[Cu,Zn]-Superoxide dismutase mutants of the swine pathogen Actinobacillus pleuropneumoniae are unattenuated in infections of the natural host.
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.
Sheehan
B J
BJ
Molecular Infectious Diseases Group, Department of Paediatrics, Imperial College School of Medicine, St. Mary's Campus, London W2 1PG, United Kingdom.
Langford
P R
PR
Rycroft
A N
AN
Kroll
J S
JS
D000189:Actinobacillus Infections / Q000662:veterinary*; D016977:Actinobacillus pleuropneumoniae / Q000201:enzymology / Q000235:genetics / Q000472:pathogenicity*; D000818:Animals; D008168:Lung / Q000473:pathology; D016254:Mutagenesis, Insertional; D011001:Pleuropneumonia / Q000662:veterinary*; D013482:Superoxide Dismutase / Q000235:genetics*; D013481:Superoxides / Q000494:pharmacology; D013552:Swine; D013553:Swine Diseases / Q000382:microbiology*; D014886:Weaning
D013481:Superoxides; D013482:Superoxide Dismutase