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Antibiotics acquisition

To evaluate antimicrobial management program and evaluate impact on cost and quality of patient care OA Historical control None DCA Gross savings in antibiotic acquisition cost 483,032/yr Cost associated with service considered, but not quantified... [Pg.316]

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]

Resistance to trimethoprim can be due to the acquisition of plasmid encoded non-allelic variants of the chromosomal DHFR enzyme that are antibiotic unsusceptible. The genes may be part of transposons that then insert into the chromosome. For instance, in gram-negative bacteria the most widespread gene is dhfrl on transposon Tn7. [Pg.774]

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). [Pg.182]

Some of the previous sections have described the acquisition of low-level resistance to various antibiotics by alterations in the cell membrane causing decreased uptake of the drugs. These have normally have characterized as changes in components such as porins which result in a decrease of penetration by antibiotics. [Pg.196]

Diarrhea is a well-known complication of antibiotic therapy. Rates of antibiotic-associated diarrhea (AAD) vary from 5 to 25%. Some antibiotics are more likely to cause diarrhea than others, specifically, those that are broad spectrum and those that target anaerobic flora. This paper reviews the effects of antibiotics on the fecal flora as well as host factors which contribute to AAD. Clinical features and treatment of AAD are also described. Prevention of AAD rests on wise antibiotic policies, the use of probiotics and prevention of acquisition in the hospital setting. Data from clinical trials suggest that poorly absorbed antimicrobials might have a decreased risk of causing AAD and Clostridium difficile-associated disease, as concluded from studies of antibiotics used for preoperative bowel decontamination and poorly absorbed antibiotics used for traveler s diarrhea. Controlled trials would prove this but are not yet available. Probiotics may be a good adjunct to poorly absorbed antibiotics to minimize the risk of diarrhea associated with antibiotics. [Pg.81]

Prevention of acquisition of C. difficile in a hospital setting includes careful attention to hand washing, disposable gloves, wise antibiotic policies and enteric precautions. [Pg.87]

Resistance to antibiotics is usnally due to the acquisition of genes that express enzymes that can inactivate the antibiotics (e.g. P-lactamase degrades the lactam ring in penicillin (see below) or that can modify the structure of proteins that are necessary for the antibiotic to enter the... [Pg.410]

Fig. 1 Mechanisms of antibiotic resistance acquisition (a) and spreading in a community over time (b). Arrows indicate horizontal gene transfer processes and R acquired antibiotic resistance gene... Fig. 1 Mechanisms of antibiotic resistance acquisition (a) and spreading in a community over time (b). Arrows indicate horizontal gene transfer processes and R acquired antibiotic resistance gene...
In comparison with culture-dependent procedures, culture-independent methods are more sensitive and have an increased potential to survey the diversity of antibiotic resistance genes in the environment. A weakness of these methods is the impossibility to elucidate about the bacteria in the community that host specific resistance determinants. On the other hand, the possibility to explore the genetic environment (mobile element, associated genes, promoter, etc.) in which the resistance determinant is integrated offers relevant clues about the gene transfer potential and gene acquisition history. [Pg.188]

Waste water treatment is accompanied by bacterial community rearrangements which may lead to changes (increases or decreases) of the percentages of antimicrobial-resistant bacteria in the final effluent when compared with the raw inflow. Additionally, sewage treatment offers privileged conditions to favour antibiotic resistance acquisition and/or selection (see Sect. 3). Although some authors reported significant decreases of resistance to aminopenicillins (presumptive Acinetobacter and Enterobacteriaceae), cephaloporins (Acinetobacter) and... [Pg.192]

A number of characteristics of plasmids are significant in relation to the development of bacterial resistance. These include the encoding of resistance capability for as many as six unrelated antibiotics in the same DNA material, the capacity to transfer from one cell to another and thus disseminate the resistance, and the mobilization by which ordinarily nontransferable gene fragments can be transferred by the plasmid from one bacterial cell to others. Plasmids are of varying size and have been identified in most bacteria. Their majority carries resistance determinants for two or more antibiotics not of the same chemical class. It appears that two identical plasmids cannot coexist in one cell, but plasmids of different groups can occur, increasing even further the possibilities for resistance spread. The transfer or acquisition of other plasmid-mediated characteristics, such... [Pg.258]

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

The unique feature of MRSA is based on the acquisition of a low-affinity penicillin-binding protein for beta-lactam antibiotic molecules (the penicillin-binding protein 2A), which allows the bacteria to carry on synthesis of its cell wall, whereas the other penicillin-binding proteins are already inactivated by the high concentration of methicillin or other beta-lactamase-resistant beta-lactam antibiotics. [Pg.490]


See other pages where Antibiotics acquisition is mentioned: [Pg.104]    [Pg.773]    [Pg.62]    [Pg.77]    [Pg.185]    [Pg.197]    [Pg.249]    [Pg.204]    [Pg.238]    [Pg.238]    [Pg.334]    [Pg.81]    [Pg.197]    [Pg.173]    [Pg.197]    [Pg.200]    [Pg.201]    [Pg.88]    [Pg.137]    [Pg.177]    [Pg.199]    [Pg.202]    [Pg.235]    [Pg.108]    [Pg.396]    [Pg.258]    [Pg.291]    [Pg.188]    [Pg.312]    [Pg.59]    [Pg.315]    [Pg.104]    [Pg.773]    [Pg.2856]    [Pg.927]    [Pg.67]   
See also in sourсe #XX -- [ Pg.708 ]




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