Ceftiofur sodium, a broad-spectrum cephalosporin antibiotic, was evaluated for safe use in horses. Male or female horses were allotted to groups and were given either saline solution (control), or 2.2, 6.6, or 11 mg of an aqueous solution of ceftiofur sodium/kg of body weight/d, IM, for 30 or 31 days. These dosages are expressed in terms of the ceftiofur free acid, and represent 1 to 5 times the proposed therapeutic dosage (2.2 mg/kg/d) administered for 3 times the maximal recommended duration of 10 days. Some of the horses were euthanatized and necropsied on day 31 or 32. The other horses were evaluated for an additional 30 days, and some were euthanatized and necropsied on day 60. The following types of data were collected: clinical observation; physical examination; pelleted food consumption; body weight; hematologic, serum biochemical, and urinalysis findings; organ weight; gross necropsy observations; and histopathologic findings. Ceftiofur sodium was generally well tolerated at the exaggerated doses and treatment durations used in these safety studies. Slight to mild decrease in pelleted food consumption was detected in horses given 6.6 or 11 mg of ceftiofur sodium/kg/d. Decreased food consumption began on day 2 and lasted for approximately 9 to 12 days. Generally, mild skeletal muscle irritation was detected by gross and microscopic examination of the injection sites of horses given ceftiofur sodium. Prevalence and severity of the muscle irritation tended to increase with increasing concentration of the dosing solution. Increases in serum aspartate transaminase and creatine kinase activities were detected in some of the ceftiofur-treated horses, and were attributed to mild skeletal muscle irritation at the injection sites. Slight increases in numbers of circulating neutrophils and plasma concentration of fibrinogen were detected in the blood of some ceftiofur-treated horses, and were attributed to mild inflammation at the injection sites or possibly in the large intestine because of a change in bacterial flora.

Sixteen healthy ponies were inoculated IV with Ehrlichia risticii-infected P388D1 mouse monocytes. Of the 16 ponies, 15 developed clinical signs of equine ehrlichial colitis. Twenty-four hours after onset of fever (rectal temperature > 38.8 degrees C), 7 ponies were treated with 25 mg of erythromycin stearate/kg of body weight and 10 mg of rifampin/kg, given orally every 12 hours for 5 days. The remaining 8 ill ponies served as nontreated controls. All ponies were observed for progression of clinical signs typical of equine ehrlichial colitis. Within 12 hours of initiation of treatment, 4 of the 7 treated ponies had rectal temperature < 38.4 C and, within 24 hours, 6 of the 7 ponies had rectal temperature < 38.3C. In contrast, all control ponies had rectal temperature > 39.2 C at 24 hours (P < 0.05). Of the 7 treated ponies, 4 no longer had signs of mental depression after the second day of treatment, and only 1 of the 7 ponies had mild signs of depression after the third day of treatment. In contrast, control ponies had high mental depression score during the observation period (P < 0.05). Feed intake improved in ponies of the treatment group, with feed intake of 4 of the 7 ponies returning to normal; the other 3 ponies were only mildly anorectic by the second day of treatment. Control ponies progressively decreased their feed intake during the observation period (P < 0.05). One control pony and 2 treated ponies developed diarrhea before the treatment/observation period began. Only 1 treated pony developed diarrhea after treatment began. Of the 8 control ponies, 7 developed diarrhea. Profound decrease in borborygmal sounds with silent periods lasting longer than 3 minutes was observed in 7 of the 8 control ponies. Only 1 of the 7 treated ponies had such profound decrease in borborygmi (P < 0.05). The decrease in borborygmal sounds progressed in the control ponies during the observation period. None of the treated ponies continued to have decreased borborygmi after treatment day 2 (P < 0.05). Of the 8 control ponies, 2 were euthanatized; all treated ponies survived. In survivors, signs lasted 8 to 17 (mean, 10) days in control ponies but only 1 to 5 (mean, 2.9) days in treated ponies.

Serum lipoprotein concentrations, routine serum biochemical values, and morphologic changes of the liver were evaluated in cats undergoing weight loss. Food was withheld from 6 obese and 6 control cats for 3 days (days 0 to 2), followed by feeding 50% of previous food intake for 26 days (days 3 to 28). Percutaneous liver biopsy specimens were obtained from all cats on days 0, 7, 14, and 28. Blood samples for serum biochemical analysis and lipoprotein profiles were obtained on days 0, 3, 7, 14, and 28. All cats lost weight throughout the study, and none developed signs of chemical illness, including those of idiopathic hepatic lipidosis syndrome. Serum total cholesterol concentrations decreased initially in all cats, but rapidly returned to normal after day 3 in obese cats, suggesting altered cholesterol metabolism during dietary restriction. Low-density lipoprotein concentrations decreased throughout the study in control cats, but were unchanged in obese cats. Examination of liver biopsy specimens from each cat revealed minimal lipid accumulation in all specimens, although some specimens contained hydropic degeneration.

The bioavailability and pharmacokinetics of ibuprofen, a nonsteroidal antiinflammatory drug, was studied in healthy Shetland ponies. Ibuprofen was administered IV, as a suspension, and as a solid solution oral paste to ponies from which food was withheld. The suspension paste was also administered to ponies that received hay and water ad libitum. Both formulations had an absolute bioavailability of about 80%. Bioavailability was not influenced by feeding.

