title: Lethal infection by Bordetella pertussis mutants in the infant mouse model.
abstract: Different aspects of lethal infection of infant mice with Bordetella pertussis were examined. Mutants deficient in vir-regulated genes were tested for the ability to cause a lethal infection in the infant mouse model. Adenylate cyclase toxin-hemolysin and pertussis toxin were required to cause a lethal infection at low doses. Mixed infection caused by challenging the mice with an equal number of pertussis toxin and adenylate cyclase toxin-hemolysin mutants at a dose at which neither alone was lethal was also unable to cause a lethal infection. Production of the filamentous hemagglutinin and the dermonecrotic toxin was not required to cause a lethal infection. Nine other mutants in vir-regulated genes whose phenotypes have yet to be determined were also tested. Only two of these mutants were impaired in the ability to cause a lethal infection. Expression of fimbriae does not appear to affect the dose required to cause a lethal infection; however, fimbrial expression was correlated with the later stages of a nonlethal, persistent infection. Growth of the bacteria in MgSO4, a condition which reversibly suppresses expression of the genes required for virulence, did not alter the ability of the bacteria to cause a lethal infection. Auxotrophic mutants deficient in leucine biosynthesis were as virulent as the parental strain; however, mutants deficient in methionine biosynthesis were less virulent. A B. parapertussis strain was much less effective in promoting a lethal infection than any of the wild-type B. pertussis strains examined. A persistent infection in the lungs was observed for weeks after challenge for mice given a sublethal dose of B. pertussis, and transmission from infected infants to the mother was never observed.
authors.affiliation: Department of Microbiology and Immunology, Medical College of Virginia, Richmond 23298.
authors.forename: A A
authors.initials: AA
authors.lastname: Weiss
authors.forename: M S
authors.initials: MS
authors.lastname: Goodwin
mesh_terms: D037361:Adenylate Cyclase Toxin; D000262:Adenylyl Cyclases / Q000235:genetics; D000818:Animals; D001885:Bordetella Infections / Q000382:microbiology*; D001886:Bordetella pertussis / Q000235:genetics / Q000472:pathogenicity*; D004252:DNA Mutational Analysis; D010861:Fimbriae, Bacterial / Q000276:immunology; D005798:Genes, Bacterial; D005816:Genetic Complementation Test; D006460:Hemolysin Proteins / Q000235:genetics; D051379:Mice; D008807:Mice, Inbred BALB C; D037342:Pertussis Toxin; D012703:Serotyping; D010566:Virulence Factors, Bordetella / Q000235:genetics
chemical_list: D037361:Adenylate Cyclase Toxin; D006460:Hemolysin Proteins; D010566:Virulence Factors, Bordetella; D037342:Pertussis Toxin; D000262:Adenylyl Cyclases