Jump to content

Plasmid-mediated resistance: Difference between revisions

Add links
From Wikipedia, the free encyclopedia
Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
consistent citation formatting; templated cites
Alter: pages, doi, issue, journal. Add: duplicate_vauthors, doi-access, pmc. Removed proxy/dead URL that duplicated identifier. Formatted dashes. | Use this tool. Report bugs. | #UCB_Gadget
Line 1: Line 1:
[[Image:Example plasmid.svg|right|thumb|200px|An example plasmid with two areas of [[antibiotic resistance]] coding [[DNA]] (1,2) and an [[origin of replication]] (3).]]
[[Image:Example plasmid.svg|right|thumb|200px|An example plasmid with two areas of [[antibiotic resistance]] coding [[DNA]] (1,2) and an [[origin of replication]] (3).]]
'''Plasmid-mediated resistance''' is the transfer of [[antibiotic resistance]] genes which are carried on [[plasmid]]s.<ref>{{cite journal | vauthors = San Millan A | title = Evolution of Plasmid-Mediated Antibiotic Resistance in the Clinical Context | journal = Trends in Microbiology | volume = 26 | issue = 12 | pages = 978–985 | date = December 2018 | pmid = 30049587 | doi = 10.1016/j.tim.2018.06.007 }}</ref> Plasmids possess mechanisms that ensure their independent replication as well as those that regulate their replication number and guarantee stable inheritance during cell division. By the [[Bacterial conjugation|conjugation]] process, they can stimulate lateral transfer between bacteria from various genera and kingdoms.<ref>{{Cite web |title=conjugation (prokaryotes) {{!}} Learn Science at Scitable |url=https://www.nature.com/scitable/definition/conjugation-prokaryotes-290/ |access-date=2023-01-06 |website=www.nature.com |language=en}}</ref> Numerous plasmids contain addiction-inducing systems that are typically based on toxin-antitoxin factors and capable of killing daughter cells that don't inherit the plasmid during cell division.<ref>{{cite journal | vauthors = Tsang J | title = Bacterial plasmid addiction systems and their implications for antibiotic drug development | journal = Postdoc Journal | volume = 5 | issue = 5 | pages = 3–9 | date = May 2017 | pmid = 28781980 | pmc = 5542005 | url = https://pubmed.ncbi.nlm.nih.gov/28781980/ }}</ref> Plasmids often carry multiple [[antibiotic resistance]] genes, contributing to the spread of [[Multidrug resistance|multidrug-resistance]] (MDR).<ref>{{cite journal | vauthors = Nikaido H | title = Multidrug resistance in bacteria | journal = Annual Review of Biochemistry | volume = 78 | issue = 1 | pages = 119–146 | date = 2009-06-01 | pmid = 19231985 | pmc = 2839888 | doi = 10.1146/annurev.biochem.78.082907.145923 }}</ref> Antibiotic resistance mediated by MDR plasmids severely limits the treatment options for the infections caused by [[Gram-negative bacteria]], especially family [[Enterobacteriaceae]].<ref name=":0">{{cite journal | vauthors = Schultsz C, Geerlings S | title = Plasmid-mediated resistance in Enterobacteriaceae: changing landscape and implications for therapy | journal = Drugs | volume = 72 | issue = 1 | pages = 1–16 | date = January 2012 | pmid = 22191792 | doi = 10.2165/11597960-000000000-00000 | s2cid = 42306704 }}</ref> The global spread of MDR plasmids has been enhanced by [[selective pressure]] from antimicrobial medications used in medical facilities and when raising animals for food.<ref>{{cite journal | vauthors = Mathers AJ, Peirano G, Pitout JD | title = The role of epidemic resistance plasmids and international high-risk clones in the spread of multidrug-resistant Enterobacteriaceae | journal = Clinical Microbiology Reviews | volume = 28 | issue = 3 | pages = 565–591 | date = July 2015 | pmid = 25926236 | pmc = 4405625 | doi = 10.1128/CMR.00116-14 }}</ref>
'''Plasmid-mediated resistance''' is the transfer of [[antibiotic resistance]] genes which are carried on [[plasmid]]s.<ref>{{cite journal | vauthors = San Millan A | title = Evolution of Plasmid-Mediated Antibiotic Resistance in the Clinical Context | journal = Trends in Microbiology | volume = 26 | issue = 12 | pages = 978–985 | date = December 2018 | pmid = 30049587 | doi = 10.1016/j.tim.2018.06.007 }}</ref> Plasmids possess mechanisms that ensure their independent replication as well as those that regulate their replication number and guarantee stable inheritance during cell division. By the [[Bacterial conjugation|conjugation]] process, they can stimulate lateral transfer between bacteria from various genera and kingdoms.<ref>{{Cite web |title=conjugation (prokaryotes) {{!}} Learn Science at Scitable |url=https://www.nature.com/scitable/definition/conjugation-prokaryotes-290/ |access-date=2023-01-06 |website=www.nature.com |language=en}}</ref> Numerous plasmids contain addiction-inducing systems that are typically based on toxin-antitoxin factors and capable of killing daughter cells that don't inherit the plasmid during cell division.<ref>{{cite journal | vauthors = Tsang J | title = Bacterial plasmid addiction systems and their implications for antibiotic drug development | journal = Postdoc Journal | volume = 5 | issue = 5 | pages = 3–9 | date = May 2017 | pmid = 28781980 | pmc = 5542005 }}</ref> Plasmids often carry multiple [[antibiotic resistance]] genes, contributing to the spread of [[Multidrug resistance|multidrug-resistance]] (MDR).<ref>{{cite journal | vauthors = Nikaido H | title = Multidrug resistance in bacteria | journal = Annual Review of Biochemistry | volume = 78 | issue = 1 | pages = 119–146 | date = 2009-06-01 | pmid = 19231985 | pmc = 2839888 | doi = 10.1146/annurev.biochem.78.082907.145923 }}</ref> Antibiotic resistance mediated by MDR plasmids severely limits the treatment options for the infections caused by [[Gram-negative bacteria]], especially family [[Enterobacteriaceae]].<ref name=":0">{{cite journal | vauthors = Schultsz C, Geerlings S | title = Plasmid-mediated resistance in Enterobacteriaceae: changing landscape and implications for therapy | journal = Drugs | volume = 72 | issue = 1 | pages = 1–16 | date = January 2012 | pmid = 22191792 | doi = 10.2165/11597960-000000000-00000 | s2cid = 42306704 }}</ref> The global spread of MDR plasmids has been enhanced by [[selective pressure]] from antimicrobial medications used in medical facilities and when raising animals for food.<ref>{{cite journal | vauthors = Mathers AJ, Peirano G, Pitout JD | title = The role of epidemic resistance plasmids and international high-risk clones in the spread of multidrug-resistant Enterobacteriaceae | journal = Clinical Microbiology Reviews | volume = 28 | issue = 3 | pages = 565–591 | date = July 2015 | pmid = 25926236 | pmc = 4405625 | doi = 10.1128/CMR.00116-14 }}</ref>


