Larkspur poisoning is a major cause of acute death of cattle on mountain and high plains rangelands of western United States. A nonlethal method to quantify dose response in cattle is needed to better estimate the toxicity of larkspur plants and the response of cattle to larkspur poisoning and to provide a basis for reference during studies. A numerical system of rating the clinical signs of larkspur poisoning was developed and used to describe the response of 10 Hereford cows given a repeated single daily dose of larkspur (Delphinium occidentale X barbeyi) by gavage. Larkspur poisoning resulted from a short-term cumulative effect, and a statistically significant increase in score was essentially maximal by 4 days. At the dose given, this effect did not persist for more than 4 days after cessation of dosing. Poisoning was most severe between 5 and 9 hours after dosing. Early signs of poisoning can be subtle and sometimes brief. The effect of larkspur poisoning can be exacerbated temporarily by exertion. Therefore, cattle could probably repeatedly consume an otherwise toxic daily dose, without manifesting marked signs of poisoning, if consumption decreased to a sufficient degree intermittently at 2- to 4-day intervals.

Ototoxicosis was evaluated in 6 healthy ponies given 5 mg of gentamicin/kg of body weight, q 8 h, IM. Ponies 1, 2, and 3 were dosed for 7 days and ponies 4, 5, and 6 were dosed for 14 days. Serum peak and trough concentrations of gentamicin were measured by radioimmunoassay at regular intervals. Brain stem auditory-evoked responses were recorded every 5 days up to 60 days after the first dose to monitor auditory function. Although serum gentamicin concentrations were within or above the accepted clinical therapeutic range, loss of auditory function was not observed at the frequency range (1 to 4 kHz) tested. Serum chemical values remained within the accepted clinical range and no evidence of nephrotoxicosis was observed. Seemingly, gentamicin given IM to healthy ponies was safe and had minimal risk of side effects.

The purpose of this study was to evaluate the effect of withdrawal of lactose from the diet for 72 hours on lactase activity in the jejunal mucosa of conventionally raised calves. The descending portion of the duodenum of six Holstein calves < 24 hours old was cannulated. The calves were fed milk except on days 5, 6 and 7 when they were given the same volume of an electrolyte solution. Sequential biopsy specimens of the proximal jejunal mucosa were obtained for three weeks and the lactase activity determined. Lactase activity was highest on day 1 and a trend toward decreased lactase activity from birth until three weeks was observed. Mean lactase activity was significantly (p < 0.05) higher for days 1, and 3 compared to days 9, 13 and 17. The withdrawal of milk and replacement by an electrolyte solution during three days had no significant effect on jejunal mucosal lactase activity in neonatal calves.

The cardiopulmonary effects of thiopental sodium were studied in hypovolemic dogs from completion of until 1 hour after administration of the drug. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. After stabilization at this pressure for 1 hour, 8 mg of thiopental/kg of body weight was administered IV to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to thiopental administration, heart rate and oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after thiopental administration, heart rate, mean arterial pressure, mean pulmonary arterial pressure, pulmonary vascular resistance, and mixed venous oxygen tension increased, whereas oxygen utilization ratio and arterial and mixed venous pH decreased from values measured prior to thiopental administration. Fifteen minutes after thiopental administration, heart rate was still increased; however by 60 minutes after thiopental administration, all measurements had returned to values similar to those obtained prior to thiopental administration.

Six calves with suppurative arthritis were given a single IM injection of sodium cephapirin at a dosage of 10 mg/kg of body weight. Cephapirin concentrations were serially measured in serum and in normal and suppurative synovial fluid over a 24-hour period. Mean peak serum concentration was 6.33 microliter/ml at 20 minutes after injection. The highest cephapirin concentrations in normal and suppurative synovial fluid were 1.68 and 1.96 microgram/ml, respectively, 30 minutes after injection. Overall mean cephapirin concentration in normal synovial fluid for the first 4 hours (1.04 +/- 0.612 microgram/ml) was not significantly different from that in suppurative synovial fluid (0.88 +/- 0.495 microgram/ml; P > 0.05). Elimination half-life was 0.60 hours and clearance was 1,593 ml/h/kg.

