Three-week-old weaned and colostrum-deprived neonatal (< 1 day old) pigs were inoculated to determine the pathogenicity of 2 enterotoxigenic Escherichia coli isolates that do not express K88, K99, F41, or 987P adhesins (strains 2134 and 2171). Strains 2134 and 2171 were isolated from pigs that had diarrhea after weaning attributable to enterotoxigenic E coli infection. We found that both strains of E coli adhered in the ileum and caused diarrhea in pigs of both age groups. In control experiments, adherent bacteria were not seen in the ileum of pigs < 1 day old or 3 weeks old that were noninoculated or inoculated with a nonpathogenic strain of E coli. These control pigs did not develop diarrhea. Antisera raised against strains 2134 and 2171 and absorbed with the autologous strain, grown at 18 C, were used for bacterial-agglutination and colony-immunoblot assays. Both absorbed antisera reacted with strains 2134 and 2171, but not with strains that express K99, F41, or 987P adhesins. A cross-reaction was observed with 2 wild-type K88 strains, but not with a K12 strain that expresses K88 pili. Indirect immunofluorescence with these absorbed antisera revealed adherent bacteria in frozen sections of ileum from pigs infected with either strain. We concluded that these strains are pathogenic and express a common surface antigen that may be a novel adhesin in E coli strains that cause diarrhea in weaned pigs.

Postoperative abdominal fluid changes were compared in 2 groups of horses; those undergoing double small-colon resection and anastomosis (n = 10) and those undergoing exploratory celiotomy alone (n = 5). Peritoneal fluid was collected before surgery and on postoperative days 1, 3, 5, and 7. Total and differential nucleated cell counts, RBC numbers, and total protein and fibrinogen concentrations were evaluated. In both groups, all values were significantly higher than normal on the first postoperative day (after small-colon resection and anastomoses, WBC = 130,350 +/- 23,310 cells/microliter, RBC 7,389,000 +/- 6,234,000 cells/microliter, total protein = 3.63 +/- 0.16 g/dl; after exploratory celiotomy alone, WBC = 166,620 +/- 34,340 cells/microliter, RBC = 295,000 +/- 86,070 cells/microliter, total protein 4.38 +/- 0.54 g/dl). The number of total peritoneal nucleated cells and RBC significantly decreased after the first postoperative day, whereas total protein and fibrinogen concentrations, percent neutrophils, and percent mononuclear cells remained unchanged. None of the values had returned to normal by postoperative day 7 (after small-colon resection and anastomoses, WBC = 45,600 +/- 8,765 cells/microliter, RBC = 95,390 +/- 53,380 cells/microliter, total protein = 4.39 +/- 0.23 g/dl; after exploratory celiotomy alone, WBC = 43,340 +/- 7,746 cells/microliter, RBC = 12,860 +/- 11,790 cells/microliter, total protein = 3.92 +/- 2.20 g/dl.) The resection and anastomosis group had a significantly lower total protein concentration on the first postoperative day and a significantly higher mean total RBC count over the entire 7-day postoperative evaluation than did horses that underwent celiotomy alone. Other values in the 2 groups of horses did not differ significantly. As a result, there was insufficient evidence to conclude that resection and anastomosis of the small colon in healthy horses causes a different inflammatory response than does manipulation of the intestine alone.

Experimental evidence indicates that maintenance of urinary pH less than or equal to 6.4 is the single most effective means of preventing feline struvite crystalluria or urolithiasis of noninfectious causes. This may be accomplished by dietary acidification, but must be moderated to avoid potential adverse effects of excessive acidification, including bone demineralization, negative calcium balance, potassium depletion, and renal disease. Effects of chronic dietary phosphoric acid supplementation on acid-base balance and on mineral and bone metabolism were investigated in adult, domestic cats. One group of 6 cats was fed a basal, naturally acidifying diet without added acidifiers, and another group of 6 cats was fed 1.7% dietary phosphoric acid. Changes observed during 12 months of study included development of noncompensated metabolic acidosis, increased urinary calcium excretion, and lower but positive calcium balance in cats of both groups. Urinary pH decreased in cats of both groups, but was significantly (P < 0.05) and consistently maintained less than or equal to 6.4 in cats given dietary phosphoric acid. Urinary phosphorus excretion increased in cats of both groups, but was significantly (P < 0.05) greater in phosphoric acid-supplemented cats, leading to lower overall phosphorus balance as well. Potassium balance decreased in cats of both groups, but was only transiently negative in the phosphoric acid-supplemented cats midway through the study, and normalized at positive values thereafter. Plasma taurine concentration was not affected by dietary acidification, and remained well within the acceptable reference range for taurine metabolism. Double labeling of bone in vivo with fluorescent markers was followed by bone biopsy and histomorphometric measurement of several static and dynamic variables of bone formation. Overall indices of bone formation decreased in cats of both groups with age and confinement, but were not affected by dietary phosphoric acid supplementation. Dietary supplementation with phosphoric acid used as the principal inorganic P source to achieve moderate and stable degree of urinary acidification, did not appear over the course of 1 year, to have induced adverse effects on mineral, bone, or taurine balance in these adult domestic cats.

