In vitro effects of a mixture of Escherichia coli heat-stable enterotoxins (STa and STb) on isolated jejunum of 3-week-old male pigs were studied, using everted intestinal sac techniques. Heat-stable enterotoxins increased chloride secretion and chloride absorption in everted intestinal sacs. The increase of secretory flux was greater than that for absorptive flux. Vasoactive intestinal peptide (6 x 10-9M) increased chloride secretion, but had no effect on chloride absorption. Neither vasoactive intestinal peptide nor pilocarpine (10-5M) had additive effect to ST. Secretory effects of ST were not blocked by atropine 2 x 10-5M), clonidine (10-6M), or morphine (4.2 X 10-6M).

Hybridomas were selected for secretion of monoclonal antibodies directed against pseudorabies virus (PRV) glycoproteins. Each monoclonal antibody was capable of neutralizing PRV in vitro in the presence of complement. This panel of antibodies was used in passive immunization studies to protect mice and swine from PRV-induced mortality. The most protective antibody in mice was 3A4, specific for PRV glycoprotein gp50, which afforded as high as 100% protection. Although antibody 3A4 was partially protective in swine, antibody 3D11, which is specific for PRV glycoprotein gIII, afforded greater protection-83% protection when ascitic fluid was used and 100% protection when immunoglobulin concentrated from cell cultures was used at a dose of 150 mg/pig. These studies demonstrated that monoclonal antibodies may be useful for short-term prophylaxis against PRV-induced disease and that antibody directed against either PRV gylcoprotein gIII or gp50 is sufficient to protect animals from PRV-induced mortality.

Blood samples from sarcoptic mite-infested pigs were evaluated for effects of mite infestation and cold and ambient temperatures on lymphocyte blastogenic responses and for effects of mite infestation on serum cortisol concentrations. In experiment 1, sarcoptic mite-infested and noninfested pigs were housed in cold (5 to 15 C fluctuating) and thermoneural (25 C) environmental chambers for 5 weeks. Differences were not observed (P greater than 0.10) in blastogenic responses to phytohemagglutin or pokeweed mitogen between lymphocytes from infested and noninfested pigs on postinfestation days (PID) 7, 21, 28, and 35 in either environmental chamber. When lymphocytes from noninfested pigs were cultured with sera from infested pigs, alterations of blastogenic responses were not detected. Cortisol values were higher (P less than 0.05) in sera from sarcoptic mite-infested pigs, compared with those from noninfested pigs, at 4 PM on PID 14 and at 4 AM and 10 AM on PID 15. Cortisol values were higher (P less than 0.05) in sera obtained at 10 AM on PID 14 and at 10 AM on PID 15 from pigs housed in cold chambers, compared with those from pigs housed in thermoneutral chambers. Interactive effects between sarcoptic mite infestation and cold ambient temperatures were not observed. At 4 AM on PID 15 (experiment 2), cortisol values were higher (P less than 0.05) in sera of infested pigs, compared with those in noninfested pigs. Seemingly, sarcoptic mange in pigs did not alter mitogen-induced lymphocyte blastogenic responses, but did increase serum cortisol concentrations, indicating that sarcoptic mange may be a stressor in pigs.

A subpopulation of purified, interepithelial lymphocytes from porcine small intestinal mucosa contained cytoplasmic granules. Toluidine blue staining revealed metachromatic granules in 13.64% (606/4,450) cells. The cells had scant organelles, a single large nucleus with obvious invagination of the nuclear membrane, and prominent chromatin. Each cell contained 1 to 10 cytoplasmic membrane-bound granules, 0.6 to 1.5 microns in diameter. These findings indicated that the granular mucosal lymphocytes are related morphologically to mucosal mast cells. The presence of serotonin in the granules, confirmed by the serotonin releasing test, provided functional evidence that granular mucosal lymphocytes are related to mucosal mast cells.

Thirty-four preweaning pigs with induced enteropathogenic Escherichia coli diarrhea were treated with electroacupuncture, traditional acupuncture, or neomycin. In the group treated with electroacupuncture, points GV-1, bilateral ST-36, and Bai-hui were stimulated electrically. In the group treated with traditional acupuncture, points GV-1, bilateral ST-36, BL-20, bulb points, bilateral ear tip, and Shan-gen were used. Acupuncture points CV-12 and bilateral ST-25 also were treated with moxibustion (applying heat generated by a burning herb, Artemisia argyi). Hemoacumpuncture also was applied to Shan-gen, bilateral ear tip, and bulb points. Pigs in the third group were given neomycin orally. Five pigs were inoculated with E coli, but were not treated and served as nontreated controls. At postinoculation day 5, 60% of control pigs and greater than 80% of pigs in treated groups recovered from diarrhea. However, at postinoculation day 3, recovery rates for pigs in the control and group treated with electroacupuncture were only 20 and 27.3%, respectively; whereas pigs treated with acupuncture or neomycin attained 81.8 and 71.4% of recovery rates, respectively. Seemingly, traditional acupuncture, but not electroacupuncture, was effective in controlling induced E coli diarrhea in pigs at its early stage.

We attempted to determine whether weaning is required for induction of diarrhea in pigs with postweaning enterotoxigenic Escherichia coli infection. Three-week-old newly weaned pigs and their suckling littermates were inoculated with the K88+ enterotoxigenic E coli strain M1823B. Fourteen of 21 weaned and 12 of 20 suckling pigs were genetically resistant to intestinal adhesion by the K88+ strain of E coli; they remained healthy, and gained weight at similar rates. Both groups of K88-resistant pigs gained weight faster, and shed fewer bacteria of strain M1823B in their feces, than did their K88-susceptible counterparts. Diarrhea developed in K88-susceptible pigs in the weaned (6 of 7 pigs) and suckling (4 of 8 pigs) groups, and 1 of the 4 affected suckling pigs died from complications resulting from diarrhea. The incidences of diarrhea, weight gain rates, and the numbers of strain M1823B shed in feces of susceptible weaned and suckling pigs were not significantly (P > 0.05) different. Diarrhea scores of susceptible weaned pigs were significantly (P < 0.02) higher than those of susceptible suckling pigs on the second day after inoculation. In this experimental model, it was concluded that weaning is not required for induction of diarrhea, but may modestly increase its severity.

In vitro effects of a mixture of Escherichia coli heat-stable enterotoxins (STa and STb) on isolated jejunum of 3-week-old male pigs were studied, using everted intestinal sac techniques. Heat-stable enterotoxins increased chloride secretion and chloride absorption in everted intestinal sacs. The increase of secretory flux was greater than that for absorptive flux. Vasoactive intestinal peptide (6 x 10-9M) increased chloride secretion, but had no effect on chloride absorption. Neither vasoactive intestinal peptide nor pilocarpine (10-5M) had additive effect to ST. Secretory effects of ST were not blocked by atropine 2 x 10-5M), clonidine (10-6M), or morphine (4.2 X 10-6M).

First-litter commerical cross-bred gilts were treated with levamisole (1.5, 2.5, or 3.5 mg/kg of body weight) weekly during the last 4 weeks of gestation, because similar treatment of dairy heifers had improved postpartum maternal health and neonatal survival. In the gilts, differences in reproductive performance were not found on the basis of pig survival at birth, pig survival at weaning, birth weight, or weaning weight. Also differences between treated and control gilts were not found in response of circulating lymphocytes to mitogen stimulation (phytohemagglutinin A, concanavalin A, and pokeweed mitogen). In all gilts, the lymphocyte response to mitogen stimulation was decreased during the first week after farrowing.