (27). [Pg.97]

Antibacterial Agents. There is a continuous need for new antibiotics primarily as a result of bacterial resistance. There are two aspects to this phenomenon. Fkst, as the mote common pathogens are contioUed by antibiotics, less common, highly resistant organisms present mote prominent health... [Pg.475]

Resistance to Tetracyclines. The tetracyclines stiU provide inexpensive and effective treatment for several microbial infections, but the emergence of acquired resistance to this class of antibiotic has limited their clinical usehilness. Studies to define the molecular basis of resistance are underway so that derivatives having improved antibacterial spectra and less susceptibiUty to bacterial resistance may be developed. Tetracyclines are antibiotics of choice for relatively few human infections encountered in daily clinical practice (104), largely as a result of the emergence of acquired tetracycline-resistance among clinically important bacteria (88,105,106). Acquired resistance occurs when resistant strains emerge from previously sensitive bacterial populations by acquisition of resistance genes which usually reside in plasmids and/or transposons (88,106,107). Furthermore, resistance deterrninants contained in transposons spread to, and become estabUshed in, diverse bacterial species (106). [Pg.182]

The nature of the conditions of intensive production, however, can increase the risk of diseases and infections which can spread very rapidly and devastate large numbers of animals." Thus it is common practice for producers of poultry to add coccidiostats to their diets and vaccines to their drinking water in order to prevent coccidiosis and other infectious diseases such as bronchitis and Newcastle disease. A similar problem exists for intensively reared fish, where it is necessary to add antibiotics to their diets. A problem with intensively reared fish is that their diet is added directly into the water in which they live thus drugs and other additives in the diet are relatively easily dispersed into the local environment of fish farms, where they can increase bacterial resistance and also cause problems such as algal blooms. [Pg.92]

The phenomenon of bacterial resistance to antibiotics was already known by the pioneers of the era of antibiotics, like Paul Ehrlich, who coined the term selective toxicity as the basic principle of antimicrobial therapeutics, as well as Gerhard Domagk, the inventor of the sulfonamide drugs, and Sir Alexander Fleming, the discoverer of the penicillins. When penicillin G was introduced into clinical practice in 1944, as many as 5% of the isolates of Staphylococcus aureus were resistant to penicillin, while 5 years later the percentage was 50%. [Pg.102]

That bacterial resistance predates the era of clinical use of antibiotics by several hundred millions of years is the recent result of genomic sequence data mining from antibiotic-producing microorganisms. These are supposed to be the inventors of antibiotic resistance genes which they had developed to protect themselves from the lethal action of their own antibiotics [4]. [Pg.102]

Leclercq R, Courvalin P (1991) Bacterial resistance to macrolide, lincosamide, and streptogramin antibiotics by target modification. Antimicrob Agents Chemother 35 1267-1272... [Pg.106]

Bacterial resistance can be caused by actively pumping antibiotics out of the cell and therefore decreasing the concentration at the target site. Drug efflux systems in bacteria are classified into four major groups based on their sequence homologies and functional similarities (Table 3). [Pg.772]

Lambert PA (2005) Bacterial resistance to antibiotics modified target sites. Adv Drug Deliv Rev 29 1471-1485... [Pg.775]

Because the natural penicillins have been used for many years, drug-resistant strains of microorganisms have developed, making the natural penicillins less effective than some of the newer antibiotics in treating a broad range of infections. Bacterial resistance has occurred within tire penicillins. Bacterial resistance is the ability of bacteria to produce substances that inactivate or destroy the penicillin. One example of bacterial resistance is tiie ability of certain bacteria to produce penicillinase, an enzyme that inactivates penicillin. The penicillinase-resistant penicillins were developed to combat this problem. [Pg.65]

Employed as a sodium salt, fusidic acid (Fig. 5.14B) is achve against many types of Gram-positive bacteria, especially staphylococci, although streptococci are relatively resistant. It is employed in the treatment of staphylococcal infections, including strains resistant to other antibiotics. However, bacterial resistance may occur in vitro and in vivo. [Pg.112]

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. [Pg.181]

Several factors are known to influence biocidal activity these include the period of contact, biocide concentration, pH, temperature, the presence of oigartic matter and the nature and condition of the microorgartisms being treated. Bacterial resistance to antibiotics is a well-established phenomenon and has been widely studied for luar years. By contrast, the mechanisms of insusceptibility to non-antibiotic chemical agents are less well understood. [Pg.263]

Empirical antibiotic selection for acute bacterial rhinosinusitis should incorporate patient risk factors for bacterial resistance. [Pg.1061]


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See also in sourсe #XX -- [ Pg.115 ]




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