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Journal of Clinical Microbiology, May 1998, p. 1260-1265, Vol. 36, No. 5
The Aerobiology Group, Division of Animal
Health and Husbandry, Department of Clinical Veterinary Science,
University of Bristol, Langford, North Somerset BS18 7DU, United
Kingdom
Received 14 October 1997/Returned for modification 15 January
1998/Accepted 29 January 1998
Pigs reared in intensive production systems are continuously
exposed to ammonia released by the microbial degradation of their excrement. Exposure to this gas has been shown to increase the severity
of the disease progressive atrophic rhinitis by facilitating colonization of the pig's upper respiratory tract by Pasteurella multocida. The etiological mechanism responsible for this synergy was investigated by studying the colonization kinetics of P. multocida enhanced by ammonia and comparing them with those
evoked by an established disease model. Three-week-old Large White
piglets were weaned and allocated to five experimental groups (groups A
to E). Pigs in groups A and B were exposed continuously to ammonia at
20 ppm for the first 2 weeks of the study. Pigs in group C were
pretreated with 0.5 ml of 1% acetic acid per nostril on days
0095-1137/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Effects of Ammonia Inhalation and Acetic Acid
Pretreatment on Colonization Kinetics of Toxigenic Pasteurella
multocida within Upper Respiratory Tracts of Swine
2 and
1 of the study. On day 0 all the pigs in groups A, C, and D were
inoculated with 1.4 × 108 toxigenic P. multocida organisms given by the intranasal route. The kinetics
of P. multocida colonization were established by testing
samples obtained at weekly intervals throughout the study. The study
was terminated on day 37, and the extent of turbinate atrophy was
determined by using a morphometric index. The results of the study
showed that exposure to aerial ammonia for a limited period had a
marked effect on the colonization of toxigenic P. multocida
in the nasal cavities of pigs, which resulted in the almost total
exclusion of commensal flora. In contrast, ammonia had only a limited
effect on P. multocida colonization at the tonsil. The
exacerbation of P. multocida colonization by ammonia was
restricted to the period of ammonia exposure, and the number of
P. multocida organisms colonizing the upper respiratory
tract declined rapidly upon the cessation of exposure to ammonia.
During the exposure period, the ammonia levels in mucus recovered from the nasal cavity and tonsil were found to be 7- and 3.5-fold higher, respectively, than the levels in samples taken from unexposed controls.
Acetic acid pretreatment also induced marked colonization of the nasal
cavity which, in contrast to that induced by ammonia, persisted
throughout the time course of the study. Furthermore, acetic acid
pretreatment induced marked but transient colonization of the tonsil.
These findings suggest that the synergistic effect of ammonia acts
through an etiological mechanism different from that evoked by acetic
acid pretreatment. A strong correlation was found between the numbers
of P. multocida organisms isolated from the nasal cavity
and the severity of clinical lesions, as determined by using a
morphometric index. The data presented in the paper highlight the
potential importance of ammonia as an exacerbating factor in
respiratory disease of intensively reared livestock.
*
Corresponding author. Mailing address: The Aerobiology
Group, Division of Animal Health and Husbandry, Department of Clinical Veterinary Science, University of Bristol, Langford, North Somerset BS18 7DU, United Kingdom. Phone: (01179) 289338. Fax: (01934) 853443. E-mail: Tim.Hamilton{at}bris.ac.uk.
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