Bacterial resistance, acquired mechanism

In general terms, bacterial resistance to antibacterial agents can be considered as being either intrinsic (innate, a natural property) or acquired, for example, by mutation or by the acquisition of a plasmid or transposon (jumping gene) [105]. Resistance to mercury [103, 122-125] and to other cations and anions [103, 122, 123, 125] is well characterized. The mechanisms involved in resistance to some metals, including silver, are summarized in Table 7.1. 

Acquired bacterial resistance to the tetracyclines has become widespread in animal populations and has severely reduced the usefulness of these drugs. Resistance to the tetracyclines results from plasmid-mediated mechanisms that prevent the active transport of the drug into the bacterial cell or increase the efflux of drug from the bacterial cell. 

MECHANISMS OF BACTERIAL RESISTANCE TO PENICILLINS AND CEPHALOSPORINS A sensitive strain may acquire resistance by mutations that decrease the affinity of PBPs for the antibiotic. Because /5-lactam antibiotics inhibit many different PBPs, their affinity for several PBPs must decrease to confer resistance. Methidllin-resistant S. aureus are resistant via acquisition of an additional high-molecular-weight PBP (via a transposon) with a very low affinity for all /5-lactam antibiotics this mechanism is responsible for methicillin resistance in the coagu-lase-negative staphylococci. 

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]. 

Polymyxins are a group of antibiotics which disrupt bacterial cell membranes. Two mechanisms of acquired resistance to the polymyxins have been identified (Russell Chopra 1996). 

Macrolide antibiotics target the bacterial ribosome and inhibit the bacterial protein biosynthesis. Many gram-negative bacteria are inherently resistant to mac-rolides because their outer membrane is impermeable to macrolides. Several mechanisms of acquired resistance have been reported. In some cases, resistance is conferred by methylation of ribosomes by methylase enzymes, the genes of... 

A major mechanism of acquired resistance to the penicillins is bacterial production of enzymes called P-lactamases. These enzymes hydrolyze the penicillin P lactam ring that is necessary for its activity. p-Lactamases with a strong proclivity for penicillins are called penicillinases. Because most strains of Staphylococcus aureus and many strains of Staphylococcus epidermidis produce penicillinase, penicillins G andV are not effective against these gram-positive bacteria. 

There is also a correlation between the sensitivity of mammalian and bacterial cells growing in vitro to alkylating agents and their ability to repair alkylated DNA. Other mechanisms of action have been proposed to account for the effects of individual alkylating agents33-35. While these may play a role, it is quite clear that cells with acquired resistance to one alkylating agent are cross resistant to all others and indicates that all act by a common pathway. 

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