Antibiotic Resistance Plasmids in Bacteria

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Antibiotic Resistance Plasmids in Bacteria

Don B Clewell, University of Michigan, Ann Arbor, Michigan, USA

Published online: February 2014

DOI: 10.1002/9780470015902.a0001491.pub3

Full Article on Wiley Online Library

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Abstract

Antibiotic resistance plasmids are bacterial extrachromosomal elements that carry genes conferring resistance to one or more antibiotics. They are notorious for their ability to transfer by conjugation between bacterial species and are significantly involved in the emergence and dissemination of multiple drug resistance associated with bacterial infections in humans. The information provided here includes some of the history and nature of antibiotic resistance as well as how plasmids have become significantly involved as intercellular carriers via the phenomenon of bacterial conjugation. The manner by which resistance determinants are able to move onto plasmids via their initial association with transposons and integrons is discussed. The existence of elements with both transpositional and conjugative properties, such as the conjugative transposons and integrative conjugative elements, is also noted.

Key Concepts:

Multiple antibiotic resistance represents a serious and growing clinical problem with regard to bacterial infections in humans.
Resistance genes are commonly found on plasmids, which are small extrachromosomal elements commonly found in bacteria.
Plasmids can vary widely with regard to their size and copy number in the cell.
Plasmids are commonly able to move from one bacterial cell to another by a mechanism known as conjugation, which involves cell‐to‐cell contact followed by transfer of a copy of plasmid DNA from a donor to a recipient.
Genes conferring antibiotic resistance are commonly found on elements known as integrons and transposons, which facilitate movement between different replicons such as between the bacterial chromosome and a plasmid.
Some transposable elements, known as conjugative transposons, also carry resistance traits; and, although unable to replicate autonomously, they can move from one bacterial cell to another by a plasmid‐like mechanism.
Excessive use of antibiotics in the treatment of human infections has, over time, contributed to the emergence and selection of resistant bacteria in the gut, a phenomenon that includes passage of resistance traits between nonpathogens and pathogens.

Keywords: conjugative transposon; horizontal transfer; insertion sequence; integron; plasmid; transposon

Article Title:	Antibiotic Resistance Plasmids in Bacteria
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	Figure 1. The generation of cell‐to‐cell contact involved in conjugation. (a) An E. coli cell with its plasmid‐encoded pilus structure binding to the recipient (plasmid‐free) cell and retracting in order to generate direct contact between the two cells. (b) An En. faecalis donor cell undergoing a plasmid‐encoded mating response to a peptide sex pheromone secreted by a recipient cell. The donors synthesise an ‘aggregation substance’ that coats the surface and facilitates adherence to recipients upon random collision. Once a copy of the plasmid is acquired, the resulting transconjugant cell shuts down or masks the endogenous pheromone and becomes a potential donor. Interestingly, transconjugants continue to produce other peptide pheromones able to induce a mating response by donors carrying different families of conjugative plasmids. A plasmid‐free strain can actually make up to six different pheromones, and probably many more.
	Figure 2. Diagram of the erythromycin‐resistance transposon Tn917 originally identified in En. faecalis. The element is a little more than 5000 bp long and is bounded by 38‐bp inverted repeats (LR, left repeat; RR, right repeat) indicated by the short arrows at the left and right ends. IR (internal repeat) is also a 38‐bp repeat, which conceivably could work together with RR to move part of the element without the erythromycin resistance gene erm, although this has not actually been demonstrated. tnpA encodes the transposase and tnpR encodes a ‘resolvase’ that acts subsequent to the transposase in ‘resolving’ a cointegrate structure that represents an intermediate in the transposition process. The resistance determinant of Tn917 is inducible, in that a subinhibitory concentration of erythromycin greatly enhances the level of the erm product by an increase in transcription. This can also have an effect downstream by increasing the expression of the transposition genes, which can lead to an increase in the frequency of movement of the element.
	Figure 3. Structure of an integron. The arrows indicate the relative orientation of the various components. P is the promoter that fires backwards from a site within the 5‐prime end of the integrase determinant intI (intI has its own promoter (the circle at the beginning of the arrow) upstream). attI is the site where new cassettes enter and become part of the integron. Cassettes move by excision via a ‘loop‐out’ involving flanking recombination sequences (i.e. 59‐base element (59‐be) sequences). The nonreplicating circular element containing one 59‐be then enters at the attI sequence. Expression is greatest at the head of the line because it is closest to the promoter P; and exposure to a given antibiotic will select for movement of the appropriate cassette to this position.