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.