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Antibiotic Resistance Mechanisms


             With regard to the genetic mechanisms of antibiotic resistance, there are advantages in .
             having resistance genes carried on a plasmid. Some chromosomal resistance mutations hinder .
             growth, whereas resistance genes generally do not. Furthermore, plasmid-determined resistance.
             can be amplified by gene duplication to produce higher levels of resistance or it can be carried on .
             a segment of DNA that can transpose from one replicon to another, allowing greater flexibility in.
             resistance diffusion1. In addition, resistance to multiple antibiotics can be packaged on one .
             plasmid.
             Probably the most important advantage is that plasmid-determined resistance can spread .
             to new hosts via the process of conjugation. The ability to transfer and receive genetic material in .
             this fashion is mostly confined to Gram-negative bacteria. The plasmid found in resistant Gram-.
             negative bacteria consists of two elements: (a) a resistance transfer factor (RTF) that allows the .
             cell to conjugate and transfer a copy of the plasmid to another cell; (b) one or more linked genes .
             each conferring resistance to a specific antibiotic2. The entire complex of RTF and resistance .
             genes is known as an R-factor and takes the form of a circular, double-stranded DNA molecule. .
             The synthesis of hair-like structures called pili is under the control of the RTF component of the .
             R-factor and is essential to the transfer of an R-factor2. Although the exact mechanism of plasmid .
             transfer is currently unknown, the presence of multiple copies of the resistance genes leads to .
             enhanced levels of resistance to certain antibiotics. .
             There is absolutely no doubt that the presence of R+ bacteria (those having an R-factor) in .
             microbial populations associated with infections can result in the emergence of a drug-resistant.
             population of cells during antibiotic therapy. However, the emergence of an R+ population of.
             bacteria during antibiotic therapy is more likely the result of a selection process for resistant cells.


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