Twelve male cats were fed 2 diets that differed in the source of P. In diet 1 (1.4% P), 62.7% of P originated from poultry, meat, and fish meal, and the remainder from other organic ingredients of food. In diet 2 (1.6% P), 63.5% of P was derived from neutral monobasic/dibasic salts, and the remainder from other organic ingredients of the food. The P intake was nearly the same with both diets, but there was a significant (P less than 0.05) difference between diets in the percentage of ingested P that was excreted in the urine (14.7 +/- 5.3% for diet 1; 34.9 +/- 8.4% for diet 2), and in 6-day urinary P excretion (774 +/- 290 mg for diet 1; 2,004 +/- 556 mg for diet 2). The P concentrations in urine samples obtained by cystocentesis after cats ate were significantly (P less than 0.05) higher when cats were fed diet 2 than when those same cats were fed diet 1. Plasma P concentrations increased after ingestion of diet 2, but were unchanged after ingestion of diet 1. Seemingly, urinary excretion of P was markedly influenced by dietary composition. Diets with the same P content have potential for different biologic effects because of differences in availability of P.

Ten Holstein heifers were fed a selenium-deficient (SeD) diet (0.04 mg of Se/kg on a total ration dry-matter basis) 3 months before calving and throughout their first lactation. A selenium-supplemented (SeS) diet (2 mg of Se/head/d) was fed to a group of 10 heifers. In about the 14th week of lactation, the cows were challenge-exposed to Escherichia coli by administering 15 to 40 colony-forming units (CFU) into 1 mammary gland. Selenium concentration microgram/ml) in blood around the time of challenge exposure was 0.033 +/-0.002 (mean +/- SEM) in SeD and 0.132 /-0.006 in SeS cows. Infections were established in all challenge-exposed quarters. The frequency of quarter atrophy and agalactia, and reduction in whole-udder milk yield in the first 4 days after challenge exposure, were greater (P < 0.05) in the SeD cows. Log10 peak bacterial concentrations in milk were higher (P < 0.05) in SeD (7.63 +/- 0.34 CFU/ml) than in SeS cows (5.57 0.66 CFU/ml). Mean log bacterial concentration was significantly higher (P < 0.05) from 12 to 20 hours after challenge exposure in SeD than in SeS cows. Duration of infection was significantly greater (P < 0.05) in SeD (162.0 +/- 12.0) than in SeS cows (114.4 +/- 18.0 hours). Milk somatic cell counts increased significantly more slowly (P < 0.05) in SeD than in SeS cows from 8 to 16 hours after challenge exposure. Ratios of milk somatic cells to bacteria in milk were significantly lower (P < 0.05) in SeD than in SeS cows at l2 and 16 hours after challenge exposure.

Phagocytic and oxidative metabolic activities of bovine blood neutrophils were determined in the presence of glycolytic (NaF) and cytoskeletal (colchicine, cytochalasin B, and prostaglandin E1) inhibitors. Phagocytosis and postphagocytic oxidative metabolic activity, measured by nitroblue tetrazolium reduction, were determined using zymosan, Escherichia coli, Staphylococcus aureus, or Streptococcus agalactiae. Sodium fluoride (1.25 micromolar to 1.25 mM concentrations) did not significantly (P greater than 0.05) inhibit phagocytosis of S aureus and Str agalactiae, whereas phagocytosis of zymosan and E coli was significantly (P less than 0.05) inhibited only at 1.25 mM concentration. Colchicine at 1.25 nM to 1.25 micromolar conce ntrations significantly inhibited phagocytosis of zymosan and E coli, but not of S aureus and Str agalactiae. Cytochalasin B at 1.25 nM to 1.25 micromolar concentrations significantly inhibited phagocytosis of zymosan and all 3 bacteria, whereas prostaglandin E1 was noninhibitory at similar concentrations. Nitroblue tetrazolium reduction, in general, was not significantly affected by NaF and cytoskeletal inhibitors.

