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Infection and Immunity, November 1998, p. 5244-5251, Vol. 66, No. 11
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Bordetella avium Virulence Measured In Vivo and In Vitro

Louise M. Temple,1 Alison A. Weiss,2,dagger Kimberly E. Walker,2,Dagger H. John Barnes,3,4 Vern L. Christensen,5 David M. Miyamoto,1 Celia B. Shelton,4 and Paul E. Orndorff4,*

Department of Biology, Drew University, Madison, New Jersey 079401; Department of Microbiology and Immunology, Medical College of Virginia, Richmond, Virginia 232982; and Department of Food Animal and Equine Medicine,3 Department of Poultry Science,5 and Department of Microbiology, Pathology, and Parasitology, College of Veterinary Medicine,4 North Carolina State University, Raleigh, North Carolina 27606

Received 23 April 1998/Returned for modification 4 June 1998/Accepted 24 August 1998

Bordetella avium causes an upper-respiratory-tract disease called bordetellosis in birds. Bordetellosis shares many of the clinical and histopathological features of disease caused in mammals by Bordetella pertussis and Bordetella bronchiseptica. In this study we determined several parameters of infection in the domestic turkey, Meleagris galapavo, and compared these in vivo findings with an in vitro measure of adherence using turkey tracheal rings. In the in vivo experiments, we determined the effects of age, group size, infection duration, and interindividual spread of B. avium. Also, the effect of host genetic background on susceptibility was tested in the five major commercial turkey lines by infecting each with the parental B. avium strain and three B. avium insertion mutants. The mutant strains lacked either motility, the ability to agglutinate guinea pig erythrocytes, or the ability to produce 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 between inoculation and tracheal culture was optimal, since an avirulent mutant (unable to produce dermonecrotic toxin) persisted for a shorter time. Communicability of the B. avium parental strain between confined birds was modest, but a nonmotile mutant was less able to spread between birds. There were no host-associated differences in susceptibility to the parental strain and the three B. avium mutant strains just mentioned: in all turkey lines tested, the dermonecrotic toxin- and hemagglutination-negative mutants were avirulent whereas the nonmotile mutants showed no loss of virulence. Interestingly, the ability of a strain to cause disease in vivo correlated completely with its ability to adhere to ciliated tracheal cells in vitro.

* Corresponding author. Mailing address: Department of Microbiology, Pathology, and Parasitology, North Carolina State University, College of Veterinary Medicine, Raleigh, NC 27606. Phone: (919) 829-4207. Fax: (919) 829-4455. E-mail: Paul_Orndorff{at}ncsu.edu.

dagger Present address: Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati, Cincinnati, OH 45267.

Dagger Present address: Center for Vaccine Development, Baltimore, MD 21201.

Infection and Immunity, November 1998, p. 5244-5251, Vol. 66, No. 11
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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Copyright © 1998 by the American Society for Microbiology. All rights reserved.