We investigated small-volume (5 ml/kg) 7% NaCl in 6% dextran 70 (HS/D70) as an alternative to large-volume (60 ml/kg) 0.9% NaCl for treatment of experimentally induced canine gastric dilatation-volvulus (GDV) shock. The stomach was surgically displaced and then distended with an intragastric balloon in 11 dogs anesthetized with pentobarbital. All dogs were subjected to GDV for 180 minutes before partial decompression and resuscitation. Hemodynamic values, blood gas values, and plasma volume were measured during control, shock, and resuscitation periods. Resuscitation started with 1 group (n = 6) receiving 5 ml of HS/D70/kg, IV, over 5 minutes, and the other group (n = 5) receiving 60 ml of 0.9% NaCl/kg, IV, over 60 minutes. Both groups received a surgical maintenance dosage (20 ml/kg/h of 0.9% NaCl after initial resuscitation. Resuscitative effects of small-volume HS/D70 were similar to large-volume 0.9% NaCl during the first hour of treatment; however, cardiac output was significantly higher in the HS/D70 group for the last 2 hours of resuscitation. Changes in heart rate, left ventricular pressure change, and systemic vascular resistance appeared to be responsible for improved perfusion. Mixed venous oxygen partial pressure data supported improved perfusion in the HS/D70 group. Packed cell volume remained higher in the HS/D70 group, indicating less hemodilution and improved oxygen delivery. Resuscitation of this GDV-induced shock model was better sustained with small-volume HS/D70, compared with conventional large-volume 0.9% NaCl.

In vitro adherence to intestinal epithelial cells by enterotoxigenic Escherichia coli strains bearing K88, K99, F41, or 987P adhesins and of their variants not bearing adhesins (K88-, K99-, or F41-) was investigated in European Large White and Chinese Meishan pigs. Possible relationship between adherence and virulence was also examined. The K88-positive (K88+) strain strongly adhered to intestinal epithelial cells from 26 of 28 Large White pigs. This strain had previously been found to be highly virulent for Large White pigs. The only surviving pig was of nonadherent phenotype, and cells from 4 dehydrated moribund pigs had strong adherence. By contrast, the same K88+ strain found previously to have little pathogenicity for Meishan pigs adhered with variable intensity to cells from 17 of 23 Meishan pigs; correlation was not evident between adherence and virulence. The K99+F41+ strain of porcine origin and the F41+ strain generally adhered strongly to cells from 24 and 23 Meishan pigs, respectively, and to cells from 25 of 26 Large White pigs. Correlation was not found between adherence and virulence for the 2 strains. A K99+F41+ strain of bovine origin adhered to cells from 20 of 22 Meishan and 22 of 23 Large White pigs, and a K99-F41+ variant adhered to cells from 19 of 23 Meishan and 23 of 24 Large White pigs. The adhesin-negative variants never adhered to intestinal epithelial cells. Strain 987 known not to readily produce 987P adhesin after in vitro growth never adhered to cells during the test. Results indicated that K88, K99, and F41 adhesins were responsible for in vitro adherence and, except for the K88+ strain in Large White pigs, adherent phenotype was not a sufficient condition to make a pig susceptible to enterotoxigenic E coli. The contribution of physiologic factors and their genetic origin to the degree of resistance of the individual is not yet completely understood for every enterotoxigenic E coli strain and breed of pig.

Plasma concentrations of porcine growth hormone (PGH) were similar in healthy pigs and those with atrophic rhinitis (AR), therefore, observed reduced growth rates and feed efficiency in naturally infected pigs with AR were not attributed to low concentrations of plasma PGH. Also, pituitary glands in both groups of pigs were responsive to growth hormone-releasing hormone (GHRH) challenge by increasing PGH secretion. Administration of clonidine hydrochloride to pigs naturally infected with AR failed to elicit any significant change (5.3 +/- 1.4 ng/ml) in the plasma concentration of PGH within a 45-minute bleeding interval. The pretreatment concentrations of PGH were similar in specific-pathogen-free toxin-treated and specific-pathogen-free control groups, but they increased significantly in toxin-treated pigs (20.7 +/- 8.2 ng/ml) within 15 minutes after GHRH injection. Porcine growth hormone release in toxin-treated pigs was variable; however, all pigs did not respond to GHRH administration: 3 responded with an increase in PGH release (35.6 +/- 10.6 ng/ml), 2 did not respond (6.7 +/- 0.5 ng/ml), and 1 had a decrease in PGH release (3.9 ng/ml). Therefore, the observed reduced growth rates reported in the literature may be attributed to factors at the target level of PGH action, such as insufficient or down-regulation of PGH receptors, changes or impaired ability in the PGH receptor-binding characteristics, and inability of PGH receptor complex to transduce signal. Toxins are known to modulate signal transduction pathways. It has been speculated that serotype-D Pasteurella multocida toxin may influence growth by its effect on signal transduction from PGH receptor complex on the cell membrane to the interior of the cell. This would account for the presence of high concentrations of PGH in the plasma and a functionally competent hypophysis cerebri, which responded to GHRH injection that have retarded growth in pigs affected with AR.