The uptake of colostral IgG and IgM, their serum half-lives, and the rates of endogenous synthesis of IgG and IgM were evaluated in 6 newborn foals fed bovine colostrum (principals) and 6 foals allowed to suckle their dams (controls). The principal foals were fed 400 ml of bovine colostrum (IgG, 10,000 mg/dl and IgM, 200 mg/dl) at 2-hour intervals, from 2 to 20 hours after foaling (total dose, 4 L). Serum IgG and IgM concentrations were determined by single radial immunodiffusion from birth to 98 days of age. At foaling, principal foals had no detectable serum equine IgG, but 1 control foal had serum equine IgG of 185 mg/dl. AFter ingestion of colostrum, there was no significant difference in the maximal serum bovine IgG concentration (range, 1,350 to 3,300 mg/dl) in the principal foals, and maximal serum equine IgG concentration (range, 500 to 6,000 mg/dl). The calculated biological bovine and equine IgG half-life in the principal and control groups was 9.4 and 26 days, respectively. Endogenous IgG synthesis was first detected in 1 principal foal at 3 days of age, but was detected first between 28 and 42 days in the other principal foals. Starting on day 56 there was no significant difference in serum equine IgG concentration between groups. At foaling, foals in both groups had low equine IgM concentrations. In the control foals, there was marked individual variation in the increases in equine IgM concentration (range, 5 to 73 mg/dl) after ingestion of colostrum. With the exception of day 49 after foaling, there was no statistical difference between groups for serum IgM concentration after day 3, and both groups had parallel rates of IgM synthesis. Bovine IgM was undetectable at foaling and maximal serum concentration ranged from 200 to 350 mg/dl following ingestion of colostrum. The calculated bovine and equine IgM half-lives were 8 and 5 days, respectively. The coefficients of absorption of bovine IgG and IgM were 30.9 and 84, respectively, in the principal foals. In the control foals, the coefficient of absorption of equine IgG and IgM was 35 and 30, respectively. One principal foal was excluded from the study because it died of aspiration pneumonia at 2 days of age.

Tissue specimens from muscle, liver, kidney, and injection sites were collected, and serum was obtained from 3 calves euthanatized on each of posttreatment days 5 and 22. Calves were treated with 6.7, 13.4, or 20 mg of oxytetracycline (OTC)/kg of body weight, IM, once daily for 3 days; these dosages are 1, 2, and 3 times the label dose, respectively. One control calf was euthanatized on each of posttreatment days 5 and 22. In treated male calves killed 2 days after the last injection, OTC residues were detected in all tissues and serum, using high-performance liquid chromatography. Tissues from all injection sites also were considered positive for antimicrobial residues, using swab test on premises (STOP), microbial inhibition test (MIT), and thin-layer chromatography-biautography (TLCB) test. Kidney tissues from a calf given 13.4 mg of OTC/kg and kidney and liver tissues from a calf given 20 mg of OTC/kg also were considered positive, using the MIT and TLCB. Results of the STOP only were considered positive for the liver and kidney of a calf given 20 mg of OTC/kg, but substitution of Saskatoon antibiotic medium-3 for the original medium (antibiotic medium-5) allowed the STOP to detect residues in these tissues from all treated calves. In female calves killed 19 days after the last injection, the STOP, MIT, and TLCB procedures revealed positive results for tissues from some injection sites, but revealed negative results for other tissues. High-performance liquid chromatographic analyses detected OTC in tissues from injection sites from all treated calves, in muscle and liver from a calf given 20 mg of OTC/kg, and in kidneys from calves given 13.4 or 20 mg of OTC/kg. The STOP, MIT, and TLCB procedures lacked the sensitivity of high-performance liquid chromatography for detection of OTC residues. However, the STOP procedure with Saskatoon antibiotic medium-3 did perform appropriately in that it failed to detect label doses in tissues from injection sites, but did detect 2 and 3 times extralabel doses after the recommended withdrawal time, and results were considered positive for all tissues after 2 days of withdrawal. A significant (P less than 0.05) loss of OTC was not observed after samples were stored at -20 C for 80 days. The highest concentration of OTC residues persisted in kidneys and tissues from injection sites.