== Properties of resistance plasmids ==
== Properties of resistance plasmids ==
Resistance plasmids by definition carry one or more antibiotic resistance genes.<ref name=":2">{{cite journal | vauthors = Bennett PM | title = Plasmid encoded antibiotic resistance: acquisition and transfer of antibiotic resistance genes in bacteria | journal = British Journal of Pharmacology | volume = 153 | issue = Suppl 1 | pages = S347-S357 | date = March 2008 | pmid = 18193080 | pmc = 2268074 | doi = 10.1038/sj.bjp.0707607 }}</ref> They are frequently accompanied by the genes encoding [[virulence]] determinants,<ref>{{cite journal | vauthors = Darmancier H, Domingues CP, Rebelo JS, Amaro A, Dionísio F, Pothier J, Serra O, Nogueira T | display-authors = 6 | title = Are Virulence and Antibiotic Resistance Genes Linked? A Comprehensive Analysis of Bacterial Chromosomes and Plasmids | journal = Antibiotics | volume = 11 | issue = 6 | pages = 706 | date = May 2022 | pmid = 35740113 | doi = 10.3390/antibiotics11060706 }}</ref> specific enzymes or resistance to toxic [[heavy metals]].<ref>{{Cite journal | vauthors = Sevim A, Sevim E |date=2015 |title=Plasmid Mediated Antibiotic and Heavy Metal Resistance in Bacillus Strains Isolated from Soils in Rize, Turkey |url=https://dergipark.org.tr/tr/download/article-file/194072 |journal=Suleyman Demirel University Journal of Natural and Applied Science |volume=19 |issue=2 |pages=133-141 |via=Süleyman Demirel University science Institute}}</ref> Multiple resistance genes are commonly arranged in the resistance cassettes.<ref name=":2" /> The antibiotic resistance genes found on the plasmids confer resistance to most of the antibiotic classes used nowadays, for example, [[Β-lactam antibiotic|beta-lactams]], [[fluoroquinolones]] and [[aminoglycoside]]s.<ref>{{cite journal | vauthors = McMillan EA, Gupta SK, Williams LE, Jové T, Hiott LM, Woodley TA, Barrett JB, Jackson CR, Wasilenko JL, Simmons M, Tillman GE, McClelland M, Frye JG | display-authors = 6 | title = Antimicrobial Resistance Genes, Cassettes, and Plasmids Present in <i>Salmonella enterica</i> Associated With United States Food Animals | journal = Frontiers in Microbiology | volume = 10 | pages = 832 | date = 2019 | pmid = 31057528 | doi = 10.3389/fmicb.2019.00832/full }}</ref>
Resistance plasmids by definition carry one or more antibiotic resistance genes.<ref name=":2">{{cite journal | vauthors = Bennett PM | title = Plasmid encoded antibiotic resistance: acquisition and transfer of antibiotic resistance genes in bacteria | journal = British Journal of Pharmacology | volume = 153 | issue = Suppl 1 | pages = S347–S357 | date = March 2008 | pmid = 18193080 | pmc = 2268074 | doi = 10.1038/sj.bjp.0707607 }}</ref> They are frequently accompanied by the genes encoding [[virulence]] determinants,<ref>{{cite journal | vauthors = Darmancier H, Domingues CP, Rebelo JS, Amaro A, Dionísio F, Pothier J, Serra O, Nogueira T | display-authors = 6 | title = Are Virulence and Antibiotic Resistance Genes Linked? A Comprehensive Analysis of Bacterial Chromosomes and Plasmids | journal = Antibiotics | volume = 11 | issue = 6 | pages = 706 | date = May 2022 | pmid = 35740113 | doi = 10.3390/antibiotics11060706 | pmc = 9220345 | doi-access = free }}</ref> specific enzymes or resistance to toxic [[heavy metals]].<ref>{{Cite journal | vauthors = Sevim A, Sevim E |date=2015 |title=Plasmid Mediated Antibiotic and Heavy Metal Resistance in Bacillus Strains Isolated from Soils in Rize, Turkey |url=https://dergipark.org.tr/tr/download/article-file/194072 |journal=Suleyman Demirel University Journal of Natural and Applied Science |volume=19 |issue=2 |pages=133–141 |via=Süleyman Demirel University science Institute}}</ref> Multiple resistance genes are commonly arranged in the resistance cassettes.<ref name=":2" /> The antibiotic resistance genes found on the plasmids confer resistance to most of the antibiotic classes used nowadays, for example, [[Β-lactam antibiotic|beta-lactams]], [[fluoroquinolones]] and [[aminoglycoside]]s.<ref>{{cite journal | vauthors = McMillan EA, Gupta SK, Williams LE, Jové T, Hiott LM, Woodley TA, Barrett JB, Jackson CR, Wasilenko JL, Simmons M, Tillman GE, McClelland M, Frye JG | display-authors = 6 | title = Antimicrobial Resistance Genes, Cassettes, and Plasmids Present in <i>Salmonella enterica</i> Associated With United States Food Animals | journal = Frontiers in Microbiology | volume = 10 | pages = 832 | date = 2019 | pmid = 31057528 | doi = 10.3389/fmicb.2019.00832 | pmc = 6479191 | doi-access = free }}</ref>


