Anecdotal descriptions of atypical FeLV infections, wherein standard clinical ELISA or immunofluorescence testing fails to detect active infections, suggest that an unknown proportion of FeLV-infected cats may go undetected. In this study, 127 viremic and nonviremic cats experimentally inoculated with FeLV were evaluated at necropsy for atypical expression of FeLV antigen. Results from viremic cats were in accordance with results of earlier studies on the pathogenesis of FeLV infection in cats, wherein antigen was found in lymphoid and epithelial tissues. Differences in time course or tissue distribution of viral antigen in some cats appeared to be attributable to the challenge virus preparations, consisting of cell-free tumor homogenate or infectious plasma. It was discovered that 5 of 19 of the FeLV challenge-exposed cats that were nonviremic had FeLV-specific antigens in select tissues (bone marrow, spleen, lymph node, and small intestine) 6 to 75 weeks after inoculation. These results indicated an additional category of possible outcomes for cats exposed to FeLV. Localized FeLV infection, as described here, may explain the discordance between clinical disease and laboratory testing for FeLV.

The 43 monoclonal antibody raised against feline T cells was found to react with a single-chain glycoprotein of Mr 72,000 that is present on most thymocytes, 60% of lymph node cells, 20% of splenocytes, and 45% of blood mononuclear cells. All CD4+ and CD8+ T cells were found to express the 43-reactive determinant, as did a small subpopulation of CD4-/CD8-/IgM- lymphocytes in the periphery. The 43-reactive determinant was not detected on B cells, macrophages, or other types of blood cells. The 43 antigen was phosphorylated in resting and activated T cells. Its expression was upregulated by stimulation with phorbol myristate acetate and with phytohemagglutinin. When added to concanavalin A-stimulated T-cell cultures in low concentrations, the 43 antibody was found to augment mitogenesis. The data indicate that this antibody may identify a CD5 homologue on feline T cells.

We investigated the biochemical composition of blood from Holstein cows, native breed (criollas), and cows descended from fighting bulls (Vacas de lidia) raised at an altitude of 3,000 m (moderately high altitude, MHA), and compared the results with those from Holsteins and cows of similar genetic ancestry as the criollas (scrub cows), both raised at sea level (SL), to determine blood biochemical values characteristic of adaptation to high altitude. Only potassium and calcium concentrations were similar among groups. Glucose concentration was lower in MHA cows, with the exception of Vacas de lidia. Serum bicarbonate concentration was lower in MHA cows; this finding can be explained by hyperventilation in the hypoxic environment. Serum magnesium concentration was lower in SL and MHA Holsteins than in other groups. Serum phosphate concentration was lower in scrub cows, MHA Holsteins, and criollas than in other groups. Cholesterol concentrations were lower in SL Holsteins, whereas triglycerides were higher in scrub cows and MHA Vacas de lidia. Concentration of high-density lipoprotein was significantly greater in Vacas de lidia and less in MHA criollas than in the other groups. Uric acid and total protein were higher in MHA groups. Using radioimmunoassay for human proteins, thyroxine-binding globulin was undetectable. Total and free thyroxine and free triiodothyronine were higher in scrub cows, followed by Vacas de lidia; lower values were detected in SL and MHA Holsteins and MHA criollas.

The abomasa of 1,949 slaughtered feedlot cattle, 45 necropsied feedlot cattle that died 2 to 45 days after arrival, and 45 necropsied pastured cattle were opened and examined. Of these organs, 484, 1, and none, respectively, contained erosions. The slaughtered cattle were fattened at 3 locations: 1,305 with 430 eroded abomasa were fed a ration of corn in northeastern Colorado; 144 cattle with 4 affected abomasa fed a ration of milo in south-central Arizona; and 500 cattle with 50 affected abomasa fed a ration of milo and corn in northwestern Texas. The redbrown lesions developed late during the second semester of fattening and were located mostly on fundic folds. Those on fold edges were linear and were 2 to 15 cm long, whereas those on fold sides were punctate and were 2 to 15 mm in diameter. Normal fold edges contained fewer goblet cells and less surface mucus than did fold sides. Eroded folds had disruption of surface epithelium, damage to endothelial cells, and dilated, thrombosed, congested, and ruptured capillaries. Mean pH values of 16 normal and 17 eroded abomasa were 4.7 and 3.9, respectively. Necrosis of all tissue toward the mucosal surface of erosions was extensive. The cause of gastric erosion in cattle is not known.

We evaluated the efficacy of buparvaquone in eliminating infection with Babesia equi of European origin in carrier horses and in splenectomized horses with experimentally induced acute infection. When administered at the rate of 5 mg/kg of body weight, IV, 4 times at 48-hour intervals, buparvaquone prompted rapid abatement of parasitemia. However, secondary and tertiary recrudescent parasitemias invariably returned with establishment of the carrier state. Buparvaquone, at the dosage evaluated, had transitory therapeutic efficacy against acute B equi infection in splenectomized horses, but was unable alone to clear carrier infection.

Glycoprotein I (gI) phenotypes and genotypes of 4 pseudorabies viral diagnostic isolates were evaluated by use of in vitro DNA amplification, monoclonal antibody binding, gI-specific serodiagnostic responses, and in vivo virulence approaches. Three viruses were avirulent and did not elicit gI-specific serologic responses, react with gI-specific monoclonal antibodies, or contain gI epitope-encoding DNA sequences. The fourth virus was virulent and did elicit a gI-specific serodiagnostic response. Compared with reference virulent pseudorabies viruses, however, the fourth isolate had reduced reactivity with a group of gI monoclonal antibodies and had a single nucleotide sequence substitution with a corresponding putative amino acid change in the epitopically dominant portion of the gI molecule. Presumably, the first 3 isolates represented diagnostic recoveries of viruses derived from gI-deleted modified-live pseudorabies viral vaccines, whereas the fourth isolate was a virulent but gI-aberrant wild-type virus. Thoroughly assessing the gI status of pseudorabies viral diagnostic isolates was considered to be essential in evaluating the epidemiologic importance of these viruses and in monitoring the validity of gI-based vaccine companion tests now used worldwide in pseudorabies control and eradication programs.

The effect of xylazine on the arrhythmogenic dose of epinephrine (ADE) was studied in 9 horses. Anesthesia was induced by administration of guaifenesin (50 mg/kg of body weight, IV) followed by thiamylal (4 to 6 mg/kg, IV) and was maintained at 1 minimal alveolar concentration MAC) of halothane (0.89%). Base apex ECG and facial artery pressure were recorded. Epinephrine was infused in a sequence of arithmetically spaced increasing rates (initial rate 0.25 (Lg/kg/min) for a maximum of 10 minutes. The ADE was defined as the lowest epinephrine infusion rate to the nearest 0.25 microgram/kg/min at which at least 4 premature ventricular depolarizations occurred in a 15-second period. Xylazine (1.1 mg/kg, IV) was administered after the control ADE was determined. Xylazine did not significantly alter the ADE (control, 1.12 +/- 0.38 microgram/kg/min; xylazine, 1.21 +/- 0.46 microgram/kg/min). Blood pressure increased transiently for 8 minutes after xylazine administration. Baseline systolic and diastolic arterial pressures and heart rate were not significantly different from control baseline pressures and heart rate 15 minutes after xylazine administration. Blood pressure and heart rate increased significantly during control and xylazine ADE determinations. Significant differences in pH, PaO2, PaCO2, or base excess were not observed between baseline and ADE in the control or xylazine groups. One horse developed atrial fibrillation, and 2 horses developed ventricular fibrillation during ADE determinations.

Histomorphometric and scanning electron microscopic analyses were carried out on 74 embryos and fetuses and 20 sheep (early postnatal to adult age). Histodifferentiation of the rumen took place at 33 days of fetal fife. Ruminal pillars were observed at 42 days, and at 61 days, ruminal papillae appeared as evaginations of the epithelial stratum basale. Neutral mucopolysaccharides first appeared in epithelial cells at 46 days of fetal life; thereafter, numbers decreased gradually and subsequently stabilized in postnatal life. Acid mucopolysaccharides, mucins, and mucoid compounds were not detected. Age and diet were recognized as factors that determine the structure of the ruminal mucosa. Growth curves and formulas were set out for each tissue layer.

A study was conducted to determine the effect of mono-phosphoryl lipid A (MPL) and trehalose dimycolate (TDM) as adjuvants on the protective responses in BALB/c mice vaccinated with Brucella abortus salt-extractable protein (BCSP) or proteinase-K-treated B abortus lipopolysaccharide (PKLPS). Mice were vaccinated with different doses of BCSP or PKLPS given alone or in combination with MPL or TDM. Mice were challenge-exposed 4 weeks later with virulent B abortus strain 2308. Two weeks after challenge exposure, the number of B abortus colony-forming units (CFU) per spleen, spleen weights, and spleen cell interleukin 1 production were measured. Serum IgG and IgM concentrations specific for vaccinal immunogens were measured before and after challenge exposure with B abortus. Spleen weights and mean B abortus CFU per vaccine group were significantly lower in BCSP- and PKLPS-vaccinated mice, compared with those of nonvaccinated control mice. Monophosphoryl lipid A enhanced the suppression of splenic infection when given with the BCSP vaccine, but not when given with the PKLPS vaccine. Trehalose dimycolate had no effect on mean CFU when given with BCSP, but incorporation of TDM resulted in a significant increase in mean CFU when given with PKLPS. Spleen weights in BCSP- or PKLPS-vaccinated mice were not different when these vaccines were combined with MPL or TDM. Because of the wide variation in the results, we could not conclude that vaccination with BCSP or PKLPS alone, or in combination with MPL altered spleen cell interleukin-1 production in B abortus-infected mice. Increased host protection as defined by decreased CFU could not be related consistently to increased BCSP- or PKLPS-specific serum IgG or IgM antibodies introduced by any of the vaccines. These results do not eliminate a role for antibodies in the protection observed.

Twenty-four healthy dogs > 8 years old were recruited. In each instance, arterial blood gas tensions were analyzed. The alveolar-to-arterial oxygen gradient (P[a-a]02) was calculated to assess adequacy of pulmonary gas exchange. Thoracic radiographs were evaluated to ensure lack of visible signs of pulmonary disease and that lung features were similar to those in aged dogs of previous reports. Unlike findings in aged human beings, arterial partial pressure of oxygen (PaO2) was not decreased in this group of aged dogs (mean +/- SD, 102.9 +/- 7.8 mm of Hg). Similarly, P(a-a)02 also Was not increased. The thoracic radiographic findings were consistent with those of previous reports of pulmonary changes in aged dogs. The extent of radiographic abnormalities and the PaO2 were not correlated.