We determined that the protein profiles of 14 isolates from animals with hemorrhagic septicemia were relatively homogeneous and could be placed in 2 distinct groups on the basis of their country of origin. Such differences correlated with the serotypic properties of the individual isolates; hemorrhagic septicemia isolates of Asian and North American origin (Carter B) had a major protein band with an apparent molecular mass of 32 kDa, whereas those of African origins (Carter E) had a major protein band with an apparent molecular mass of 37 kDa. The possession of a major 32-kDa protein band appeared to be unique to Carter B isolates, suggesting that electrophoresis may be a useful nonserologic technique for the identification of organisms of this serotype. Other major bands with apparent molecular masses of 27, 45, and 47 kDa were shared by all strains, regardless of their serotype. The lipopolysaccharides were of low molecular mass and relatively uniform from 1 isolate to the next.

Inclusion of lactose in the diets of chickens has been determined to reduce cecal colonization with Salmonella typhimurium. We hypothesized, therefore, that dietary lactose may be a practical means for reducing the prevalence of Salmonella contamination of chicken products. Because some strains of Salmonella are atypical and ferment lactose, we investigated the effects of dietary lactose on cecal colonization with lactose-fermenting S typhimurium. Broiler chicks were inoculated intracloacally with Lac+ S typhimurium selected for resistance to novobiocin and rifampicin. The chicks also were inoculated orally with certain anaerobes that do not effectively inhibit colonization by S typhimurium, but do appear essential for lactose mediated inhibition of cecal colonization. Control chicks were not given dietary lactose, and chicks in the experimental group were fed a diet containing 7% lactose. Enumeration of Lac+ S typhimurium in cecal contents revealed dietary lactose to be effective at controlling this organism. Control was correlated with changes in cecal pH and increases in undissociated volatile fatty acids, especially propionic acid.

An experiment was conducted to determine whether a persistent Salmonella newport infection could be established in swine, to determine duration of shedding and distribution of the organism in internal organs, and to determine whether changes occurred in antimicrobial susceptibility or plasmid profile of the organism during the course of long-term infection. Naturally farrowedSalmonella-free pigs (n = 22) were orally exposed to a multiply antimicrobial-resistant zoonotic strain of S newport when they were 7 weeks old. Tonsillar and rectal swab specimens were examined bacteriologically for S newport during the first week after exposure, then weekly for 7 weeks. Fecal samples were likewise examined weekly or every 2 weeks for 28 weeks after exposure. Necropsies of 2 or 3 randomly selected pigs were conducted at 2, 4, 8, 12, 16, 20, 24, and 28 weeks after exposure. A total of 45 specimens/pig representing the following internal organs or tissues were examined bacteriologically for S newport: liver, spleen, kidney, gallbladder, heart, heart blood, lung, stomach, and tonsils; segments of the intestinal tract with corresponding lymph nodes; and lymph nodes from lymphocenters of the head and neck, thoracic cavity, thoracic limbs, abdominal viscera, and abdominal wall. Exposure to S newport induced a mild and transient clinical response. The organism was recovered from 97% of tonsillar swab specimens and 89% of rectal swab specimens collected during 7 weeks after exposure and from 98% of fecal samples collected during 28 weeks after exposure. At necropsy, S newport was recovered most frequently from tonsils (86.4%), followed by segments of the intestinal tract from ileum to rectum (81.8% recovery from cecal contents), and from mandibular (68.2%), jejunal (50%), and ileocolic (45.5%) lymph nodes. Sporadic recoveries of the organism were made from other lymph nodes and from gallbladder, stomach, kidney, spleen, liver, and heart, varying from 2 to 20 weeks after exposure. The cranial portion of jejunum, medial iliac lymph nodes, dorsal superficial cervical lymph node, and heart blood of all pigs were culture-negative. Of 26 representative isolates of S newport recovered from body organs or feces during 28 weeks after exposure, 4 (15.4%) underwent changes in antimicrobial susceptibility pattern. Changes in plasmid profile of the organism were not detected during longterm infection of swine.

