title: Histopathologic changes in kidney and liver correlate with streptococcal pyrogenic exotoxin B production in the mouse model of group A streptococcal infection.
abstract: Previous studies show that isogenic mutants deficient in streptococcal pyrogenic exotoxin B (SPE B) cause less mortality and skin tissue damage than wild-type strains of Streptococcus pyogenes when inoculated into mice via an air pouch. In this study, the growth and dissemination of bacteria, pathologic changes in various organs, and their correlation with SPE B production were examined. Bacterial numbers in the air pouch from wild-type strain NZ131-infected mice increased at 48 h, while those from speB mutant SW510-infected mice continuously reduced. Mice infected with NZ131 developed bacteremia and greater dissemination in the kidney, liver, and spleen; those infected with SW510 showed either no or slight bacteremia and dissemination. Co-inoculation of SW510 with recombinant SPE B showed a higher bacterial count in the air pouch, bacteremia, and organ dissemination compared to co-inoculation with a C192S mutant lacking protease activity. The histopathologic changes examined showed lesions in kidney and liver in the NZ131-infected but not in SW510-infected mice. The elevation in sera of BUN, AST, and ALT correlated positively with renal and liver impairment. Taken together, SPE B produced during S. pyogenes infection plays a pathogenic role. A direct effect of SPE B on vessel permeability change was also demonstrated.
authors.affiliation: Department of Nursing, I-Shou University, Kaohsiung, Taiwan.
authors.forename: Chih-Feng
authors.initials: CF
authors.lastname: Kuo
authors.forename: Yueh-Hsia
authors.initials: YH
authors.lastname: Luo
authors.forename: Hsiu-Yueh
authors.initials: HY
authors.lastname: Lin
authors.forename: Kuen-Jeng
authors.initials: KJ
authors.lastname: Huang
authors.forename: Jiunn-Jong
authors.initials: JJ
authors.lastname: Wu
authors.forename: Huan-Yao
authors.initials: HY
authors.lastname: Lei
authors.forename: Ming T
authors.initials: MT
authors.lastname: Lin
authors.forename: Woei-Jer
authors.initials: WJ
authors.lastname: Chuang
authors.forename: Ching-Chuan
authors.initials: CC
authors.lastname: Liu
authors.forename: Ying-Tai
authors.initials: YT
authors.lastname: Jin
authors.forename: Yee-Shin
authors.initials: YS
authors.lastname: Lin
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D016470:Bacteremia; D001426:Bacterial Proteins; D001806:Blood Urea Nitrogen; D002199:Capillary Permeability; D015169:Colony Count, Microbial; D004195:Disease Models, Animal; D005098:Exotoxins / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D017353:Gene Deletion; D005798:Genes, Bacterial; D007668:Kidney / Q000382:microbiology / Q000473:pathology*; D008099:Liver / Q000382:microbiology / Q000473:pathology*; D008565:Membrane Proteins; D051379:Mice; D008807:Mice, Inbred BALB C; D016254:Mutagenesis, Insertional; D020125:Mutation, Missense; D010447:Peptide Hydrolases / Q000235:genetics / Q000502:physiology; D013154:Spleen / Q000382:microbiology / Q000473:pathology; D013290:Streptococcal Infections / Q000235:genetics / Q000382:microbiology* / Q000473:pathology*; D013297:Streptococcus pyogenes / Q000235:genetics / Q000254:growth & development / Q000472:pathogenicity*
chemical_list: D001426:Bacterial Proteins; D005098:Exotoxins; D008565:Membrane Proteins; C117980:SpeA protein, Streptococcus pyogenes; C027951:erythrogenic toxin; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D010447:Peptide Hydrolases