Skip Navigation

This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (34)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Courvalin, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Courvalin, P.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Journal of Antimicrobial Chemotherapy (1996) 37, 855-869
© 1996 The British Society for Antimicrobial Chemotherapy

other

The Garrod Lecture Evasion of antibiotic action by bacteria

P. Courvalin*

Department of Biology, University of California San Diego 9500 Gilman Drive, La Jolla, CA 92093-0116, USA

Received 18 October 1995; accepted 22 January 1996

Antibiotics have reduced the mortality from infectious diseases but not the prevalence of these diseases. Use, and often abuse, of antimicrobial agents encourages the evolution of bacteria toward resistance, often resulting in therapeutic failure. This evolution is due to the emergence of ‘new’ resistance mechanisms and to the spread of well-characterized mechanisms of resistance to the majority of bacterial species. Bacterial resistance can be intrinsic or acquired. Intrinsic resistance is species or genus specific and delineates the spectrum of activity of the antibiotic. Acquired resistance is present in only certain strains of a species or of a genus. The latter results from mutation in a gene located in the host chromosome or a plasmid or from acquisition of new genetic information by a bacterium, mainly by conjugation or transformation. In this review, recent developments in the understanding of biochemical mechanisms and the genetics of resistance is considered for the clinically important antibiotic families.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J Antimicrob ChemotherHome page
D. Metcalf, C. Robinson, D. Devine, and S. Wood
Enhancement of erythrosine-mediated photodynamic therapy of Streptococcus mutans biofilms by light fractionation
J. Antimicrob. Chemother., July 1, 2006; 58(1): 190 - 192.
[Abstract] [Full Text] [PDF]

Home page
 J Antimicrob ChemotherHome page
S. Wood, D. Metcalf, D. Devine, and C. Robinson
Erythrosine is a potential photosensitizer for the photodynamic therapy of oral plaque biofilms
J. Antimicrob. Chemother., April 1, 2006; 57(4): 680 - 684.
[Abstract] [Full Text] [PDF]

Home page
 BMJHome page
S. G B Amyes
Treatment of staphylococcal infection
BMJ, April 30, 2005; 330(7498): 976 - 977.
[Full Text] [PDF]

Home page
 J Antimicrob ChemotherHome page
P. E. Varaldo
Antimicrobial resistance and susceptibility testing: an evergreen topic
J. Antimicrob. Chemother., July 1, 2002; 50(1): 1 - 4.
[Full Text] [PDF]

Home page
 J Med MicrobiolHome page
G. RAPONI, M. C. GHEZZI, M. T. LUN, G. BIGOTTI, P. G. NATALI, and C. MANCINI
Protective features of monoclonal antibodies to Escherichia coli during experimental infection of mice with homologous and heterologous serotypes of E. coli
J. Med. Microbiol., March 1, 2000; 49(3): 253 - 260.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.