Affiliation:
1. Aerobiology Group, Division of Animal Health and Husbandry, Department of Clinical Veterinary Science, University of Bristol, Langford, North Somerset BS40 5DU,1 and
2. Institute for Animal Health, Compton Laboratory, Compton, Newbury, Berkshire RG20 7NN,2 United Kingdom
Abstract
ABSTRACT
Pigs reared commercially indoors are exposed to air heavily contaminated with particulate and gaseous pollutants. Epidemiological surveys have shown an association between the levels of these pollutants and the severity of lesions associated with the upper respiratory tract disease of swine atrophic rhinitis. This study investigated the role of aerial pollutants in the etiology of atrophic rhinitis induced by
Pasteurella multocida
. Forty, 1-week-old Large White piglets were weaned and divided into eight groups designated A to H. The groups were housed in Rochester exposure chambers and continuously exposed to the following pollutants: ovalbumin (groups A and B), ammonia (groups C and D), ovalbumin plus ammonia (groups E and F), and unpolluted air (groups G and H). The concentrations of pollutants used were 20 mg m
−3
total mass and 5 mg m
−3
respirable mass for ovalbumin dust and 50 ppm for ammonia. One week after exposure commenced, the pigs in groups A, C, E, and G were infected with
P. multocida
type D by intranasal inoculation. After 4 weeks of exposure to pollutants, the pigs were killed and the extent of turbinate atrophy was assessed with a morphometric index (MI). Control pigs kept in clean air and not inoculated with
P. multocida
(group H) had normal turbinate morphology with a mean MI of 41.12% (standard deviation [SD], ± 1.59%). In contrast, exposure to pollutants in the absence of
P. multocida
(groups B, D, and F) induced mild turbinate atrophy with mean MIs of 49.65% (SD, ±1.96%), 51.04% (SD, ±2.06%), and 49.88% (SD, ±3.51%), respectively. A similar level of atrophy was also evoked by inoculation with
P. multocida
in the absence of pollutants (group G), giving a mean MI of 50.77% (SD, ±2.07%). However, when
P. multocida
inoculation was combined with pollutant exposure (groups A, C, and E) moderate to severe turbinate atrophy occurred with mean MIs of 64.93% (SD, ±4.64%), 59.18% (SD, ±2.79%), and 73.30% (SD, ±3.19%), respectively. The severity of atrophy was greatest in pigs exposed simultaneously to dust and ammonia. At the end of the exposure period, higher numbers of
P. multocida
bacteria were isolated from the tonsils than from the nasal membrane, per gram of tissue. The severity of turbinate atrophy in inoculated pigs was proportional to the number of
P. multocida
bacteria isolated from tonsils (
r
2
= 0.909,
P
< 0.05) and nasal membrane (
r
2
= 0.628,
P
< 0.05). These findings indicate that aerial pollutants contribute to the severity of lesions associated with atrophic rhinitis by facilitating colonization of the pig’s upper respiratory tract by
P. multocida
and also by directly evoking mild atrophy.
Publisher
American Society for Microbiology
Subject
Microbiology (medical),Clinical Biochemistry,Immunology,Immunology and Allergy
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