File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Facilitation of horizontal transfer of antimicrobial resistance by transformation of antibiotic-induced cell-wall-deficient bacteria

TitleFacilitation of horizontal transfer of antimicrobial resistance by transformation of antibiotic-induced cell-wall-deficient bacteria
Authors
Issue Date2003
PublisherChurchill Livingstone. The Journal's web site is located at http://www.elsevier.com/locate/mehy
Citation
Medical Hypotheses, 2003, v. 61 n. 4, p. 503-508 How to Cite?
AbstractIt is universally accepted that the use of antibiotics will lead to antimicrobial resistance. Traditionally, the explanation to this phenomenon was random mutation and horizontal gene transfer and amplification by selective pressure. Subsequently, a second mechanism of antibiotic-induced antimicrobial resistance acquisition was proposed, when Davies et al. discovered that genes encoding antimicrobial resistance are present in bacteria that produce antibiotics, and during the process of antibiotic purification from these antibiotic-producing organisms, remnants of the organisms' DNA that contain antibiotic resistance genes are also co-extracted, and can be recovered in antibiotic preparations. In addition to selective pressure and antimicrobial resistance genes in antibiotic preparations, we hypothesize the third mechanism by which administration of antibiotics leads to antimicrobial resistance. β-Lactams and glycopeptides damage bacteria by inhibiting cell wall murein synthesis. During the process, cell-wall-deficient forms are generated before the bacteria die. These cell-wall-deficient forms have an increased ability to uptake DNA by transformation. It has been demonstrated that plasmids encoding antimicrobial resistance of Staphylococcus aureus can be transformed to Bacillus subtilis after the B. subtilis was treated with penicillin or lysostaphin, a chemical that damage the cell walls of some Gram-positive bacteria; and that short treatment of Escherichia coli with antibiotics disturbing bacterial cell wall synthesis rendered the cells capable of absorbing foreign DNA. Since bacteria occupying the same ecological niche, such as the lower gastrointestinal tract, is common, bacteria are often incubated with foreign DNA encoding resistance coming from the administration of antibiotics or other bacteria that undergone lysis unrelated to antibiotic-induced killing. As few as a single antibiotic resistant gene is taken up by the cell-wall-deficient form, it will develop into a resistant clone, despite most of the other bacteria are killed by the antibiotic. If the hypothesis is correct, one should reduce the use of antibiotics that perturb bacterial cell wall synthesis, such as β-lactams, which is the largest group being manufactured, in both humans and animals, in order to reduce the acquisition of antibiotic resistance through this mechanism. In contrast to the old theory that antibiotics only provide selective pressures for the development of antimicrobial resistance, antibiotics by themselves are able to generate the whole chain of events towards the development of antimicrobial resistance. Antibiotics provide a source of antimicrobial resistance genes, facilitate the horizontal transfer of antimicrobial resistance genes through facilitating transformation, and provide selective pressures for amplification of the antimicrobial resistance genes. That is perhaps an important reason why antimicrobial resistance is so difficult to control. Further experiments should be performed to delineate which particular type of β-lactam antibiotics are associated with increase in transformation efficiencies more than the others, so that we can select those less resistance generating β-lactam for routine usage. © 2003 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/78964
ISSN
2015 Impact Factor: 1.136
2015 SCImago Journal Rankings: 0.464
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWoo, PCYen_HK
dc.contributor.authorTo, APCen_HK
dc.contributor.authorLau, SKPen_HK
dc.contributor.authorYuen, KYen_HK
dc.date.accessioned2010-09-06T07:48:56Z-
dc.date.available2010-09-06T07:48:56Z-
dc.date.issued2003en_HK
dc.identifier.citationMedical Hypotheses, 2003, v. 61 n. 4, p. 503-508en_HK
dc.identifier.issn0306-9877en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78964-
