RESISTANCE OF SWINE TO BORDETELLA RHINITIS 
W. p. Switzer* 
Knowledge of the mechanisms of resistance to bac- 
terial and mycoplasmal infections of the respiratory 
tract of man and animals has developed more slowly 
than our knowledge of respiratory resistance to viral 
infections. This is probably due to our lack of under- 
standing of the processes by which these larger, extra- 
cellular microorganisms attach to the epithelial surfaces 
and resist removal by mucociliary action and to our 
lack of information about the ability of substances pro- 
duced by the host to prevent this initial colonization. 
INTRODUCTION 
Swine are an excellent model for the study of 
respiratory tract resistance to bacterial and 
mycoplasmal diseases. Both classes of organ- 
isms produce economically significant, wide- 
spread, chronic respiratory infections in 
swine. In spite of this, it has been demon- 
strated that at least in the case of one chronic 
bacterial infection, the respiratory surface is 
capable of developing a remarkable resistance 
to reinfection.^ 
A discussion of this specific bacterial infec- 
tion, i.e. bordetella rhinitis will illustrate some 
of the aspects of this experimental model. 
DISCUSSION 
Bordetella rhinitis of swine is a chronic dis- 
ease due to infection of the respiratory system 
with Bordetella bronchiseptica. The infecting 
bacterium is not exclusively a swine strain since 
isolates from several species of animals have 
been demonstrated to infect swine." On initial 
infection the organism may colonize any level 
of the respiratory tract but it is most likely to 
colonize the tracheal and nasal epithelium.*' It 
remains localized primarily on the epithelial 
surface and does not usually invade the tissue. 
Even though it is localized on the surface, it 
* Veterinary Medical Research Institute, Iowa State University, 
Ames, Iowa 50010. 
exerts an eftect on deeped tissues, especially the 
osteocytes and osteoblasts of the nasal turbinate 
bones. This is manifested as a progressive re- 
sorption and hypoplasia (atrophic rhinitis). 
There is also a fibroplastic reaction in the sub- 
mucosa and a metaplasia and hyperplasia of 
the epithelium. These lesions are believed to be 
the result of a diffusable endotoxin-like material 
produced by the microcolonies localized on the 
surface.! The specific action of this diffusable 
product on the osteoblasts and osteocytes may 
be similar to its demonstrated ability to impair 
mitochrondial membrane function. ^i'^" *'^ 
Recovery of infected swine usually proceeds 
so that the lung and tracheal infection is elimi- 
nated before the nasal infection is cleared. It 
has been suggested that the ethmoid crypts are 
among the last areas of the nasal cavity to elimi- 
nate this infection.!^ Since the organisms are 
localized primarily on the epithelial surface and 
since the nasal cavity is accessible to nasal sam- 
ple collection, the infection can be followed by 
collection and culturing of nasal samples. 
The natural history of this disease in a group 
of comparably aged pigs housed together gives 
an insight into the spread/and recovery from 
this infection as determined by recovery of the 
organisms from nasal swabs. The anticipated 
rate of recovery is given in Figure 1. The actual 
recovery observed in a group of naturally in- 
fected pigs is given in Figure 2.^ Study of these 
figures reveal that some of the baby pigs be- 
come infected within the first week of life by 
exposure to chronically infected dams. These 
young pigs serve as good aerosol transmitters 
and establish an aerosol epizootic within the 
group of closely housed young pigs. For this 
reason, naturally infected pigs sampled at 4 
to 10 weeks of age have the highest percent of 
infected pigs as well as the greatest numbers of 
B. bronchiseptica present. 
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