It is very common for the resistance genes or entire resistance cassettes to be re-arranged on the same plasmid or be moved to a different plasmid or chromosome by means of recombination systems. Examples of such systems include [[integron]]s, [[Transposable element|transposons]], and IS''CR''-promoted gene mobilization.<ref name=":2" />
It is very common for the resistance genes or entire resistance cassettes to be re-arranged on the same plasmid or be moved to a different plasmid or chromosome by means of recombination systems. Examples of such systems include [[integron]]s, [[Transposable element|transposons]], and IS''CR''-promoted gene mobilization.<ref name=":2" />


Most of the resistance plasmids are conjugative, meaning that they encode all the needed components for the transfer of the plasmid to another bacterium,<ref name="pmid25481925">{{cite journal | vauthors = Zatyka M, Thomas CM | title = Control of genes for conjugative transfer of plasmids and other mobile elements | journal = FEMS Microbiology Reviews | volume = 21 | issue = | pages = 291–319 | date = 1998 | pmid = 25481925 | doi = 10.1111/j.1574-6976.1998.tb00355.x }}</ref> and that isn't present in mobilizable plasmids. According to that, Mobilizable plasmids are smaller in size (usually < 10 kb) while conjugative plasmids are largger (usually > 30 kb) due to the considerable size of DNA required to encode the conjugation mechanisms that allow for cell-to-cell conjugation.<ref name=":2" />
Most of the resistance plasmids are conjugative, meaning that they encode all the needed components for the transfer of the plasmid to another bacterium,<ref name="pmid25481925">{{cite journal | vauthors = Zatyka M, Thomas CM | title = Control of genes for conjugative transfer of plasmids and other mobile elements | journal = FEMS Microbiology Reviews | volume = 21 | issue = 4| pages = 291–319 | date = 1998 | pmid = 25481925 | doi = 10.1111/j.1574-6976.1998.tb00355.x }}</ref> and that isn't present in mobilizable plasmids. According to that, Mobilizable plasmids are smaller in size (usually < 10 kb) while conjugative plasmids are largger (usually > 30 kb) due to the considerable size of DNA required to encode the conjugation mechanisms that allow for cell-to-cell conjugation.<ref name=":2" />


==R-factor==
==R-factor==
{{About|the plasmid|information about the residual factor in crystallography|R-factor (crystallography)|section=TRUE}}
{{About|the plasmid|information about the residual factor in crystallography|R-factor (crystallography)|section=TRUE}}
'''R-factors''' are also called a resistance factors, are [[plasmid]]s that contain [[antibiotic resistance]] genes.<ref>{{Cite web |title=R-Factor |url=https://www.vedantu.com/biology/r-factor |access-date=2023-01-08 |website=VEDANTU}}</ref> Resistance genes are ones that give rise to proteins that modify the antibiotic or pump it out. They are different from mutations that give bacteria resistance to antibiotics by preventing the antibiotic from getting in or changing the shape of the target protein.<ref>{{cite journal | vauthors = Peterson E, Kaur P | title = Antibiotic Resistance Mechanisms in Bacteria: Relationships Between Resistance Determinants of Antibiotic Producers, Environmental Bacteria, and Clinical Pathogens | journal = Frontiers in Microbiology | volume = 9 | pages = 2928 | date = 2018 | pmid = 30555448 | doi = 10.3389/fmicb.2018.02928/full }}</ref> R-factors have been known to contain up to ten resistance genes. They can also spread easily as they contain genes for constructing pili, which allow them to transfer the R-factor to other bacteria.<ref>{{cite journal | vauthors = Tao S, Chen H, Li N, Wang T, Liang W | title = The Spread of Antibiotic Resistance Genes In Vivo Model | journal = The Canadian Journal of Infectious Diseases & Medical Microbiology = Journal Canadien Des Maladies Infectieuses Et De La Microbiologie Medicale | volume = 2022 | pages = 3348695 | date = 2022-07-18 | pmid = 35898691 | pmc = 9314185 | doi = 10.1155/2022/3348695 }}</ref> R-factors have contributed to the growing antibiotic resistance crisis because they quickly spread resistance genes amongst bacteria.<ref>{{cite book | vauthors = Campbell N |title=Biology A Global Approach |date=2018 |publisher=Pearson |location=New York |isbn=978-1-292-17043-5 |page=633 |edition=11th }}</ref>
'''R-factors''' are also called a resistance factors, are [[plasmid]]s that contain [[antibiotic resistance]] genes.<ref>{{Cite web |title=R-Factor |url=https://www.vedantu.com/biology/r-factor |access-date=2023-01-08 |website=VEDANTU}}</ref> Resistance genes are ones that give rise to proteins that modify the antibiotic or pump it out. They are different from mutations that give bacteria resistance to antibiotics by preventing the antibiotic from getting in or changing the shape of the target protein.<ref>{{cite journal | vauthors = Peterson E, Kaur P | title = Antibiotic Resistance Mechanisms in Bacteria: Relationships Between Resistance Determinants of Antibiotic Producers, Environmental Bacteria, and Clinical Pathogens | journal = Frontiers in Microbiology | volume = 9 | pages = 2928 | date = 2018 | pmid = 30555448 | doi = 10.3389/fmicb.2018.02928 | pmc = 6283892 | doi-access = free }}</ref> R-factors have been known to contain up to ten resistance genes. They can also spread easily as they contain genes for constructing pili, which allow them to transfer the R-factor to other bacteria.<ref>{{cite journal | vauthors = Tao S, Chen H, Li N, Wang T, Liang W | title = The Spread of Antibiotic Resistance Genes In Vivo Model | journal = The Canadian Journal of Infectious Diseases & Medical Microbiology = Journal Canadien des Maladies Infectieuses et de la Microbiologie Medicale | volume = 2022 | pages = 3348695 | date = 2022-07-18 | pmid = 35898691 | pmc = 9314185 | doi = 10.1155/2022/3348695 | doi-access = free }}</ref> R-factors have contributed to the growing antibiotic resistance crisis because they quickly spread resistance genes amongst bacteria.<ref>{{cite book | vauthors = Campbell N |title=Biology A Global Approach |date=2018 |publisher=Pearson |location=New York |isbn=978-1-292-17043-5 |page=633 |edition=11th }}</ref>


===Transmission===
===Transmission===
Line 22: Line 22:


