Previous Article | Next Article ![]()
Clinical and Diagnostic Laboratory Immunology, March 1999, p. 199-203, Vol. 6, No. 2
Aerobiology Group,
Received 1 June 1998/Returned for modification 17 July
1998/Accepted 11 December 1998
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
1071-412X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Contributory and Exacerbating Roles of Gaseous
Ammonia and Organic Dust in the Etiology of Atrophic Rhinitis
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
(r2 = 0.909, P < 0.05) and
nasal membrane (r2 = 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.
*
Corresponding author. Mailing address: Aerobiology
Group, Division of Animal Health and Husbandry, Department of Clinical Veterinary Science, University of Bristol, Langford, North Somerset BS40 5DU, United Kingdom. Phone: 44 (0) 1179 289478. Fax: 44 (0) 1179 289612. E-mail: Tim.Hamilton{at}bris.ac.uk.
Clinical and Diagnostic Laboratory Immunology, March 1999, p. 199-203, Vol. 6, No. 2
1071-412X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»