A hospital-based case-control study was conducted to evaluate and compare risk factors for abomasal volvulus (AV) and left displaced abomasum (LDA) in cattle. Medical record abstracts were derived from 17 North American veterinary schools by the Veterinary Medical Data Program for all cattle admitted between Jan 1, 1977 and Dec 31, 1986, and for those with a diagnosis of AV or LDA. From a total of 108,956 individual cattle records, 1,036 cases of AV and 7,695 cases of LDA were identified, with a ratio of LDA to AV cases of 7.4 to 1. In-hospital mortality was 23.5% for AV and 5.6% for LDA. Age, breed, gender, and season each had significant (P < 0.05) effects on risk for AV and LDA. Risk for AV and LDA increased with increasing age, with greater risk in cattle aged 4 to 7 years. Dairy cattle were at higher risk of developing AV (adjusted odds ratio, 36.4) and LDA (adjusted odds ratio, 95.2) than were beef cattle. The odds of AV in Brown Swiss cattle were significantly (P < 0.0001) lower, and the odds of LDA in Guernsey cattle were significantly (P < 0.0001) higher than those in Holstein cattle. Female cattle were also at higher risk of developing AV (adjusted odds ratio, 3.3) and LDA (adjusted odds ratio, 29.1) than were male cattle. The odds of AV and LDA varied considerably throughout the year, with the lowest number of cases observed in autumn. Seasonal development of AV differed significantly (P < 0.0001) from that Of LDA, with the odds of AV and LDA being highest in January and March, respectively. The medical records for all cattle with AV and LDA examined at the teaching hospital over a 10- and 5-year period, respectively, were reviewed, and the time interval since parturition, as well as the existence and nature of concurrent disease, were recorded. Proportionately fewer cases of AV than LDA developed during the first 2 weeks after parturition (28.3% of AV cases vs. 57.0% of LDA cases). Concurrent disease existed in 30.4% of AV cases and 53.6% of LDA cases, with the rates of concurrent disease differing significantly (P < 0.0001) between the 2 groups. The misclassification rate for data generated at the teaching hospital was estimated to be 6.5% for AV and 5.3% for LDA. On the basis of the findings of this study, we hypothesize that: abomasal atony is a prerequisite for AV and LDA; existence of an abdominal void immediately after parturition facilitates development of AV and LDA; normal rumen volume provides a moderately effective barrier against LDA; risk of LDA does not increase appreciably with advancing pregnancy; and the direction of abomasal displacement (AV or LDA) after abomasal atony and dilation is influenced principally by rumen volume.

Macromolecular permeability of the small intestine was tested in four 3-week-old gnotobiotic pigs inoculated with porcine rotavirus strain RV277 (group A). Pigs were administered 125I-labeled polyvinylpyrrolidone (molecular weight [mol wt], 40,000) orally 1 day before and 2 and 24 hours after virus inoculation, and blood samples were obtained every 6 hours. Eight hours after rotavirus inoculation, pigs had watery diarrhea. Increased permeation of 125I-labeled polyvinylpyrrolidone was not observed after clinical signs of infection had developed. Serum total protein and urea nitrogen concentrations increased slightly at the end of the study, probably as a consequence of dehydration. Differences in blood glucose concentration were not seen. At 48 hours after viral inoculation, macromolecular permeability was tested morphologically by injecting horseradish peroxidase (mol wt, 40,000) into the jejunal lumen just distally to the ligamentum colicoduodenale. After an incubation period of 20 minutes, small segments of jejunum were obtained for stereomicroscopic, histologic, and ultrastructural investigations. Moderate hyperregenerative villus atrophy was found. Ultrastructural changes of the villus epithelium were minor, and increased macromolecular permeation was not observed.

The anatomy of the nasolacrimal duct of llamas was examined grossly and radiographically in 2 llamas. Dacryocystorhinography was performed on cadaver heads, using a radiographic aqueous contrast agent. Anatomic casts of the nasolacrimal apparatus were obtained by cannulation of the duct and use of polyurethane cast material. Dacryocystorhinography accurately revealed the nasolacrimal apparatus and compared favorably with gross dissections and polyurethane casts.

Several pharmaceutical compounds were evaluated for their ability to selectively inhibit activated coagulation factor-XIII-like enzyme activity (eg, XIIIa) in pooled equine plasma. Presence of coagulation factor-XIIIa -like enzyme activity in plasma was established by assay procedures involving incorporation of the fluorescent amine compound, monodansylcadaverine, into purified casein, which served as a protein substrate. Pharmaceuticals inhibitory to coagulation factor-XIIIa -like enzyme activity were recognized by plasma gel formation of high spectrophotometric transmittance (transparency), solubility of transparent fibrin gels in concentrated urea solution, in conjunction with simultaneous depletion of native fibrinogen fractions, and production of fibrin monomer. Compounds acting primarily as anticoagulants were recognized by lack of plasma gel formation, but retaining high spectrophotometric transmittance and no detectable depletion of native fibrinogen fractions. Compounds failing to inhibit either thrombin-mediated fibrinogen-fibrin transformation (ie, coagulation) or coagulation factor-XIIIa -like enzyme activity were recognized by opaque plasma gels caused by fibrin polymerization, low spectrophotometric transmittance values, and coinciding with depletion of native fibrinogen fractions. Pharmaceuticals capable of exerting selective inhibition of coagulation factor-XIIIa -like enzyme activity were further classified as competitive inhibitors of phase 1 (carbamide) or phase 2 (terminal amine) of the transglutamination process.