=== Beta-lactam resistance ===
=== Beta-lactam resistance ===
B-lactamases are antibiotic-hydrolyzing enzymes that typically cause resistance to b-lactam antibiotics. These enzymes are prevalent in Streptomyces, and together with related enzymes discovered in pathogenic and non-pathogenic bacteria, they form the protein family known as the "b-lactamase superfamily".<ref>{{cite journal | vauthors = Peterson E, Kaur P | title = Antibiotic Resistance Mechanisms in Bacteria: Relationships Between Resistance Determinants of Antibiotic Producers, Environmental Bacteria, and Clinical Pathogens | journal = Frontiers in Microbiology | volume = 9 | pages = 2928 | date = 2018 | pmid = 30555448 | doi = 10.3389/fmicb.2018.02928/full }}</ref> it is hypothesized that b-lactamases also serve a double purpose, such as housekeeping and antibiotic resistance.<ref>{{cite journal | vauthors = Martínez JL | title = Ecology and Evolution of Chromosomal Gene Transfer between Environmental Microorganisms and Pathogens | journal = Microbiology Spectrum | volume = 6 | issue = 1 | pages = 6.1.06 | date = January 2018 | pmid = 29350130 | doi = 10.1128/microbiolspec.MTBP-0006-2016 | vauthors = Baquero F, Bouza E, Gutiérrez-Fuentes J, Coque TM }}</ref>
B-lactamases are antibiotic-hydrolyzing enzymes that typically cause resistance to b-lactam antibiotics. These enzymes are prevalent in Streptomyces, and together with related enzymes discovered in pathogenic and non-pathogenic bacteria, they form the protein family known as the "b-lactamase superfamily".<ref>{{cite journal | vauthors = Peterson E, Kaur P | title = Antibiotic Resistance Mechanisms in Bacteria: Relationships Between Resistance Determinants of Antibiotic Producers, Environmental Bacteria, and Clinical Pathogens | journal = Frontiers in Microbiology | volume = 9 | pages = 2928 | date = 2018 | pmid = 30555448 | doi = 10.3389/fmicb.2018.02928 | pmc = 6283892 | doi-access = free }}</ref> it is hypothesized that b-lactamases also serve a double purpose, such as housekeeping and antibiotic resistance.<ref>{{cite journal | DUPLICATE_vauthors = Martínez JL | title = Ecology and Evolution of Chromosomal Gene Transfer between Environmental Microorganisms and Pathogens | journal = Microbiology Spectrum | volume = 6 | issue = 1 | pages = 6.1.06 | date = January 2018 | pmid = 29350130 | doi = 10.1128/microbiolspec.MTBP-0006-2016 | vauthors = Baquero F, Bouza E, Gutiérrez-Fuentes J, Coque TM }}</ref>


Both narrow spectrum beta-lactamases (e.g. penicillinases) and [[Extended-spectrum beta-lactamase|extended spectrum beta-lactamases]] (ESBL) are common for resistance plasmids in ''Enterobacteriaceae''. Often multiple beta-lactamase genes are found on the same plasmid hydrolyzing a wide spectrum of beta-lactam antibiotics.<ref name=":0" />
Both narrow spectrum beta-lactamases (e.g. penicillinases) and [[Extended-spectrum beta-lactamase|extended spectrum beta-lactamases]] (ESBL) are common for resistance plasmids in ''Enterobacteriaceae''. Often multiple beta-lactamase genes are found on the same plasmid hydrolyzing a wide spectrum of beta-lactam antibiotics.<ref name=":0" />
Line 29: Line 29:
ESBL enzymes can hydrolyze all beta-lactam antibiotics, including cephalosporins, except for the carpabepenems. The first clinically observed ESBL enzymes were mutated versions of the narrow spectrum beta-lactamases, like TEM and SHV. Other ESBL enzymes originate outside of family Enterobacteriaceae, but have been spreading as well.<ref name=":0" />
ESBL enzymes can hydrolyze all beta-lactam antibiotics, including cephalosporins, except for the carpabepenems. The first clinically observed ESBL enzymes were mutated versions of the narrow spectrum beta-lactamases, like TEM and SHV. Other ESBL enzymes originate outside of family Enterobacteriaceae, but have been spreading as well.<ref name=":0" />


In addition, since the plasmids that carry ESBL genes also commonly encode [[Antibiotic resistance|resistance]] determinants for many other antibiotics, ESBL strains are often resistant to many non-beta-lactam antibiotics as well,<ref>{{cite journal | vauthors = Hussain T, Jamal M, Nighat F, Andleeb S | title = Broad spectrum antibiotics and resistance in non-target bacteria: an example from tetracycline | journal = Journal of Pure and Applied Microbiology | date = 2014 | volume = 8 | issue = 4 | pages = 2667-2671 | doi = }}</ref> leaving very few options for the treatment.
In addition, since the plasmids that carry ESBL genes also commonly encode [[Antibiotic resistance|resistance]] determinants for many other antibiotics, ESBL strains are often resistant to many non-beta-lactam antibiotics as well,<ref>{{cite journal | vauthors = Hussain T, Jamal M, Nighat F, Andleeb S | title = Broad spectrum antibiotics and resistance in non-target bacteria: an example from tetracycline | journal = Journal of Pure and Applied Microbiology | date = 2014 | volume = 8 | issue = 4 | pages = 2667–2671 | doi = }}</ref> leaving very few options for the treatment.


