BORDETELLA-AVIUM VIRULENCE MEASURED IN-VIVO AND IN-VITRO

Citation
Lm. Temple et al., BORDETELLA-AVIUM VIRULENCE MEASURED IN-VIVO AND IN-VITRO, Infection and immunity (Print), 66(11), 1998, pp. 5244-5251
Citations number
40
Categorie Soggetti
Immunology,"Infectious Diseases
ISSN journal
00199567
Volume
66
Issue
11
Year of publication
1998
Pages
5244 - 5251
Database
ISI
SICI code
0019-9567(1998)66:11<5244:BVMIAI>2.0.ZU;2-J
Abstract
Bordetella avium causes an upper-respiratory-tract disease called bord etellosis in birds. Bordetellosis shares many of the clinical and hist opathological features of disease caused in mammals by Bordetella pert ussis and Bordetella bronchiseptica. In this study we determined sever al parameters of infection in the domestic turkey, Meleagris galapavo, and compared these in vivo findings with an in vitro measure of adher ence using turkey tracheal rings. In the in vivo experiments, we deter mined the effects of age, group size, infection duration, and interind ividual spread of B. avium. Also, the effect of host genetic backgroun d on susceptibility was tested in the five major commercial turkey lin es by infecting each with the parental B. avium strain and three B. av ium insertion mutants. The mutant strains lacked either motility, the ability to agglutinate guinea pig erythrocytes, or the ability to prod uce dermonecrotic toxin. The susceptibilities of 1-day-old and 1-week- old turkeys to B. avium were the same, and challenge group size (5, 8, or 10 birds) had no effect upon the 50% infectious dose. Two weeks be tween inoculation and tracheal culture was optimal, since an avirulent mutant (unable to produce dermonecrotic toxin) persisted for a shorte r time. Communicability of the B. avium parental strain between confin ed birds was modest, but a nonmotile mutant was less able to spread be tween birds. There were no host-associated differences in susceptibili ty to the parental strain and the three B. avium mutant strains just m entioned: in all turkey lines tested, the dermonecrotic toxin- and hem agglutination-negative mutants were avirulent whereas the nonmotile mu tants shelved no loss of virulence. Interestingly, the ability of a st rain to cause disease in vivo correlated completely with its ability t o adhere to ciliated tracheal cells in vitro.