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.