==== Carbapenemases ====
==== Carbapenemases ====

Revision as of 19:34, 9 January 2023

An example plasmid with two areas of antibiotic resistance coding DNA (1,2) and an origin of replication (3).

Plasmid-mediated resistance is the transfer of antibiotic resistance genes which are carried on plasmids.[1] Plasmids possess mechanisms that ensure their independent replication as well as those that regulate their replication number and guarantee stable inheritance during cell division. By the conjugation process, they can stimulate lateral transfer between bacteria from various genera and kingdoms.[2] Numerous plasmids contain addiction-inducing systems that are typically based on toxin-antitoxin factors and capable of killing daughter cells that don't inherit the plasmid during cell division.[3] Plasmids often carry multiple antibiotic resistance genes, contributing to the spread of multidrug-resistance (MDR).[4] Antibiotic resistance mediated by MDR plasmids severely limits the treatment options for the infections caused by Gram-negative bacteria, especially family Enterobacteriaceae.[5] The global spread of MDR plasmids has been enhanced by selective pressure from antimicrobial medications used in medical facilities and when raising animals for food.[6]

Properties of resistance plasmids

Resistance plasmids by definition carry one or more antibiotic resistance genes.[7] They are frequently accompanied by the genes encoding virulence determinants,[8] specific enzymes or resistance to toxic heavy metals.[9] Multiple resistance genes are commonly arranged in the resistance cassettes.[7] The antibiotic resistance genes found on the plasmids confer resistance to most of the antibiotic classes used nowadays, for example, beta-lactams, fluoroquinolones and aminoglycosides.[10]

It is very common for the resistance genes or entire resistance cassettes to be re-arranged on the same plasmid or be moved to a different plasmid or chromosome by means of recombination systems. Examples of such systems include integrons, transposons, and ISCR-promoted gene mobilization.[7]

Most of the resistance plasmids are conjugative, meaning that they encode all the needed components for the transfer of the plasmid to another bacterium,[11] and that isn't present in mobilizable plasmids. According to that, Mobilizable plasmids are smaller in size (usually < 10 kb) while conjugative plasmids are largger (usually > 30 kb) due to the considerable size of DNA required to encode the conjugation mechanisms that allow for cell-to-cell conjugation.[7]

R-factor

This section is about the plasmid. For information about the residual factor in crystallography, see R-factor (crystallography).

R-factors are also called a resistance factors, are plasmids that contain antibiotic resistance genes.[12] Resistance genes are ones that give rise to proteins that modify the antibiotic or pump it out. They are different from mutations that give bacteria resistance to antibiotics by preventing the antibiotic from getting in or changing the shape of the target protein.[13] R-factors have been known to contain up to ten resistance genes. They can also spread easily as they contain genes for constructing pili, which allow them to transfer the R-factor to other bacteria.[14] R-factors have contributed to the growing antibiotic resistance crisis because they quickly spread resistance genes amongst bacteria.[15]

Transmission

Bacteria containing F-factors (said to be "F+") have the capability for horizontal gene transfer; they can construct a sex pilus, which emerges from the donor bacterium and ensnares the recipient bacterium, draws it in, and eventually triggers the formation of a mating bridge, merging the cytoplasms of two bacteria via a controlled pore. This pore allows the transfer of genetic material, such as a plasmid. Conjugation allows two bacteria, not necessarily from the same species, to transfer genetic material one way.[16] Since many R-factors contain F-plasmids, antibiotic resistance can be easily spread among a population of bacteria. Also, R-factors can be taken up by "DNA pumps" in their membranes via transformation, or less commonly through viral mediated transduction, or via bacteriophage, although conjugation is the most common means of antibiotic resistance spread. They contain the gene called RTF (Resistance transfer factor).

Enterobacteriaceae

Escherichia coli bacteria on the right are sensitive to two beta-lactam antibiotics, and do not grow in the semi-circular regions surrounding the antibiotics. E. coli bacteria on the left are resistant to beta-lactam antibiotics, and grow next to one antibiotic (bottom) and are less inhibited by another antibiotic (top).

it is a family of Gram-negative rod-shaped (bacilli) bacteria, the pathogenic bacteria that are most frequently found in the environment and clinical cases, as a result, they are significantly impacted by the use of antibiotics in agriculture, the ecosystem, or the treatment of diseases.[17] In Enterobacteriaceae, 28 different plasmid types can be identified by PCR-based replicon typing (PBRT).The plasmids that have been frequently reported [IncF, IncI, IncA/C, IncL (previously designated IncL/M), IncN, and IncH] contain a broad variety of resistance genes.[18]

