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Abstract

Objective

To document airborne transmission of Actinobacillus pleuropneumoniae and porcine reproductive and respiratory syndrome virus (PRRSV) infection in nursery pigs.

Animals

32 two-week-old pigs obtained from 3 farms, but with similar Landrace × Yorkshire genetics for trial 1 of each experiment; 16 pigs for trial 2 of the A pleuropneumoniae experiment; and 14 pigs for trial 2 of the PRRSV experiment.

Procedure

In experiment 1, pigs were inoculated with A pleuropneumoniae serotype 1 (6/8) or were left as contacts (2/8). At the beginning of trial 1, pigs were seronegative to A pleuropneumoniae serotypes 1 and 5 on the basis of results of an ELISA, but had positive results on the A pleuropneumoniae hemolysin I (Apx1)-neutralization test. Pigs in trial 2 had negative results on both tests. Pigs of trial 1 of experiment 2 were inoculated with a PRRSV virulent field isolate (MN-1b); pigs of trial 2 were inoculated with the virus reference strain VR-2332. Aerosol-exposed pigs were placed on the other side of the air duct and kept there for 2 to 7 weeks depending on evidence of airborne transmission.

Results

In trial 1 of experiment 1, evidence of airborne transmission was not found. In trial 2, most airborne-exposed pigs died as a result of A pleuropneumoniae infection 12 days after initiation of the experiment. In trial 1 of experiment 2, all inoculated pigs (8/8) seroconverted, but only 2 of 8 contact-exposed pigs seroconverted. Aerosol-exposed pigs did not seroconvert nor was virus isolated. In trial 2, all inoculated and contact-exposed pigs seroconverted. All aerosol-exposed pigs seroconverted after 21 days, and virus was isolated at 16 days.

Conclusions

A pleuropneumoniae was transmitted by air at a distance of 1 m when pigs were fully susceptible to the organism. Transmission of PRRSV appeared to be strain dependent; when reference strain VR-2332 was used, airborne transmission of PRRSV was documented. (Am J Vet Res 1997;58:828–832)

Free access
in American Journal of Veterinary Research

Abstract

Objective—To establish a model for inheritance of gluten-sensitive enteropathy (GSE) in Irish Setters.

Animals—44 dogs of a 6-generation family of Irish Setters with GSE and 7 healthy Irish Setters.

Procedure—Phenotype of each dog was determined after oral administration of gluten in the weaning diet, using morphometric evaluation of jejunal biopsies (all generations) and measurement of small intestinal permeability by use of a lactulose-rhamnose permeation test (generations 1, 2, and 3). Overall probability for each of 4 genetic models of inheritance (autosomal recessive, autosomal dominant, sex-linked recessive, and sex-linked dominant) accounting for segregation of partial villus atrophy within the entire family was calculated.

Results—The autosomal recessive model was most tenable and was 56,250 times more likely to account for segregation of partial villus atrophy than the autosomal dominant model, assuming disease prevalence of 0.8%. Both sex-linked models were untenable. These conclusions were robust to the error attached to estimation of disease prevalence. High intestinal permeability without morphometric jejunal abnormalities in 4 of 20 dogs in the 3 youngest generations suggested heterogeneity of lesions associated with GSE.

Conclusions—Genetic transmission of GSE is under the control of a single major autosomal recessive locus. (Am J Vet Res 2000;61:462–468)

Full access
in American Journal of Veterinary Research