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World Health Organization : Year 1995 : Communicable Diseases and Emerging Infectious Diseases ; Bvi, No. 95.7: World Health Organization Scientific Working Group on Monitoring and Management of Bacterial Resistance to Antimicrobial Agents

By World Health Organization

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Book Id: WPLBN0000047758
Format Type: PDF eBook
File Size: 1.3 MB
Reproduction Date: 2005
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Title: World Health Organization : Year 1995 : Communicable Diseases and Emerging Infectious Diseases ; Bvi, No. 95.7: World Health Organization Scientific Working Group on Monitoring and Management of Bacterial Resistance to Antimicrobial Agents  
Author: World Health Organization
Volume:
Language: English
Subject: Health., Public health, Wellness programs
Collections: Medical Library Collection, World Health Collection
Historic
Publication Date:
Publisher: World Health Organization

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Organization, W. H. (n.d.). World Health Organization : Year 1995 : Communicable Diseases and Emerging Infectious Diseases ; Bvi, No. 95.7. Retrieved from http://hawaiilibrary.net/


Description
Medical Reference Publication

Excerpt
Resistance to p-lactam drugs can be mediated either by p-lactamases or by changes in the orr-a nism's penicillin-bindin-g .pr oteins. While O-lactamases are aresent in both Gram-wositive and Gram-negative organisms, resistance mediated by changes in penicillin-binding proteins is primarily important in Gram-positive org-a nisms. Amino-dv.c oside resistance can be caused bv: enzvmes that modify the drug; reduced uptake by the bacterium; or changes in ribosomal thBt reduce or prevent binding of the drug to the active site. Genes encoding aminoglycoside resistance are commonly found on plasmids and transposable elements. Fluoroquinolone resistance is mediated by decreased uptake of the drug into the bacterial cell, or by changes in the DNA gyrase subunits. 1Ir;lmatic incretises in fluoroquinolone resistance in strains of methicillin-resistant Staphylococcus nureus have been observed when fluoroquinolones are used extensively for control of staphylococctil infections. Alteration of the target site is an important mechanism of resistance for macrolides (such as etythromycin), clindamycin, tetra~ycline, glycopeptides (such as vancomycjn), and rifampim. Enzymatic inactivation is important for chloramphenicol and eventually in macrolides. Finally, trimethoprim and sulfonamide resistance usually occur through acquisition of new genes that encode alternate metabolic enzymes that are insensitive to the action of these drugs.

Table of Contents
Table of Contents Page 1. Introduction 2. The nature and costs of resistance 2.1 A brief review of bacterial resistance to antimicrobial agents 2.2 The economies of resistance 2.3 Epidemiology of resistance 2.4 The lack of new microbial agents 2.5 Selective pressure and population genetics 2.6 The search for new anti-infectives 2.7 The clinical impact of resistance 3. Recent increases in resistance Beta-lactamases Aminoglycosides Trimethoprim Quinolones Methicillin-resistant Stafl6ococcus aureus Beta-haemolytic Streptococci Streptococcus pneumoniae Enterococci Neisseria Anaerobes Tuberculosis Entetic infections 4. How to modify conditions to limit resistance 4.1 In bacteria of human populations 4.2 in bacteria of animals and other reservoirs 4.3 In bacteria in special environments 4.4 Perspectives on chemotherapy 4.5 Small peptide antibiotics 4 Anticipation of future patterns of drug-resistant infections

 

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