Members of family Enterobacteriaceae, for example, Escherichia coli or Klebsiella pneumoniae pose the biggest threat regarding plasmid-mediated resistance in hospital- and community-acquired infections.[5]

Beta-lactam resistance

B-lactamases are antibiotic-hydrolyzing enzymes that typically cause resistance to b-lactam antibiotics. These enzymes are prevalent in Streptomyces, and together with related enzymes discovered in pathogenic and non-pathogenic bacteria, they form the protein family known as the "b-lactamase superfamily".[19] it is hypothesized that b-lactamases also serve a double purpose, such as housekeeping and antibiotic resistance.[20]

Both narrow spectrum beta-lactamases (e.g. penicillinases) and extended spectrum beta-lactamases (ESBL) are common for resistance plasmids in Enterobacteriaceae. Often multiple beta-lactamase genes are found on the same plasmid hydrolyzing a wide spectrum of beta-lactam antibiotics.[5]

Extended spectrum beta-lactamases (ESBL)

ESBL enzymes can hydrolyze all beta-lactam antibiotics, including cephalosporins, except for the carpabepenems. The first clinically observed ESBL enzymes were mutated versions of the narrow spectrum beta-lactamases, like TEM and SHV. Other ESBL enzymes originate outside of family Enterobacteriaceae, but have been spreading as well.[5]

In addition, since the plasmids that carry ESBL genes also commonly encode resistance determinants for many other antibiotics, ESBL strains are often resistant to many non-beta-lactam antibiotics as well,[21] leaving very few options for the treatment.

Carbapenemases

Carbapenemases represent type of ESBL which are able to hydrolyze carbapenem antibiotics that are considered as the last-resort treatment for ESBL-producing bacteria. KPC, NDM-1, VIM and OXA-48 carbapenemases have been increasingly reported worldwide as causes of hospital-acquired infections.[5]

Quinolone resistance

Quinolone resistance genes are frequently located on the same plasmid as the ESBL genes. Examples of resistance mechanisms include different Qnr proteins, aminoglycose acetyltransferase aac(6')-Ib-cr that is able to hydrolyze ciprofloxacin and norfloxacin, as well as efflux transporters OqxAB and QepA.[5]

Aminoglycoside resistance

Aminoglycoside resistance genes are also commonly found together with ESBL genes. Resistance to aminoglycosides is conferred via numerous aminoglycoside-modifying enzymes and 16S rRNA methyltransferases.[5]

small RNAs

Study investigating physiological effect of pHK01 plasmid in host E.coli J53 found that the plasmid reduced bacterial motility and conferred resistance to beta-lactams. The pHK01 produced plasmid-encoded small RNAs and mediated expression of host sRNAs. These sRNAs were antisense to genes involved in replication, conjugate transfer and plasmid stabilisation : AS-repA3 (CopA), AS-traI, AS-finO, AS-traG, AS-pc02 . The over-expression of one of the plasmid-encoded antisense sRNAs: AS-traI shortened t lalog phase of host growth.[22]