Twenty-four dogs with induced, severe chronic renal failure were allotted to 2 groups of 12 each. Group-A dogs were fed a 0.4% phosphorus (P)/0.6% calcium, 32% protein diet, and group-B dogs were fed a 1.4% P/1.9% calcium, 32% protein diet. Dogs were studied over 24 months to determine clinical status, survival, blood biochemical alterations, glomerular filtration rate (GFR), urinary excretion of P and protein, renal morphologic changes, and renal tissue concentrations of calcium, P, and magnesium. Group-A dogs developed statistically significant differences from group-B dogs in several blood biochemical values (PCV and total solids, calcium, P, potassium, sodium, chloride, total CO2 (TCO2), anion gap, and parathyroid hormone concentrations) and in urinary P excretion. Mean (+/- SEM) GFR values in group-A and group-B dogs were nearly identical when diets were initiated (group A = 0.73 +/- 0.05 ml/min/kg of body weight; group B = 0.72 +/- 0.08 ml/min/kg), but significantly (P = 0.0346) lower GFR developed in group-B than in group-A dogs over time. At 24 months, GFR in survivors was 0.83 +/- 0.08 and 0.63 +/- 0.15 ml/min/kg for dogs of groups A and B, respectively. Other measurements favored the hypothesis that P/calcium restriction was beneficial, but values failed to reach statistical significance. Survival was greater at 24 months in group-A than in group-B (7 vs 5) dogs, and renal tissue concentrations of calcium and P were higher in group-B than in group-A dogs. Differences were not detected between groups in urinary excretion of protein and in the type or severity of renal lesions. We conclude that P/calcium restriction at 32% protein intake is beneficial to dogs with chronic renal failure, but that the degree of restriction imposed in group-A dogs of this study did not prevent development of abnormalities. Factors other than dietary P/calcium intake may have a role in progression of renal failure to uremia.

Cat foods containing propylene glycol (PG) induce Heinz body formation in feline erythrocytes. To further study the hematologic importance of dietary PG, 21 adult cats were allotted to 3 groups of 7 each and fed diets containing 0, 6, or 12% PG on a dry-weight basis. Cats fed PG had a dose-related increase in Heinz bodies within 2 weeks, and the increase persisted throughout the study. Although only slight changes occurred in PCV, hemoglobin concentration, and RBC count, punctate reticulocytes were significantly increased in the group fed 12% PG. Mean RBC survival was decreased in the groups fed 6 or 12% PG by 30 and 55%, respectively, compared with the control group. These data indicate that PG-containing diets cause a dose-dependent erythrocyte destruction, even when fed at concentrations as low as 6%.

The effects of 2 liquid formula diets differing in protein source were evaluated in orphan foals. The response of 7 foals fed a diet containing casein as the protein source, and 6 foals fed a diet containing a combination of whey and casein, was compared with the response in a reference group of 8 mare-raised foals. Orphaned foals were fed 150 kcal/kg of body weight/d, divided into 6 equal feedings of 25 kcal/kg. Formula intake was comparable among the experimental groups, and foals fed the liquid formula diet grew as well as mare-raised foals. There was no difference among groups in mean daily body weight gain, wither height, heart girth, body temperature, pulse, respiration rate, capillary refill time, or skin tenting. Insulin and blood glucose concentrations increased in both groups of foals fed formula diets, returning to prefeeding values within 4 hours. Differences among groups were found for serum alkaline phosphatase, alanine transaminase, cholesterol, creatinine, and glucose values; all other serum chemical values were comparable among groups. Plasma amino acid determinations revealed that arginine and ornithine were significantly lower in foals in both experimental groups than in reference foals, suggesting that arginine may have been the limiting amino acid in these diets. Diarrhea developed in foals in all treatment groups, but in most cases was self-limiting. These results suggest that the protein source of liquid formula diets may be less important in foals than in infants.

Nutritional and physiologic effects of clinically apparent and subclinical Ostertagia ostertagi infections were studied in 3 groups of 5 calves each. Group-1 calves were inoculated with 100,000 Ostertagia ostertagi third-stage larvae (L3)/calf/wk for 14 weeks. Group-2 calves were inoculated with 10,000 L3/calf/wk for 14 weeks, and group-3 calves were not inoculated. Calves in group 1 had decreased dry matter intake and feed utilization from 4 weeks after initial inoculation. Group-2 calves had no changes in dry matter intake, but had decreased feed utilization at 12 and 14 weeks. Calves with clinically apparent infections (group 1) lost a mean weight of 11.8 kg, whereas calves with subclinical infections (group 2) lost a mean of 46.6 kg, and control calves lost a mean of 60.7 kg. Calves with O. ostertagi infections (groups 1 and 2) also had decreased carcass quality at slaughtering, which was reflected in decreased dressing weights and increased water-holding capacity of the rib-eye muscle. Calves in groups 1 and 2 also had lower carcass yield and rib-eye muscle weight, and group-1 calves had decreased protein content. Results of hematologic, pathologic, parasitologic, and clinical examinations mirrored nutritional changes.