Nineteen purebred Beagles of various ages (4, 5, 13,and 47 weeks) were inoculated with North American Trypanosoma cruzi isolates obtained from an opossum (Tc-O), armadillo (Tc-A), or a dog (Tc-D). Dogs were grouped on the basis of clinical outcome of infection. During the acute stage of disease, dogs of group 1 (n = 7 inoculated with Tc-O or Tc-A) died or were euthanatized because of the severity of disease. Dogs of group 2 (n = 5 inoculated with Tc-O or Tc-A) developed acute disease, but survived to develop chronic disease. Dogs of group 3 (n = 7Tc-D-inoculated dogs) developed neither acute nor chronic disease. Dogs of group 4 (n = 4-2 dogs 13 weeks old and 2 dogs 47 weeks old) served as noninoculated controls. Clinical signs associated with severe acute myocarditis developed in dogs of groups 1 and 2 between postinoculation day (PID) 15 and 28. Generalized lymphadenopathy and lymphocytosis were observed in all dogs of groups 1, 2, and 3 between PID 14 and 17. Serum alanine transaminase and aspartate transaminase activities and urea nitrogen concentration were high, and glucose concentration was low prior to death of dogs in group 1. Serum activities of isoenzymes of creatine kinase were significantly (P < 0.05) high in only 1 dog (group 1), whereas serum lactate dehydrogenase isoenzyme activities were not significantly high in any dog. Parasitemia was detected by examination of thick blood smears as early as PID 3, peaked by PID 17 in most dogs, and was not detected by PID 33 in dogs of groups 1 and 2. Parasitemia was documented by blood culture results in dogs of groups 2 and 3 at various times throughout the study. Dogs infected at an older age generally had lesser degree of parasitemia and higher survival rate than did dogs infected at a younger age. Dogs of group 2 did not manifest clinical signs of disease for 27 to 120 days prior to onset of chronic disease. Ventricular-based arrhythmias and exercise intolerance developed in all dogs of group 2 at various times by PID 120. Two dogs developed signs of biventricular heart failure.

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 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.

Noninvasive determination of anal and genitoanal reflexes was evaluated in clinically normal cats. Thirty adult mixed-breed cats (15 sexually intact or castrated males, 15 sexually intact or spayed females) were sedated by IV administration of ketamine, acetylpromazine, and atropine. Anal reflexes were recorded from the anal sphincter muscle after ipsilateral and contralateral electrical stimulation of the perineal skin. Genitoanal reflexes were recorded from the anal sphincter muscle after electrical stimulation of the penis or clitoris. An anal sphincter response to tibial nerve stimulation was attempted. Anal reflexes from ipsilateral and contralateral stimulations and a genitoanal reflex were detected in all cats. Anal sphincter responses to tibial nerve stimulation were inconsistent (4/30) and were not included in any analyses. Anal reflexes had response latencies of 7.5 to 12.0 ms (ipsilateral stimulation) and 6.5 to 13 ms (contralateral stimulation). Genitoanal reflexes had latencies of 9.0 to 13.0 ms (males) and 6.5 to 9.0 ms (females). Anal reflex latencies were significantly (P < 0.05) longer for contralateral, opposed to ipsilateral, stimulation and were significantly (P < 0.05) longer in males than in females. Genitoanal reflex latencies were also significantly (P < 0.05) longer in males than in females, reflecting the more peripheral stimulation site in males. Anal reflex responses could be recorded in 2 feline clinic patients with such severe perineal trauma that pudendal nerve function could not be manually evaluated. A potentially favorable prognosis was given in each instance on the basis of detection of the response. One cat eventually recovered. The other was euthanatized because of other problems, and the sacral part of the spinal cord, sacral nerve roots, and pudendal nerves were found to be intact at necropsy.

Sixteen Holstein cows were used to test the effect of postmilking teat treatment on colonization and intramammary infection by Staphylococcus aureus on chapped teats. Treatments were (1) chapping the teat and using 1% I2/10% glycerin postdip solution, (2) 1% I2/10% glycerin postdip solution on nonchapped teats, (3) chapping the teat and using 10% glycerin postdip solution, (4) chapping the teat and not using a postdip solution. All mammary glands were free of S aureus teat skin colonization and intramammary infection at the start of the study. Teats selected for chapping were dipped in 1N NaOH prior to 3 applications of S aureus broth culture; cultures were applied at 12-hour intervals on all teats. Treatments were applied after each milking for 30 days and were initiated after the second broth dip. Teat skin swab specimens and milk samples were collected before treatment application. Teat skin condition was scored daily. Nonchapped teats (treatment 2) did not support skin or orifice colonization by S aureus. Treatment-1 teats healed most rapidly and supported less colonization in skin and orifice than did treatment-3 and -4 teats. Teat skin scores and skin colonization were lower for treatment-3 than treatment-4 teats. A correlation between teat skin colonization and teat skin conditions was found. Two intramammary infections were found in treatment-4 quarters and 1 in a treatment-3 quarter. On the basis of our findings, we concluded that poor teat skin condition will more readily support S aureus colonization, that a dip of 1% I2 with glycerin helped reduce S aureus colonization and was associated with faster healing, and that glycerin in teat dips may be of value in preventing colonization by S aureus and in promoting healing.