The purpose of this study was to experimentally reproduce swine infertility and respiratory syndrome (SIRS). Six multiparous sows were intranasally inoculated at 93 days of gestation with lung homogenates from clinically affected pigs, and 3 additional sows were similarly inoculated with a virus isolated in cell culture from the lung homogenate (SIRS virus, isolate ATCC VR-2332). Inoculated sows developed transient anorexia, farrowed up to 7 days prematurely, and delivered a mean of 5.8 live pigs and 6.0 dead fetuses/litter. Clinical signs of disease were not observed in 3 sham-inoculated control sows that delivered a mean of 12.7 live pigs and 0.3 stillborn fetuses/litter. The sirs virus was isolated from 50 of 76 live-born and stillborn fetuses from the 9 infected fitters. Virus was not isolated from 26 autolyzed fetuses or 15 control pigs. Six of 9 inoculated sows developed neutralizing antibodies to SIRS virus. The reproductive effects found in these experiments were identical to those found in field cases. On the basis of our findings, virus isolate ATCC VR-2332 causes the reproductive failure associated with SIRS.

Seventy-five pigs from 4 facilities were examined for Salmonella choleraesuis by use of bacteriologic culture of feces, blood, WBC (buffy coat), mononuclear leukocytes, and neutrophils. The organism was isolated from 0 of 75 fecal samples, compared with isolation from 39 of 75 purified neutrophil preparations. Of the pigs that did not have Salmonella isolated from feces or blood, but had S choleraesuis isolated from neutrophils, 6 were further examined. These pigs from 2 groups again had culture performed at least 3 successive times to test for repeatability and to determine optimal number of neutrophils required for Salmonella isolation. These same pigs were euthanatized and necropsied. Nineteen tissue specimens from each pig were obtained for culture, but S choleraesuis was isolated only from neutrophil samples. Results indicate that neutrophils may contribute to the carrier state in pigs and should be cultured when attempting to identify S choleraesuis carrier swine.

Equine alpha1-acid glycoprotein (alpha-1AG) was isolated from equine serum by successive ammonium precipitation, anion- and cation-exchange chromatographies, and gel filtration. Purified equine alpha-1AG had a molecular weight of 46,000 +/- 1,000, and contained 31.4% carbohydrate. Gel isoelectric focusing revealed an isoelectric point range of 2.8 to 3.7. With immunoelectrophoresis, it was found that alpha-1AG migrated to the alpha-1-globulin region. Single radial immunodiffusion was used for quantitative measurement of alpha-1AG in equine serum. In clinically normal foals, serum alpha-1AG was undetectable (less than or equal to 20 micrograms/ml) in less than or equal to 7-day-old foals, but was detected by 14 days. The alpha-1AG concentration (mean +/- SD) increased to reach mean adult values of 99.23 +/- 26.90 micrograms/ml by 1 year of age. The alpha-1AG concentration in pregnant mares decreased at 2 to 3 months before parturition, then gradually increased until 1 day after parturition, when a brief decrease was observed. The concentration increased again at 2 weeks after foaling, then a decrease was observed, after which the alpha-1AG concentration increased again by 2 to 4 months after parturition. The concentration of serum alpha-1AG quickly rose to peak values 2 to 3 days after castration and jejunojejunostomy in adult horses, returning to baseline values by 14 to 28 clays after surgery. The alpha-1AG was concluded to be an acutephase reactive protein in horses.