Mice with a severe combined immunodeficiency in B and T lymphocytes and natural killer cells (SCID-beige) were inoculated intranasally with sialodacryoadenitis (SDA) virus, a coronavirus of rats. Animals were killed at designated intervals and tissues were examined for evidence of viral infection by light microscopy and immunofluorescence microscopy. Based on these criteria, there was no evidence that these immundeficient mice were susceptible to infection with SDA virus.

The purpose of this study was to evaluate a commercial enzyme-linked immunosorbent assay (ELISA) for human von Willebrand factor antigen (vWF:Ag) with respect to its potential value in quantitating the protein in canine plasma. The assay was a sandwich technique using F(ab')2 fragments specific for von Willebrand factor (vWF) and a peroxidase conjugated rabbit anti-vWF second antibody, with a microplate as the support surface. Canine plasmas were assayed by ELISA, and by Laurell electroimmunoassay (EIA), our reference methodology. The ELISA had a within-day variation of 1.21-4.44% and a between-day variation of 0.85-4.88% depending on the level of vWF:AG. The sensitivity of the assay was less than 0.1% vWF:AG. The range of vWF:AG concentrations in plasmas from 24 clinically normal dogs compared favorably with the range for the same plasmas when assayed by EIA (ELISA = 60-152% of normal; EIA = 50-142% of normal). In 121 canine plasmas with vWF:AG concentrations (as assessed by EIA) ranging from undetectable levels (< 6% of normal) to 142% of normal, there was good correlation with measurements made by ELISA (correlation coefficient = 0.835). It was concluded that this commercial ELISA technique could be used to provide reliable, same-day measurements of canine plasma vWF:AG. Since it requires no special equipment other than a microplate reader and washer it is particularly suitable for laboratories lacking the electrophoretic expertise or equipment required for EIA.

Fourteen adult beavers (Castor canadensis) weighing 16.5 +/- 4.14 kg (mean +/- SD) were anesthetized for surgical implantation of radio telemetry devices. Beavers were anesthetized with diazepam (0.1 mg/kg) and ketamine (25 mg/kg) administered IM, which provided smooth anesthetic induction and facilitated tracheal intubation. Anesthesia was maintained with halothane in oxygen via a semiclosed circle anesthetic circuit. Values for heart rate, respiratory rate, esophageal temperature, direct arterial blood pressure, end-tidal halothane concentration, and end-tidal CO2 tension were recorded every 15 minutes during the surgical procedure. Arterial blood samples were collected every 30 minutes to determine pH, PaO2, and PaCO2. Values for plasma bicarbonate, total CO2, and base excess were calculated. Ventilation was spontaneous in 7 beavers and controlled to maintain normocapnia (PaCO2 approx 40 mm of Hg) in 7 others. Vaporizer settings were adjusted to maintain a light surgical plane of anesthesia. Throughout the surgical procedure, all beavers had mean arterial pressure < 60 mm of Hg and esophageal temperature < 35 C. Mean values for arterial pH, end-tidal CO2, PaO2, and PaCO2 were significantly (P < 0.05) different in spontaneously ventilating beavers, compared with those in which ventilation was controlled. Respiratory acidosis during halothane anesthesia was observed in spontaneously ventilating beavers, but not in beavers maintained with controlled ventilation. All beavers recovered unremarkably from anesthesia.

The hematologic and pathologic effects of orally administered L-tryptophan and indoleactic acid and of L-tryptophan administered IV were studied in ponies. Sixteen adult Shetland ponies were allotted into 4 experimental groups. Group 1 consisted of 5 ponies (1-5) given 0.6 g of tryptophan/kg of body weight in a water slurry via stomach tube. Group 2 included 4 ponies (6-9) given 0.35 g of tryptophan/kg orally. Group-3 ponies (10-13) were given 0.35 g of indoleacetic acid/kg orally. Group 4 consisted of 3 ponies (14-16) given a single 4-hour IV infusion of 0.1 g of tryptophan/kg. Restlessness, increased respiratory rate, hemolysis, and hemoglobinuria were detected in 4 of the 5 group-1 ponies. Only pony 7 in group 2 developed hemolysis, hemoglobinuria, and a significant increase in respiratory rate. Renal pathologic lesions, consistent with hemoglobinuric nephrosis, were seen in ponies 2, 4, 5, and 7. Bronchiolar degeneration was evident in 4 of 9 ponies given tryptophan orally. The importance of these respiratory lesions was unknown. Clinical or pathologic abnormalities were not noticed in the ponies of groups 3 and 4. Mean plasma tryptophan values increased significantly in groups 1 and 2 at 6 hours after dosing. A second peak of tryptophan was detected in both groups at 12 hours. Values returned to predose values by 48 hours. Plasma indole and 3-methylindole concentrations were detectable in only 2 ponies (4 and 7). In vitro incubations of cecal fluid from ponies 6, 8, and 9 yielded a percentage conversion of tryptophan to indole of 16.75%, 5.84%, and 7.96%, respectively. 3-Methylindole was not produced. These results suggested that indole was the major metabolite of orally administered tryptophan in these ponies.

