Effects of the endophyte Acremonium coenophialum in tall fescue on pregnant mares and foal viability were evaluated. Twenty-two mature pregnant mares were randomly chosen to graze either Kentucky-31 tall fescue that was free from A coenophialum (endophyte-free, EF) or tall fescue infected with A coenophialum (endophyte-present, EP) after the first 90 days of pregnancy through parturition. Concentrations of pyrrolizidine and ergopeptine alkaloids were significantly greater in EP grass, compared with EF pasture. Ten of 11 mares grazing EP pasture had obvious dystocia. Mean duration of gestation was significantly greater for the EP group, compared with the EF group. Foal survivability was severely reduced among mares grazing Ep fescue with only 1 foal surviving the natal period. Udder development and lactation were low in mares grazing EP grass. The absence of clinical problems in mares grazing EF grass implicated the endophyte as the causative agent of reproductive problems and perinatal foal mortality in pregnant mares grazing endophyte-infected fescue grass. Caution should be exercised in allowing pregnant mares to graze pastures infected with the endophyte A coenophialum.

Five adult 40- to 50-kg female sheep were surgically fitted with a reentrant cannulae placed in the proximal part of the duodenum just distal to the pylorus. By diversion of abomasal outflow, this model has been shown to produce hypochloremic metabolic alkalosis accompanied by dehydration, hypokalemia, and hyponatremia. Each sheep was subjected to 3 separate, 12-hour IV treatment trials, in each case preceded by a control period of 48 hours, and a diversion period of 36 to 96 hours, during which a hypochloremic (Cl- less than or equal to 60 +/- 2 mEq/L) metabolic alkalosis with hypokalemia and hyponatremia was produced. Treatment 1, consisting of 6 L of isotonic Na gluconate, was designed to replace volume without replenishing the Cl- deficit. Although hydration improved, plasma Cl- decreased further, and the sheep became increasingly weak and depressed. Treatment 2, consisting of 2 L of 1.8% NaCl, was designed to replace the Cl- deficit without replacing total volume. Plasma Na+ and Cl- concentrations returned to normal during the 12 hours of treatment; acid-base balance and plasma K+ concentrations returned to normal within 36 hours of treatment. During treatment 3 (control, no treatment), measured metabolic values changed minimally. We concluded that the IV replacement of Cl- without K+ is effective in the correction of experimentally induced hypochloremic metabolic alkalosis in sheep.

Sixty-three drugs, belonging to 10 chemical classes, were tested in vitro to determine effects on phagocytosis of 32P-labeled Staphylococcus aureus by neutrophils isolated from milk. Within each class, the number of antibiotics tested were: nonsteroidal anti-inflammatory drugs (NSAID; 8), peptolids (2), aminoglycosides (8), tetracyclines and fusidic acid (4), beta-lactam antibiotics (25), secretolytic agents (2), macrolides (5), polypeptides (2), and antibacterial quinolones (8). Percentage of phagocytosis was determined after incubating (2 hours at 37 C) 12.5 X 10(6) viable neutrophils, 200 X 10(6) 32P-labeled S aureus with antibiotics and 5% skimmed milk. Concentrations of antibiotics tested were 1,000, 500, and 10 microgram/ml of incubation media. When compared with nonantibiotic controls at the highest drug concentration, the NSAID acetylsalicylic acid and centrophenoxine increased phagocytosis 23.2 and 8.8%, respectively, and benzydamine, indomethacin, phenylbutazone, ibuprofen, and acetominophen decreased phagocytosis 22.8, 14.2, 9.8, 27.0, and 18.2%, respectively. The peptolids novobiocin and pristinamycin decreased phagocytosis 24.5 and 22.0%, respectively. The aminoglycosides tobramycin, amikacin, and gentamicin decreased phagocytosis 21.1, 15.4, and 19.2%, respectively. For the tetracyclines and fusidic acid, minocycline and doxycycline decreased phagocytosis 39.8 and 54.2%, respectively. The beta-lactam antibiotics carfecillin, cephapirin sodium, and cephacetrile sodium decreased phagocytosis 11.2, 12.8, and 23.8%, respectively. The secretolytic agent, bromhexin, increased phagocytosis 10.8%. These data indicate that the potential for enhanced phagocytosis exists through use of some NSAID, and for depressed phagocytosis through use of aminoglycosides, peptolids, tetracyclines, and beta-lactams, as well as certain other NSAID.