References

  1. ^ San Millan A (December 2018). "Evolution of Plasmid-Mediated Antibiotic Resistance in the Clinical Context". Trends in Microbiology. 26 (12): 978–985. doi:10.1016/j.tim.2018.06.007. PMID 30049587.
  2. ^ "conjugation (prokaryotes) | Learn Science at Scitable". www.nature.com. Retrieved 6 January 2023.
  3. ^ Tsang J (May 2017). "Bacterial plasmid addiction systems and their implications for antibiotic drug development". Postdoc Journal. 5 (5): 3–9. PMC 5542005. PMID 28781980.
  4. ^ Nikaido H (1 June 2009). "Multidrug resistance in bacteria". Annual Review of Biochemistry. 78 (1): 119–146. doi:10.1146/annurev.biochem.78.082907.145923. PMC 2839888. PMID 19231985.
  5. ^ a b c d e f g Schultsz C, Geerlings S (January 2012). "Plasmid-mediated resistance in Enterobacteriaceae: changing landscape and implications for therapy". Drugs. 72 (1): 1–16. doi:10.2165/11597960-000000000-00000. PMID 22191792. S2CID 42306704.
  6. ^ Mathers AJ, Peirano G, Pitout JD (July 2015). "The role of epidemic resistance plasmids and international high-risk clones in the spread of multidrug-resistant Enterobacteriaceae". Clinical Microbiology Reviews. 28 (3): 565–591. doi:10.1128/CMR.00116-14. PMC 4405625. PMID 25926236.
  7. ^ a b c d Bennett PM (March 2008). "Plasmid encoded antibiotic resistance: acquisition and transfer of antibiotic resistance genes in bacteria". British Journal of Pharmacology. 153 (Suppl 1): S347 – S357. doi:10.1038/sj.bjp.0707607. PMC 2268074. PMID 18193080.
  8. ^ Darmancier H, Domingues CP, Rebelo JS, Amaro A, Dionísio F, Pothier J, et al. (May 2022). "Are Virulence and Antibiotic Resistance Genes Linked? A Comprehensive Analysis of Bacterial Chromosomes and Plasmids". Antibiotics. 11 (6): 706. doi:10.3390/antibiotics11060706. PMC 9220345. PMID 35740113.
  9. ^ Sevim A, Sevim E (2015). "Plasmid Mediated Antibiotic and Heavy Metal Resistance in Bacillus Strains Isolated from Soils in Rize, Turkey". Suleyman Demirel University Journal of Natural and Applied Science. 19 (2): 133–141 – via Süleyman Demirel University science Institute.
  10. ^ McMillan EA, Gupta SK, Williams LE, Jové T, Hiott LM, Woodley TA, et al. (2019). "Antimicrobial Resistance Genes, Cassettes, and Plasmids Present in Salmonella enterica Associated With United States Food Animals". Frontiers in Microbiology. 10: 832. doi:10.3389/fmicb.2019.00832. PMC 6479191. PMID 31057528.
  11. ^ Zatyka M, Thomas CM (1998). "Control of genes for conjugative transfer of plasmids and other mobile elements". FEMS Microbiology Reviews. 21 (4): 291–319. doi:10.1111/j.1574-6976.1998.tb00355.x. PMID 25481925.
  12. ^ "R-Factor". VEDANTU. Retrieved 8 January 2023.
  13. ^ Peterson E, Kaur P (2018). "Antibiotic Resistance Mechanisms in Bacteria: Relationships Between Resistance Determinants of Antibiotic Producers, Environmental Bacteria, and Clinical Pathogens". Frontiers in Microbiology. 9: 2928. doi:10.3389/fmicb.2018.02928. PMC 6283892. PMID 30555448.
  14. ^ Tao S, Chen H, Li N, Wang T, Liang W (18 July 2022). "The Spread of Antibiotic Resistance Genes In Vivo Model". The Canadian Journal of Infectious Diseases & Medical Microbiology = Journal Canadien des Maladies Infectieuses et de la Microbiologie Medicale. 2022: 3348695. doi:10.1155/2022/3348695. PMC 9314185. PMID 35898691.
  15. ^ Campbell N (2018). Biology A Global Approach (11th ed.). New York: Pearson. p. 633. ISBN 978-1-292-17043-5.
  16. ^ "Prokaryotic Cell Structure: Pili". Archived from the original on 7 December 2016. Retrieved 19 January 2017.
  17. ^ Dahal P (20 May 2022). "Enterobacteriaceae- Definition, Characteristics, Identification". Microbe Notes. Retrieved 9 January 2023.
  18. ^ Rozwandowicz M, Brouwer MS, Fischer J, Wagenaar JA, Gonzalez-Zorn B, Guerra B, et al. (May 2018). "Plasmids carrying antimicrobial resistance genes in Enterobacteriaceae". The Journal of Antimicrobial Chemotherapy. 73 (5): 1121–1137. doi:10.1093/jac/dkx488. PMID 29370371.
  19. ^ Peterson E, Kaur P (2018). "Antibiotic Resistance Mechanisms in Bacteria: Relationships Between Resistance Determinants of Antibiotic Producers, Environmental Bacteria, and Clinical Pathogens". Frontiers in Microbiology. 9: 2928. doi:10.3389/fmicb.2018.02928. PMC 6283892. PMID 30555448.
  20. ^ Baquero F, Bouza E, Gutiérrez-Fuentes J, Coque TM (January 2018). "Ecology and Evolution of Chromosomal Gene Transfer between Environmental Microorganisms and Pathogens". Microbiology Spectrum. 6 (1): 6.1.06. doi:10.1128/microbiolspec.MTBP-0006-2016. PMID 29350130. {{cite journal}}: Unknown parameter |DUPLICATE_vauthors= ignored (help)
  21. ^ Hussain T, Jamal M, Nighat F, Andleeb S (2014). "Broad spectrum antibiotics and resistance in non-target bacteria: an example from tetracycline". Journal of Pure and Applied Microbiology. 8 (4): 2667–2671.
  22. ^ Jiang X, Liu X, Law CO, Wang Y, Lo WU, Weng X, et al. (July 2017). "The CTX-M-14 plasmid pHK01 encodes novel small RNAs and influences host growth and motility". FEMS Microbiology Ecology. 93 (7). doi:10.1093/femsec/fix090. PMID 28854680.

Further reading


Retrieved from "https://en.wikipedia.org/w/index.php?title=Plasmid-mediated_resistance&oldid=1132626608"