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United States Department of Agriculture

Agricultural Research Service


item Register, Karen
item Brockmeier, Susan
item Magyar, Tibor

Submitted to: Research Workers in Animal Diseases Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 10/1/1999
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: The dermonecrotic toxin (DNT) of B. bronchiseptica is proposed to be a major virulence factor in swine atrophic rhinitis. However, its role during infection in vivo has not been definitively assessed. We constructed a DNT mutant from a virulent swine isolate by replacement of 1.8 Kb of the dnt gene with a kanamycin resistance cassette. Groups of 6 Caesarean-derived, colostrum-deprived piglets were inoculated at 7 days of age with the parent strain, the DNT mutant, or PBS. At 28 days PI, all pigs were necropsied. Results of nasal washes indicate that the mutant was significantly impaired in its ability to colonize the nasal cavity, both at 7 and 28 days PI (p</=0.07). Colonization of the turbinate was also significantly lower for the mutant than the parent strain (p=0.019). Levels of bacteria in the trachea and lung were similar for both groups, although gross lung lesions were evident only in pigs infected with the parent strain. B. bronchiseptica was not isolated at any time from pigs inoculated with PBS. Turbinate atrophy was minimal in pigs inoculated with PBS or the mutant (avg. nasal lesion scores of 0.67 and 0.33, respectively), while significant degeneration was noted in pigs infected with the parent strain (avg. nasal lesion score of 8.8). These results indicate DNT is required for maximum colonization of the upper respiratory tract. Additional experiments are necessary to determine whether the lack of turbinate atrophy in pigs infected with the mutant is directly due to the absence of DNT or is a reflection of the low levels of bacteria present. Although the absence of DNT has no effect on colonization of the lung, the toxin may have a direct role in the induction of lung lesions.

Last Modified: 09/21/2017
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