IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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 Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sheehan, B. J.
Right arrow Articles by Kroll, J. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sheehan, B. J.
Right arrow Articles by Kroll, J. S.

 Previous Article  |  Next Article 

Infection and Immunity, August 2000, p. 4778-4781, Vol. 68, No. 8
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

[Cu,Zn]-Superoxide Dismutase Mutants of the Swine Pathogen Actinobacillus pleuropneumoniae Are Unattenuated in Infections of the Natural Host

Brian J. Sheehan,1 Paul R. Langford,1 Andrew N. Rycroft,2 and J. Simon Kroll1,*

Molecular Infectious Diseases Group, Department of Paediatrics, Imperial College School of Medicine, St. Mary's Campus, London W2 1PG,1 and Department of Pathology and Infectious Diseases, The Royal Veterinary College, University of London, North Mymms, Hatfield, Hertfordshire AL9 7TA,2 United Kingdom

Received 31 January 2000/Returned for modification 17 April 2000/Accepted 1 May 2000

Actinobacillus pleuropneumoniae, the causative agent of porcine pleuropneumonia, contains a periplasmic Cu- and Zn-cofactored superoxide dismutase ([Cu,Zn]-SOD, or SodC) which has the potential, realized in other pathogens, to promote bacterial survival during infection by dismutating host-defense-derived superoxide. Here we describe the construction of a site-specific, [Cu,Zn]-SOD-deficient A. pleuropneumoniae serotype 1 mutant and show that although the mutant is highly sensitive to the microbicidal action of superoxide in vitro, it remains fully virulent in experimental pulmonary infection in pigs.


* Corresponding author. Mailing address: Molecular Infectious Diseases Group, Department of Paediatrics, Imperial College School of Medicine, St. Mary's Campus, London W2 1PG, United Kingdom. Phone: 020 7886 6220. Fax: 020 7886 6284. E-mail: s.kroll{at}ic.ac.uk.


Infection and Immunity, August 2000, p. 4778-4781, Vol. 68, No. 8
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.



This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2000 by the American Society for Microbiology. All rights reserved.