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
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