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Infection and Immunity, August 2000, p. 4778-4781, Vol. 68, No. 8
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.
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
*
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.
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