The mean area and minimal diameter of 3 histochemically determined myofiber types (1, 2A, and 2B; myosin ATPase in acid buffer) were calculated in middle gluteal muscle biopsy specimens from 62 stallions, 47 Andalusians and 15 Arabians, ranging in age from 6 to 12 years. Fourteen Andalusians and 7 Arabians were untrained, and the remainder were actively endurance-trained. The 6-month training schedules involved walking, slow trotting, and cantering. Fourteen Andalusians were moderately endurance-trained, whereas the other 19 Andalusians and 8 Arabians were strongly endurance-trained. Significant differences were not recorded between untrained and endurance-trained Arabians with respect to the area (type 1, 3,194 +/- 869 micrometers(2) and 3,150 +/- 370 micrometers(2); type 2A, 3,819 +/- 890 micrometers(2) and 3,380 +/- 356 micrometers(2); and type 2B, 4,872 +/- 962 micrometers(2) and 4,417 +/- 646 micrometers(2) or minimal diameter (type 1, 52.2 +/- 7.4 micrometers and 52.8 +/- 3.1 micrometers; type 2A, 58.1 +/- 6.7 micrometers and 55.0 +/- 2.8 micrometers; and type 2B, 65.3 +/- 6.4 micrometers and 63.4 +/- 4.3 micrometers) of the 3 fiber types, nor between untrained and endurance-trained Andalusians with respect to the area (untrained, 3,990 +/- 690 micrometers(2) moderately endurance-trained, 3,882 +/- 347 micrometers(2); and strongly endurance-trained, 3,758 +/- 510 micrometers(2)) and minimal diameter (untrained, 58.1 +/- 4.7 micrometers; moderately endurance-trained, 59.7 +/- 2.7 micrometers; and strongly endurance-trained, 58.7 +/- 4.5 micrometers) of 2A fibers. Moderately endurance-trained Andalusians had larger 2B fibers (area 18.6%; minimal diameter 14.3%) than untrained Andalusians, and the minimal diameter of type-1 and type-2B fibers was greater in strongly endurance-trained Andalusians than in untrained Andalusians (9.5% for type 1; 10.0% for type 2B). These results suggest minimal effects of endurance training on the myofiber size of adult Andalusians and Arabians, but a tendency toward increased type-1 and -2B fiber size was found for Andalusians.

Six male Beagles were inoculated with Ehrlichia canis. Transient proteinuria was confirmed during the acute phase of infection by serial determination of urinary protein-to-creatinine ratio. Peak urine protein loss, consisting principally of albumin, was observed 2.5 to 3.5 weeks after inoculation. Renal biopsy specimens were obtained before inoculation, during peak proteinuria, and 10 weeks after inoculation when proteinuria had resolved. Renal tissue was evaluated by use of light, immunofluorescent, and electron microscopy to correlate specific glomerular lesions with development of proteinuria. Histologic examination revealed perivenular and interstitial infiltrates of lymphocytes and plasma cells localized principally to the renal cortex. Glomerular lesions were minimal to absent. Immunofluorescent staining revealed moderate to marked deposition of anti-canine IgG and IgM in the glomerular tufts and mesangium. Depositions of anti-canine complement factor C3 were not observed. Immunofluorescent staining persisted 10 weeks after inoculation, despite resolution of proteinuria, and probably represented passive trapping of immunoglobulins. Ultrastructural examination revealed fusion of podocyte processes that coincided with development of proteinuria. Electron-dense deposits or changes in the basement membrane were not observed. Morphometric measurements of average podocyte process length and percentage of coverage of basement membrane by podocyte processes were used to quantify the degree of process fusion. Both measurements increased significantly (P < 0.05) during peak proteinuria, and returned to preinoculation values when proteinuria had resolved 10 weeks after E canis inoculation. These findings indicated possible minimal-change glomerulopathy, rather than immune-complex glomerulonephritis, during acute E canis infection and could explain transient proteinuria without histologic evidence of glomerular disease.

Single-dose pharmacokinetic variables of pyrimethamine were studied in horses. Pyrimethamine (1 mg/kg of body weight) was administered IV and orally to 6 adult horses, and plasma samples were obtained at frequent intervals thereafter. Plasma pyrimethamine concentration was assayed by gas chromatography, and concentration-time data were analyzed, using a pharmacokinetic computer program. The IV and oral administration data were best described by 3-compartment and 1-compartment models, respectively. The median volume of distribution at steady state after iv administration was 1,521 ml/kg and the median elimination half-time was 12.06 hours. Mean plasma concentration after oral administration fluctuated between a maximal concentration of 0.18 microgram/ml and 0.09 microgram/ml (24 hours after dosing). Bioavailability after oral administration was 56%.