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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.

Contributory and Exacerbating Roles of Gaseous Ammonia and Organic Dust in the Etiology of Atrophic Rhinitis

T. D. C. Hamilton,1,* J. M. Roe,1 C. M. Hayes,1 P. Jones,2 G. R. Pearson,1 and A. J. F. Webster1

Aerobiology Group, Division of Animal Health and Husbandry, Department of Clinical Veterinary Science, University of Bristol, Langford, North Somerset BS40 5DU,1 and Institute for Animal Health, Compton Laboratory, Compton, Newbury, Berkshire RG20 7NN,2 United Kingdom

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-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.



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