By Ola Skold(auth.)
This publication, that's the translated model of a Swedish publication, combines a basic creation of numerous antibiotics with a closer dialogue of resistance. the focal point on resistance in studying approximately antibiotics may also help destiny scientists realize the matter antibiotics resistance poses for medicinal and drug-related fields, and maybe set off extra learn and discoveries to struggle antibiotic resistant lines.
present overviews of the subject are integrated, besides particular discussions at the person mechanisms (betalactams, glycopeptides, aminoglycosides, and so forth) utilized in numerous antibacterial brokers and causes of ways resistances to these boost. tools for counteracting resistance improvement in micro organism are mentioned as well.
Chapter 1 Antibiotics: the best Triumph of clinical drugs (pages 1–19):
Chapter 2 Distribution of Antibiotics (pages 21–28):
Chapter three Sulfonamides and Trimethoprim (pages 29–68):
Chapter four Penicillins and different Betalactams (pages 69–94):
Chapter five Glycopeptides (pages 95–102):
Chapter 6 Aminoglycosides (pages 103–113):
Chapter 7 different Antibiotics Interfering with Bacterial Protein Synthesis (pages 115–131):
Chapter eight Quinolones (pages 133–145):
Chapter nine Antibacterial brokers now not on the topic of the big Antibiotic households (pages 147–166):
Chapter 10 Mechanisms for the Horizontal unfold of Antibiotic Resistance between micro organism (pages 167–186):
Chapter eleven find out how to deal with Antibiotic Resistance (pages 187–202):
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Additional info for Antibiotics and Antibiotic Resistance
The simplest mechanism includes mutational changes in the sulfonamide target enzyme dihydropteroate synthase (Fig. 1) that limit binding of the drug and thus mitigate the competition with the normal substrate p-aminobenzoic acid. Dihydropteroate synthase catalyzes the next-to-last step in the enzymic pathway leading to folic acid. In this step the pteridin nucleus of folic acid is linked to p-aminobenzoic acid. The structural similarity between sulfonamide and p-aminobenzoic acid and the high affinity of sulfonamide to the enzyme effects a competitive inhibition of dihydropteroate formation and, in turn, of folic acid formation.
Meningitidis should not exist today according to the argument described earlier for mutational sulfonamide resistance. They do, however, and are in fact common among present-day isolates of this pathogen. This means that they have not been selected away in the absence of sulfonamides. This in turn means that sulfonamide resistance has not hindered the resistant strains in their growth competition with their susceptible relatives. The fitness cost of resistance assumed must have been compensated in some way.
This is in analogy with the antifolate cytostatic drugs aminopterin (3-7) and methotrexate (3-8), the H2N N N H N N H N H N OH O Dihydrofolic acid COOH COOH 3-5 H2N N N OH H N N H H N H N O Tetrahydrofolic acid COOH COOH 3-6 N H2N N N N H N H N NH2 O Aminopterin 3-7 COOH COOH 53 TRIMETHOPRIM H2 N N N N N CH3 N H N NH2 O COOH COOH Methotrexate 3-8 latter having been used as a cytostatic agent since the 1950s. Methotrexate and aminopterin cannot be used as antibacterial agents, however, since they are not selective for bacteria.