Intestinal tissues from swine affected withproliferative enteritis were ground, filtered through a 0.65-micrometer pore membrane filter, diluted, and injected into 7-day-old embryonated hens' eggs via the yolk sac. At 2, 4, and 7 days later, yolk sac swab specimens taken from live embryos were cultured for Campylobacter species. Campylobacter hyointestinalis was recovered from eggs injected with tissues of swine with acute hemorrhagic proliferative enteritis at dilutions up to 10-4. Campylobacter mucosalis was recovered from eggs injected with tissues of swine with chronic proliferative enteritis at dilutions up to 10-6. Campylobacter coli was recovered from several specimens without lesions of proliferative enteritis and also from some specimens with lesions of proliferative enteritis. Two previously undescribed hemolytic Campylobacter species designed as hemolytic number 1 and hemolytic number 2 were recovered from normal and experimentally inoculated swine tissues. Few contaminating organisms grow in eggs and these were usually recovered at dilutions of 10-2 or less. Recovery of Campylobacter species by use of these techniques was seldom successful in tissues stored at -70 C for more than 6 months.

We report here genetic recombination between 2USDA-licensed vaccine strains of pseudorabies virus co-inoculated into swine. The vaccine strains, one of which was a conventionally attenuated strain and the other, a genetically engineered deleted strain containing a negative immunologic marker, had complementary genomes. Coinoculation resulted in the creation of novel strains of pseudorabies virus containing negative immunologic markers with restored virulence genes. Plaque-purified recombinant progeny viruses were found in 2 litters of pigs in which both strains were co-inoculated IM, a litter in which both strains were co-inoculated oronasally, and a litter in which the conventionally attenuated strain was inoculated oronasally and the genetically engineered strain was inoculated IM. Recombinant phenotypes and recombinant restriction fragment patterns were observed. The creation, spread, and potential misdiagnosis of these types of recombinant strains could disrupt control and eradication programs that are based on the serologic identification of swine infected with potentially virulent strains of pseudorabies virus.

The effect of pulsed radio frequency therapy (PRFT) was evaluated on seven ponies with no arthritis and in 28 ponies in which arthritis was created using intra-articular amphotericin B to induce synovitis in the right middle carpal joint. The ponies were divided into five treatment and two control groups. Two levels of arthritis were created and two dosage levels of PRFT were evaluated. The effect of PRFT on arthritic and nonarthritic joints was measured by comparing synovial fluid parameters, the degree and duration of lameness, the range of carpal motion, and carpus circumference, for treated and untreated groups. Lesions seen radiographically at gross pathology, and by histopathology were also compared between the treated and control groups. In the ponies with a mild form of induced arthritis, PRFT significantly (p < 0.05) reduced the severity and duration of lameness, swelling of the carpus, and the severity of gross pathological and radiographic changes. In these ponies the synovial acid phosphatase levels were lower, the mucin clot quality was superior, and the synovial protein levels were lower for the ponies receiving PRFT as compared to the arthritic ponies receiving no treatment. A dose response effect was evident. In ponies with a slightly more severe form of arthritis, PRFT was evaluated at one dosage level. The treated ponies were significantly improved over the untreated ponies with respect to carpal range of motion, degree of lameness, carpus swelling, and radiographic lesions. No deleterious effects were noted when normal, PRFT treated, middle carpal joints were compared to contralateral untreated, normal joints. It was concluded that significant beneficial effects resulted when affected ponies were treated with PRFT.

A reliable bovine viral diarrhea (BVD) viral antigen was prepared from BVD virus grown on Madin Darby bovine kidney (MDBK) cells by solubilizing the virus with detergent MEGA-10 (decanoyl-N-methylglucamide) followed by removal of hydrophobic proteins with Triton X-100 treatment. By these treatments, problems of high background associated with BVD viral antigen in the enzyme-linked immunosorbent assay (ELISA) were eliminated. With this new antigen, an ELISA was adapted to detect bovine serum antibody against BVD virus. The diagnostic specificity of the assay in 403 bovine sera collected from a BVD virus-free herd was 100%; in 296 bovine sera with serum neutralizing antibody titers of greater than or equal to 1:2, 289 sera were ELISA positive (relative sensitivity of 97.6%), two sera gave false negative reactions (0.7%) and five sera gave suspicious reactions (1.7%). These interpretations were based on positive/negative (P/N) ratio readings, i.e. a P/N ratio of < 1.50, 1.50-1.99 and greater than or equal to 2.00 were interpreted as negative, suspicious and positive reactions, respectively. The ELISA results gave excellent agreement with serum neutralization in detecting both seropositive and seronegative animals (Kappa = 0.994). The ELISA assay was considered to be technically superior to the serum neutralization test for the routine detection of BVD viral antibody in bovine sera.