Norfloxacin, a 4-quinolone antibiotic, was administered orally to 4 healthy dogs at dosages of 11 and 22 mg/kg of body weight, every 12 hours for 4 days, with a 4-week interval between dosing regimens. Serum and tissue cage fluid (TCF) norfloxacin concentrations were measured at 0, 0.5, 1, 1.5, 2, 3, 4, 5, 6, 8, 10, and 12 hours after the first and seventh dose of each dosing regimen. When administered at a dosage of 11 mg/kg, the mean peak serum concentration (Cmax) was 1.0 micrograms/ml at 1 hour, the time of mean peak concentration (Tmax) after the first dose. After the seventh dose, the Cmax was 1.4 micrograms/ml at Tmax of 1.5 hours. The Tmax for the TCF concentration was 5 hours, with Cmax of 0.3 micrograms/ml and 0.7 micrograms/ml after the first and seventh dose, respectively. When administered at a dosage of 22 mg/kg, the serum Tmax was 2 hours after the first dose, with Cmax of 2.8 micrograms/ml. After the seventh dose, the serum Tmax was 1.5 hours, with Cmax of 2.8 micrograms/ml. The Tmax for the TCF concentration was 5 hours after the first and seventh doses, with Cmax of 1.2 micrograms/ml and 1.6 micrograms/ml, respectively. After the seventh dose, the serum elimination half-life was 6.3 hours for a dosage of 11 mg/kg and was 6.7 hours for a dosage of 22 mg/kg. For serum concentration, the area under the curve from 0 to 12 hours (AUC0 leads to 12) was 8.77 micrograms.h/ml and 18.27 micrograms.h/ml for dosages of 11 mg/kg and 22 mg/kg, respectively. The corresponding AUC0 leads to 12 for the TCF concentration was 6.20 micrograms.h/ml and 16.42 micrograms.h/ml. The percentage of TCF penetration (AUC(TCF)/AUCserum) was 71% at a dosage of 11 mg/kg and 90% at a dosage of 22 mg/kg.

Water vapor-saturated air was delivered to 12 healthy housed horses for 2 hours daily for 5 days. Treatment had no effect on tracheal mucus transport rate, bronchoalveolar lavage total and differential cell counts, blood cell counts, or plasma fibrinogen concentration.

Functional capabilities of morphologically mature (segmented) and immature granulocytes (neutrophils and eosinophils) from bone marrow from cows were studied and compared with similar activities of segmented granulocytes from blood. Phagocytosis of Escherichia coli and postphagocytic oxidative metabolic stimulation, measured by nitroblue tetrazolium (NBT) reduction, were evaluated simultaneously. Phagocytosis was observed readily in segmented neutrophils, neutrophilic bands, and metamyelocytes and rarely in myelocytes. Phagocytosis was not seen in promyelocytes and myeloblasts. Neutrophilic bands and metamyelocytes were phagocytically less active than were segmented neutrophils. Washed segmented bone marrow neutrophils possessed phagocytic activity similar to that of blood neutrophils, whereas the activity of unwashed segmented bone marrow neutrophils was markedly less than that of blood neutrophils. Reduction of NBT was observed only in blood segmented neutrophils and bone marrow segmented neutrophils; the magnitude of NBT reduction was significantly (P = less than 0.005) less in bone marrow neutrophils than in blood neutrophils. Eosinophils were phagocytically less competent than were neutrophils. The NBT reduction was observed only in eosinophils from blood, but not in eosinophils from bone marrow.

Serum concentrations of iodine were determined after cattle were given ethylenediamine dihydriodide (EDDI) orally at dosages ranging from 0.0 (placebo) to 0.77 mg/kg of body weight/day. The serum iodine concentration was correlated with the dosage of EDDI. A rate of 0.11 mg EDDI/kg/day was correlated with serum iodine concentrations (20 to 80 micrograms/dl) previously found to be effective in preventing foot rot in cattle. A linear dose-response curve that was generated could be helpful in predicting dosage of EDDI if the serum iodine concentration is known.

The possibility that the canine pancreas might have an important role in the physiologic absorption of cobalamin (vitamin B12) has been explored by determining the effect of exocrine pancreatic insufficiency on cobalamin absorption and by examining the subsequent influence of bovine pancreatic enzymes and canine pancreatic juice. Exocrine pancreatic insufficiency was induced by ligation of pancreatic ducts and confirmed by indirect assessment of exocrine pancreatic function. Cobalamin absorption was determined by oral administration of cyano[58Co]cobalamin and quantitation of radioactivity in blood, urine, and feces during 48 hours. Pancreatic duct ligation resulted in a significant (P less than 0.001) decrease in cobalamin absorption, which was not restored by oral administration of bovine pancreatic enzymes, despite considerable improvements in steatorrhea and in vivo proteolytic activities. In marked contrast, malabsorption of cobalamin was significantly (P less than 0.05) reversed by oral administration of canine pancreatic juice. These results indicate that pancreatic secretions have an important role in the normal absorption of cobalamin in the dog, a role that does not appear to be attributable to pancreatic enzymes, but is consistent with the existence of a pancreatic intrinsic factor in this species.