Naturally acquired gram-negative bacterial intramammary infections (n = 160) were studied in 99 cows over a 2-year period. Escherichia coli, Klebsiella spp, Serratia spp, Enterobacter spp, and unidentified gram-negative bacteria were isolated from 28.8, 39.4, 9.4, 5.0, and 11.2%, respectively, of infected mammary glands. A majority (61%) of intramammary infections were first detected during the nonlactating period. Gram-negative bacteria isolated during the first half of the nonlactating period were predominantly Klebsiella spp, Serratia spp, and Enterobacter spp. Onset of E coli intramammary infections was more prevalent during the second half of the nonlactating period and during the first 7 days of lactation. The majority (59%) of infections were <28 days in duration, but Klebsiella spp and Serratia spp infections were of significantly (P <0.05) greater duration than infections with E coli. The greatest percentage (47%) of gram-negative bacterial intramammary infections were first detected during the summer.

The role of decreased luteal activity in embryonic loss after induced endotoxemia was studied in mares 21 to 35 days pregnant. Fourteen pregnant mares were treated daily with 44 mg of altrenogest to compensate for the loss of endogenous progesterone secretion caused by prostaglandin F2 alpha, (PGF2 alpha) synthesis and release following intravenous administration of Salmonella typhimurium endotoxin. Altrenogest was administered daily from the day of endotoxin injection until day 40 of gestation (group 1; n = 7), until day 70 (group 2; n = 5), or until day 50 (group 3; n = 2). In all mares, secretion of PGF2 alpha, as determined by the plasma 15-keto-13,14-dihydro-PGF2 alpha concentrations, followed a biphasic pattern, with an initial peak at 30 minutes followed by a second, larger peak at 105 minutes after endotoxin injection. Plasma progesterone concentrations decreased in all mares to values < 1 ng/ml within 24 hours after endotoxin injection. In group 1, progesterone concentrations for all mares were < 1 ng/ml until the final day of altrenogest treatment. In 6 of 7 mares in group 1, the fetuses died within 4 days after the end of treatment, with progesterone concentrations < than 1 ng/ml at that time. In the mare that remained pregnant after the end of treatment, plasma progesterone concentration was 1.6 ng/ml on day 41 and increased to 4.4 ng/ml on day 44. In group 2, all mares remained pregnant, even though plasma progesterone concentrations were < 1 ng/ml in 4 of 5 mares from the day after endotoxin injection until after the end of altrenogest treatment. One group-2 mare appeared to develop a secondary corpus luteum before day 70, with progesterone concentrations greater than 1 ng/ml from day 36 through day 70. Daily altrenogest administration consistently prevented pregnancy loss, which usually follows induced endotoxemia. Altrenogest administration offers a reliable and practical treatment for the prevention of fetal loss following endotoxemia in mares < 2 months pregnant. One group-3 mare remained pregnant, and in the other mare, fetal death was diagnosed 8 days after endotoxin administration, although this mare was still being treated with altrenogest. In that case fetal death was believed to be unrelated to the treatment.

The role of prostaglandin F2 alpha (PGF2 alpha) in embryonic loss following induced endotoxemia was studied in mares that were 21 to 44 days pregnant. Thirteen pregnant mares were treated with a nonsteroidal anti-inflammatory drug, flunixin meglumine, to inhibit the synthesis of PGF2 alpha caused by Salmonella typhimurium endotoxin given IV. Flunixin meglumine was administered either before injection of the endotoxin (group 1, -10 min; n = 7), or after endotoxin injection into the mares (group 2, 1 hour, n = 3; group 3, 2 hours, n = 3); 12 pregnant mares (group 4) were given only S typhimurium endotoxin. In group 4, the secretion of PGF2 alpha, as determined by plasma 15-keto-13,14-dihydro-PGF2 alpha concentrations, was biphasic, initially peaking at 30 minutes followed by a second, larger peak approximately 105 minutes after the endotoxin was given IV. When flunixin meglumine was administered at -10 minutes, synthesis of PGF2 alpha was inhibited for several hours, after administration of flunixin meglumine at 1 hour, the second secretory surge of PGF2 alpha was blocked, and administration of the drug at 2 hours did not substantially modify the secretion of PGF2 alpha. Plasma progesterone concentrations were unchanged after endotoxin injections were given in group 1. In group 2, progesterone values decreased < 2 ng/ml and remained low for several days. In group 3 and group 4, progesterone concentrations decreased to values < 0.5 ng/ml by 48 hours after endotoxin injections were given. Pregnancy continued in all 7 mares in group 1; in group 2, pregnancy continued in 2 of 3 mares; and in group 3, none of the 3 mares was pregnant by 4 days after endotoxin administration. The abortifacient effect of endotoxemia in mares < 2 months pregnant is mediated indirectly through the secretion of PGF2 alpha; compromised luteal activity and inadequate progesterone secretion are the primary causes of fetal death. Although flunixin meglumine administration can be used to prevent loss of pregnancy in cases of endotoxemia, it must be initiated at an early stage of the endotoxemia, that is, when clinical signs are often not yet apparent.