dc.description.abstractIt is universally accepted that the use of antibiotics will lead to antimicrobial resistance. Traditionally, the explanation to this phenomenon was random mutation and horizontal gene transfer and amplification by selective pressure. Subsequently, a second mechanism of antibiotic-induced antimicrobial resistance acquisition was proposed, when Davies et al. discovered that genes encoding antimicrobial resistance are present in bacteria that produce antibiotics, and during the process of antibiotic purification from these antibiotic-producing organisms, remnants of the organisms' DNA that contain antibiotic resistance genes are also co-extracted, and can be recovered in antibiotic preparations. In addition to selective pressure and antimicrobial resistance genes in antibiotic preparations, we hypothesize the third mechanism by which administration of antibiotics leads to antimicrobial resistance. β-Lactams and glycopeptides damage bacteria by inhibiting cell wall murein synthesis. During the process, cell-wall-deficient forms are generated before the bacteria die. These cell-wall-deficient forms have an increased ability to uptake DNA by transformation. It has been demonstrated that plasmids encoding antimicrobial resistance of Staphylococcus aureus can be transformed to Bacillus subtilis after the B. subtilis was treated with penicillin or lysostaphin, a chemical that damage the cell walls of some Gram-positive bacteria; and that short treatment of Escherichia coli with antibiotics disturbing bacterial cell wall synthesis rendered the cells capable of absorbing foreign DNA. Since bacteria occupying the same ecological niche, such as the lower gastrointestinal tract, is common, bacteria are often incubated with foreign DNA encoding resistance coming from the administration of antibiotics or other bacteria that undergone lysis unrelated to antibiotic-induced killing. As few as a single antibiotic resistant gene is taken up by the cell-wall-deficient form, it will develop into a resistant clone, despite most of the other bacteria are killed by the antibiotic. If the hypothesis is correct, one should reduce the use of antibiotics that perturb bacterial cell wall synthesis, such as β-lactams, which is the largest group being manufactured, in both humans and animals, in order to reduce the acquisition of antibiotic resistance through this mechanism. In contrast to the old theory that antibiotics only provide selective pressures for the development of antimicrobial resistance, antibiotics by themselves are able to generate the whole chain of events towards the development of antimicrobial resistance. Antibiotics provide a source of antimicrobial resistance genes, facilitate the horizontal transfer of antimicrobial resistance genes through facilitating transformation, and provide selective pressures for amplification of the antimicrobial resistance genes. That is perhaps an important reason why antimicrobial resistance is so difficult to control. Further experiments should be performed to delineate which particular type of β-lactam antibiotics are associated with increase in transformation efficiencies more than the others, so that we can select those less resistance generating β-lactam for routine usage. © 2003 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherChurchill Livingstone. The Journal's web site is located at http://www.elsevier.com/locate/mehyen_HK
dc.relation.ispartofMedical Hypothesesen_HK
dc.subject.meshAnti-Bacterial Agents - pharmacologyen_HK
dc.subject.meshBacteria - drug effectsen_HK
dc.subject.meshCell Wall - physiologyen_HK
dc.subject.meshDrug Resistance, Bacterialen_HK
dc.subject.meshDrug Resistance, Microbialen_HK
dc.subject.meshGene Transfer, Horizontalen_HK
dc.subject.meshModels, Theoreticalen_HK
dc.subject.meshMutationen_HK
dc.titleFacilitation of horizontal transfer of antimicrobial resistance by transformation of antibiotic-induced cell-wall-deficient bacteriaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0306-9877&volume=61&spage=503&epage=8&date=2003&atitle=Facilitation+of+horizontal+transfer+of+antimicrobial+resistance+by+transformation+of+antibiotic-induced+cell-wall-deficient+bacteriaen_HK
dc.identifier.emailWoo, PCY:pcywoo@hkucc.hku.hken_HK
dc.identifier.emailLau, SKP:skplau@hkucc.hku.hken_HK
dc.identifier.emailYuen, KY:kyyuen@hkucc.hku.hken_HK
dc.identifier.authorityWoo, PCY=rp00430en_HK
dc.identifier.authorityLau, SKP=rp00486en_HK
dc.identifier.authorityYuen, KY=rp00366en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0306-9877(03)00205-6en_HK
dc.identifier.pmid13679020-
dc.identifier.scopuseid_2-s2.0-0345598877en_HK
dc.identifier.hkuros87978en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0345598877&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume61en_HK
dc.identifier.issue4en_HK
dc.identifier.spage503en_HK
dc.identifier.epage508en_HK
dc.identifier.isiWOS:000185699800017-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridWoo, PCY=7201801340en_HK
dc.identifier.scopusauthoridTo, APC=36828058300en_HK
dc.identifier.scopusauthoridLau, SKP=7401596211en_HK
dc.identifier.scopusauthoridYuen, KY=36078079100en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats