Subclinical Toxoplasma gondii infection was induced in young and adult cats by oral administration of tissue cysts. An antibody-capture ELISA to detect anti-Toxoplasma IgM-class antibodies in the serum of cats was developed. The serologic response to experimental infection was followed in the 2 groups of cats by use of anti-Toxoplasma IgM and IgG detection. This study shows that anti-Toxoplasma IgM-class antibody titers develop early in the course of experimental infection in cats and that the combination of IgM- and IgG-class antibody titer measurement can aid in the detection of recent subclinical toxoplasmosis.

We compared the ability of 3 alpha 2-adrenoreceptor antagonists, idazoxan (0.05 mg/kg), tolazoline (2 mg/kg), and yohimbine (0.2 mg/kg) to reverse xylazine (0.3 mg/kg)-induced respiratory changes and CNS depression in 6 ewes. Once weekly, each ewe was given a random IV treatment of xylazine, followed in 5 minutes by either an antagonist or 0.9% NaCl solution. Xylazine alone caused recumbency for 54.2 +/- 5.3 minutes (mean +/- SEM). Xylazine also increased respiratory rate and decreased PaCO2 for at least 45 minutes, but did not significantly change arterial pH or PaCO2. Idazoxan and tolazoline were equally effective in reversing the respiratory actions of xylazine; however, yohimbine was less effective in reducing the respiratory rate and was ineffective in antagonizing the decreased PaO2. Idazoxan and tolazoline decreased the duration of xylazine-induced recumbency to 6.3 +/- 0.6 and 9.5 +/- 2.3 minutes, respectively, whereas yohimbine did not significantly change this effect of xylazine. Thus, at the dosages studied, idazoxan and tolazoline appeared to be more effective than yohimbine in reversing the respiratory and CNS depressant actions of xylazine in sheep.

Affinity-purified bovine immunoglobulin isotypes were bacteriolytic for Pasteurella haemolytica biotype A, serotype 1 (PHA-1). This bacteriolysis was specific and complement-dependent. The IgM and IgG1 were the most active isotypes in the classic complement cascade. These isotypes also induced bacteriolysis through the alternative complement cascade. The comparative bacteriolytic activities of IgG1 and IgM were equal within each cascade; however, the bacteriolytic activities of IgG1 and IgM were equal within each cascade; however, the bacteriolytic activities of IgG1 and IgM were lower in the alternative cascade than in the classical cascade. The IgG2 was more bacteriolytic than IgA in the classic and alternative complement pathways. Bovine immunoglobulins passively protected C57BL/6 mice from experimentally induced pasteurellosis. There were no major differences in the protection among hyperimmune sera, purified IgM, or purified IgG. Mice were protected from PHA-1 by approximately 1.9 microgram of IgG and 1.2 or 0.1 microgram of IgM. Elimination of murine complement with cobra venom factor 3 reduced PHA-1 clearance in passively immunized C57BL/6 mice. The protective effect of IgM mediated resistance was highly dependent on an intact complement system. The intact complement cascade was associated with enhanced clearance of PHA-1 from the liver. Although PHA-1 was susceptible to antibody complement-mediated bacteriolysis in vitro, the dependence on an intact complement cascade was not absolute in experimentally induced murine septicemic pasteurellosis.

A study on erythrocyte distribution was performed on 10 healthy, nonstressed adult white Pekin ducks. Results indicated 2 populations of erythrocytes, with average mean corpuscular volumes of 128.37 fl/cell and 308.50 fl/cell. Variations in erythrogram patterns were evident over time, when comparing specimens from different ducks or the same duck. There were 5 patterns of cell number/volume distribution observed between the 2 cell populations when all ducks were studied. Females had a greater change than did males when population density and volume percentage comparisons were made on erythrocyte compartments.

Data from slaughter plants (n = 3) and feedlots (n = 18) in eastern Washington were analyzed to characterize occurrence patterns of cysticercosis in Washington during 1984. Three concurrent peaks in cysticercosis rates (0.6/1,000 to 5/1,000 slaughtered cattle) were detected at 3 slaughter plants. Peaks were observed at 8 feedlots from December 1983 to March 1984, at 6 feedlots from April to July 1984, at 2 feedlots from August to October 1984, and at 3 feedlots from November 1984 to February 1985. Affected feedlots were not closely associated geographically and were feeding cattle from many, predominantely northwestern, origins. For 3 feedlots for which time in the feedlot was available for each slaughter shipment, an increase in cysticercosis rate with increasing time in the feedlot was noticed. Within these 3 feedlots, cases of cysticercosis were widely scattered spatially. The pattern of cysticercosis indicated human fecal contamination of a regionally available feed source. Of feedstuffs in use, potato waste, a byproduct of the processed potato industry, appeared to be the most likely source of Taenia saginata ova.

Exogenously administered vasopressors (sympathomimetics) were evaluated in halothane-anesthetized dogs to determine the effects of these drugs on cardiovascular function before and after hemorrhage. Six dogs were anesthetized with thiamylal sodium (20 mg/kg of body weight) and halothane (1.25 minimal alveolar concentration) in 100% oxygen. After instrumentation, cardiac output, systemic arterial blood pressure (SAP), heart rate (HR), left ventricular pressure, pulmonary arterial pressure, and an index of cardiac contractility (dP/dT) were measured. Stroke volume, cardiac index (CI), stroke index (SI), rate-pressure product, and systemic vascular resistance (SVR) were calculated. Epinephrine (0.1, 0.3, and 0.5 micrograms/kg/min [low, medium, and high doses, respectively]) and dobutamine (1, 5, and 10 micrograms/kg/min [low, medium, and high doses, respectively]) were infused. Methoxamine was given in a bolus of 0.22 mg/kg, IV. All measurements were taken at 2.5 minutes after infusion, and were repeated after removal of 40% of the estimated blood volume. Dobutamine administered at the low dose before hemorrhage increased SAP and dP/dT. At the high and medium dose, dobutamine significantly increased CI, dP/dT, and SAP with no significant change in HR or SVR. The medium dose of epinephrine was the most effective dose of epinephrine at increasing key variables (CI, SI, dP/dT). The response of CI and SI to this dose was not significantly different from the changes seen with high-dose administration of dobutamine. The dP/dT was significantly lower with epinephrine than with dobutamine, and SVR and HR were unchanged with epinephrine, except at the low dose, which decreased SVR. Methoxamine significantly decreased CI, SVR, and HR, whereas SVR and SAP were increased significantly. After hemorrhage, the only variables that had a significant change in the absolute magnitude of the response to a drug, relative to the response before hemorrhage, were a significantly reduced ability of dobutamine and methoxamine to increase SAP, and a significantly decreased ability of methoxamine to decrease CI. We concluded that dobutamine and epinephrine provide beneficial short-term support of the cardiovascular system in the halothane-anesthetized dog during acute hypovolemia.

Oxytetracycline (OTC) pharmacokinetic values in plasma and bile were ascertained after IV administration of the drug. At 6 hours after administration of 1 mg of OTC/kg of body weight, 2.15% of the dose was found in the bile and 37.6% was found in the urine. At 2 hours after administration, the peak bile-to-plasma OTC concentration ratio was 60:1. Bioavailability of OTC was 47.6% when it was administered orally to fasted turkeys and was 9.4% when administered to fed turkeys.

The in vitro reactivity of vasoconstrictive mediators that are implicated in acute laminitis was determined in palmar and plantar digital arteries and veins obtained from healthy horses and in palmar digital vessels of horses with early laminitis (Obel grade I). To obtain baseline reactivity data, 3 experiments were conducted, using healthy horses: (1) the reactivity of palmar and plantar digital arteries and veins to angiotensin II, norephinephrine, and 5-hydroxytryptamine (serotonin) were compared; (2) the direct effects of bacterial endotoxin on vascular reactivity were assessed; and (3) the reactivity of palmar digital arteries and veins to angiotensin II, norepinephrine, prostaglandin F2 alpha (PGF2 alpha), sertonin, and a thromboxane-endoperoxide analog (U46619) were determined. The vascular reactivity of these same 5 vasoconstrictors then was determined in horses with early laminitis and was compared with data from healthy (control) horses. Obel grade-I laminitis was experimentally induced in horses using carbohydrate overload. Dose responses were conducted for each agent at concentrations between 10(-8)M and 10(-4)M. The potency of a drug was defined as the mean effective concentration necessary to induce 50% of maximal contraction (EC50). There were no differences in EC50 concentrations and in maximal contractions between forelimb and hind limb arteries and veins for angiotensin II, norepinephrine, and serotonin. Incubation with endotoxin had no effect on the reactivity of arteries and veins to angiotension II, norepinephrine, and serotonin. In healthy horses, serotonin and U46619 were more potent arterial constrictors than were norepinephrine PGF2 alpha, and angiotensin II. In veins, serotonin, U46619, and angiotension II were similar in potency, and all were significantly (P less than 0.05) more potent than were norepinephrine and PGF2 alpha. Serotonin induced greater arterial constriction than did all other agents tested. There were no differences in the maximal venoconstriction induced by norepinephrine, PGF2 alpha, serotonin, and U46619. Angiotensin II induced the least amount of arterial and venous constriction. Maximal contractions were significantly (P less than 0.05) greater for veins than for arteries for all agents evaluated, except for angiotensin II. In horses with early laminitis, angiotensin II and serotonin were the most potent (smallest EC50 values) constricting agents for the arterial and venous segments and norepinephrine and PGF2 alpha were the least potent. Serotonin and norepinephrine induced significantly (P less than 0.05) greater venoconstriction than did the other agents. Angiotensin II induced the least arterial and venous contraction. For all agonists except angiotensin II, the mean EC50 values for vessels from horses with early laminitis were either similar or greater than those for vessels from control horses. The EC50 values for norepinephrine and the thromboxane analog were significantly (P less than 0.05) greater for vessels from horses with early laminitis, compared with those from control horses. The mean maximal contractions for all vasoconstrictors, except angiotensin II, were significantly (P less than 0.05) less for vessels from horses with early laminitis. Significantly greater venous-to-arterial maximal contraction ratios were found for norepinephrine and serotonin in horses with laminitis, compared with those ratios in control horses. These data suggested that the digital vasculature of horses with early laminitis was not more sensitive to the vasoconstrictor substances tested and that the vessels were significantly less repsonsive than was vasculature from the control horses. However, the venous-to-arterial contraction ratios were either the same or significantly (P less than 0.05) greater in horses with laminitis.

Exogenously administered vasopressors (sympathomimetics were evaluated in isoflurane-anesthetized dogs to determine the effects of these drugs on cardiovascular function before and after hemorrhage. Six dogs were anesthetized with thiamylal sodium (20 mg/kg of body weight) and isoflurane (1.25 minimal alveolar concentration) in 100% oxygen. After instrumentation, cardiac output, systemic arterial blood pressure, heart rate (HR), left ventricular pressure, pulmonary arterial pressure, and an index of cardiac contractility (dP/dT) were measured. Stroke volume, cardiac index (CI), stroke index (SI), rate-pressure product, and systemic vascular resistance (SVR) were calculated. Epinephrine (0.1, 0.3, and 0.5 micrograms/kg/min [low, medium, and high doses, respectively]) and dobutamine (1, 5, and 10 micrograms/kg/min [low, medium, and high doses, respectively]) were infused. Methoxamine was given in a bolus of 0.22 mg/kg, IV. All measurements were taken at 2.5 minutes after infusion, and were repeated after removal of 40% of the estimated blood volume. Before hemorrhage, administration of high doses of dobutamine and medium and high doses of epinephrine were equally effective at increasing CI and SI. The dP/dT was increase to the greatest degree by administration of high doses of dobutamine. Administration of the low dose of dobutamine increased dP/dT, whereas administration of the low dose of epinephrine increased CI, HR, and SI, and decreased SVR. The HR and SVR were not increased by administration of any dose of dobutamine or of the medium and high doses of epinephrine. However, methoxamine increased SVR and decreased HR. Methoxamine decreased CI, SI, and dP/dT, but increased systemic arterial pressure to the same degree as that attributed to administration of high doses of dobutamine and epinephrine. After hemorrhage, effectiveness of the drugs in eliciting a response was unchanged, except for a decreased ability of dobutamine to increase rate-pressure product. Further, when the results of this study were compared with those of an earlier halothane study, there were no significant differences in the response of a variable to drug infusion on the basis of the anethetic. The drugs were equally effective with halothane or isoflurane anesthesia. Results inidcated that dobutamine and ephinephrine are effective short-term treatments for hypovolemia during volume resuscitation, and that they work equally well with halothane or isoflurane anesthesia.

Lateral cecal arterial blood flow, carotid arterial pressure, heart rate, and mechanical activity in the duodenum, right ventral colon, cecal body, and cecal apex were measured in 6 conscious healthy horses for 60 minutes during and for 120 minutes after IV infusion of 0.9% NaCl solution (control) or fenoldopam. There were no significant changes in these measurements during or after infusion of 0.9% NaCl (saline) solution. Fenoldopam, a selective dopamine- 1 receptor agonist, was administered in saline solution at dosages of 0.01, 0.05, and 0.1 ug/kg/min. Intravenous infusion of fenoldopam at 0.01 ug/kg/min significantly increased heart rate, but did not change average carotid arterial pressure or lateral cecal arterial blood flow. Intravenous infusion of fenoldopam at both 0.05 and 0.1 ug/kg/min significantly increased heart rate, significantly decreased average carotid arterial pressure, and significantly increased lateral cecal arterial blood flow. Intravenous infusion of fenoldopam at 0.01, 0.05 and 0.1 ug/kg/min did not significantly change the mechanical activity measured by the area under the strain gauge defection curve for the duodenum, right ventral colon, cecal body, or cecal apex. These results suggest that dopaminergic-1 receptors are present on the colonic vascudopaminergic-1 receptors exist on the visceral smooth muscle of the duodenum, right ventral colon, cecal body, or cecal apex of horses.