The antebrachiocarpal and tarsocrural joints of 10 adult horses were randomly assigned to 1 of 4 groups. Groups were formulated and were treated as follows: group 1, control (arthrocentesis only); group 2, buffered lactated Ringer solution; group 3, 10% dimethyl sulfoxide (DMSO; w/v) in lactated Ringer solution; and group 4, 30% DMSO (w/v) in lactated Ringer solution. Joints were lavaged once with the respective solution. Prior to lavage and on days 1, 4, and 8 after lavage, all horses were evaluated for lameness and joint effusion; synovial fluid total and differential WBC counts, synovial fluid total protein concentration, and mucin clot quality were determined. Horses were euthanatized on day 8, and joints were evaluated grossly, histologically, and histochemically. Significant difference was not observed in effect of lactated Ringer solution, 10% DMSO, and 30% DMSO on any measured variable. At 24 hours after treatment, significant (P < 0.05) difference in synovial fluid WBC numbers and total protein concentration was detected between control and treated joints. Eighty percent of lavaged joints had effusion 24 hours after treatment, compared with 30% of control joints. Gross, histopathologic, or histochemical differences were not detected between treated and control joints. Results of the study indicate that buffered lactated Ringer, 10% DMSO, and 30% DMSO solutions induce similar inflammatory changes in articular structures and significantly greater inflammatory reaction than does arthrocentesis alone.

We compared the frequency and severity of osteochondrosis lesions in young Thoroughbred horses with cervical stenotic myelopathy (CSM) vs that in clinically normal Thoroughbreds of the same age. All lesions of the cervical vertebrae and appendicular skeleton were classifiedhistologically as osteochondrosis or nonosteochondrosis and were measured for severity. Minimal sagittal diameter was significantly smaller in horses with CSM from C2 through C6; no difference was detected at C7. Severity of cervical vertebral osteochondrosis was greater in the horses with CSM, however frequency was not different. Frequency and severity of nonosteochondrosis lesions were not different in cervical vertebrae or appendicular skeleton. Frequency and severity of appendicular skeleton osteochondrosis lesions were both greater in horses with CSM. Osteochondrosis and nonosteochondrosis lesions were more severe on facets at sites of compression than on facets at noncompressed sites in horses with CSM. However, compression was also observed at sites with no articular facet lesions. The association of widespread osteochondrosis and spinal canal narrowing with CSM suggests CSM may represent a systemic failure in the development or maturation of cartilage and bone.

Four methods of evaluating renal function were performed in 6 cats anesthetized with halothane in oxygen. Glomerular filtration rate (GFR) was measured simultaneously in each cat by exogenous creatinine clearance (ECC), bolus inulin clearance, and 99mTc(Sn)-diethylene-triaminepentaacetic acid (DTPA) clearance determined by 2 different methods. In the first DTPA clearancemethod (DTPA-1), we measured radioactivity in serial blood specimens to construct plasma disappearance curves for calculation of GFR. In the second DTPA clearance method (DTPA-2), we used serial external head counts of radioactivity and a single blood specimen to construct plasma disappearance curves for calculation of GFR. Bolus inulin clearance was calculated from plasma disappearance curves using a 1-compartment open pharmacokinetic model (IN-1) and a 2-compartment open pharmacokinetic model (IN-2). Glomerular filtration rates were measured over 3 hours, for creatinine and DTPA methods, and over 4 hours for the inulin methods. The GFR obtained with the reference method (ECC) was 2.56 +/- 0.61 ml/min/kg of body weight (mean +/- SD). Values for GFR determined by ECC and DTPA-1 were significantly correlated (r = 0.852; P less than or equal to 0.05). Correlationbetween ECC and DTPA 2 was not as good (r = 0.783; P less than or equal to 0.10), but the 2 DTPA methods significantly correlated with one another (r = 0.897; P less than or equal to 0.05). Regardless of the method of calculation, bolus inulin clearance was poorly correlated with ECC (IN-1: r = 0.538, P greater than or equal to 0.10; IN-2: r = 0.430, P greater than or equal to 0.10) and DTPA-1 IN-1: r = 0.601, P greater than or equal to 0.10; IN-2: r = 0.625, P greater than or equal to 0.10). The 2 methods of calculating inulin clearance were highly correlated (r = 0.927; P less than or equal to 0.01). The DTPA clearance calculated from directly measured plasma disappearance curves (DTPA-1) comparedfavorably with ECC as an estimate of GFR and appears to be a safe, reliable, and less invasive method of determining GFR incats.