title: Comparison of the course of infection of virulent Yersinia enterocolitica serotype O:8 with an isogenic sodA mutant in the peroral rabbit model.
abstract: Peroral infections of rabbits with a virulent Yersinia enterocolitica serotype O:8 wild-type strain (WA-314) and its isogenic Mn-cofactored superoxide dismutase (sodA) mutant were analyzed with respect to the following parameters: clinical findings, bacterial ability to colonize and persist in different tissues, bacterial resistance to the killing effect of leukocytes and blood sera, IgG antibody response, pathomorphological and immunomorphological changes. In comparison to WA-314, the sodA mutant was markedly impaired in its ability to disseminate into the brain and viscera, and to cause hyperthermia, leukocytosis with monocytosis, granulocytosis and initial lymphopenia. The sodA mutant strain was more susceptible to bactericidal activity of leukocytes and blood sera than the parent strain WA-314. Moreover, in comparison to WA-314, the sodA mutant was attenuated for mice after oral, intravenous, and intraperitoneal inoculation and totally avirulent for rats. Strikingly, the sodA mutation led not only to attenuation of virulence but also enhanced immunogenicity (as reflected by the specific antibody response). These features are consistent with the mild immunomorphological changes observed after infection with the sodA mutant as compared to the severe tissue lesions caused by the virulent strain WA-314. In conclusion, this study demonstrates that the sodA mutation in Y. enterocolitica leads to loss of virulence and gain of immunogenicity in rabbits. These are promising features for a live oral vaccine carrier strain.
authors.affiliation: The Stephan Angeloff Institute of Microbiology, Bulgarian Academy of Sciences, Acad G. Bontchev Str. 26, 1113 Sofia, Bulgaria. usema@bas.bg
authors.forename: Hristo M
authors.initials: HM
authors.lastname: Najdenski
authors.forename: Elica N
authors.initials: EN
authors.lastname: Golkocheva
authors.forename: Anna M
authors.initials: AM
authors.lastname: Vesselinova
authors.forename: Holger
authors.initials: H
authors.lastname: Rüssmann
mesh_terms: D000284:Administration, Oral; D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D001770:Blood Bactericidal Activity; D001921:Brain / Q000382:microbiology; D004195:Disease Models, Animal; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D051379:Mice; D008813:Mice, Inbred ICR; D009154:Mutation; D011817:Rabbits; D051381:Rats; D017208:Rats, Wistar; D012703:Serotyping; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism*; D014774:Virulence; D014781:Viscera / Q000382:microbiology; D015009:Yersinia Infections / Q000276:immunology / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology*; D015008:Yersinia enterocolitica / Q000145:classification / Q000235:genetics / Q000276:immunology / Q000472:pathogenicity*
chemical_list: D000907:Antibodies, Bacterial; D001426:Bacterial Proteins; D007074:Immunoglobulin G; C095500:SodA protein, Bacteria; D013482:Superoxide Dismutase