Pathophysiologic effects of Ostertagia ostertagi infection and their prevention by strategic anthelmintic treatments were studied in 3 groups each of 6 steer calves. Group-1 calves were noninfected controls. Group-2 calves were inoculated with 100,000 third-stage larvae on the 1st and 28th days of the experiment and grazed on pasture initially free of contamination. Group-3 calves were on a similar regimen as those in group 2, but were also treated with ivermectin 9 days after each larval inoculation. Group-2 calves had increased plasma pepsinogen and gastrin values and decreased weight gains, and total serum protein and albumin concentrations from the 2nd week of infection onward. They were anemic at 10 to 12 weeks and had lower carcass and meat quality at slaughter. Strategic anthelmintic treatments were effective in preventing these effects and calves in groups 1 and 3 had similar performances. On the basis of our findings, high pepsinogen values were related to worm burdens, whereas high gastrin concentrations were related to gastric lesions.

In mammalian species studied previously, pepsinogen consisted of biochemically different groups of isozymogens. By use of gel filtration chromatography and electrophoresis, we isolated a predominant pepsinogen from the gastric mucosa of a horse. Peptide mapping with V8 protease revealed differences with its porcine homologue. However, porcine and equine pepsinogens, when activated to pepsin, had a similar pattern of activity when hemoglobin was used as substrate. Those results suggest that differences must exist in the primary structure of the pepsinogens of the 2 species.

Eight ponies were allotted to 2 groups of 4. Group-1 ponies (1-4) were given 0.2 g of indole/kg of body weight orally and group-2 ponies (5 to 8) were given 0.1 g of indole/kg. Various physical, hematologic, and physiologic measurements were obtained after administration of indole. Intravascular hemolysis and hemoglobinuria were detected in both groups within 24 hours of dosing. Hemolysis was reflected by decreases in PCV, hemoglobin concentration, and RBC count, and an increase in indirect bilirubin. Erythrocyte fragility appeared to increase in both groups at 8 hours after dosing and peaked at 16 hours after dosing. At 72 hours after dosing, the RBC fragility value was less than predose measurements. Heinz body formation was noticed in group-2 ponies, but not in group 1. Plasma indole concentrations increased in both groups from the nondetectable predose concentrations. Group-1 values were 203% of group-2 values. In group 2, plasma indole was nondetectable by 12 hours, whereas low concentrations could still be measured in the group-1 ponies at 24 hours. Ponies in group 1 died or were euthanatized between 24 and 72 hours after dosing, whereas group-2 ponies were euthanatized between 48 and 120 hours. At necropsy, all body fat, mucous membranes, and elastic tissue were stained yellow. Hemoglobinuric nephrosis was the most prominent microscopic lesion. Results of this study indicated that indole, a metabolite of the amino acid tryptophan, causes acute intravascular hemolysis in ponies.

A study was conducted to determine whether dietary supplements with alpha-linolenic acid altered the ability of equine peritoneal macrophages to produce tumor necrosis factor (TNF) in response to endotoxin. Peritoneal macrophages were harvested from 6 healthy adult horses before and after the horses were fed a nutritionally balanced ration that contained 8% linseed oil as a source of alpha-linolenic acid. The macrophages were cultured in media containing no additives (control), endotoxin (0.5 to 50 ng/ml), or the calcium ionophore, A23187. Macrophage supernatants were collected after 6 and 24 hours' incubation and stored at -70 C. Tumor necrosis factor activity was estimated by a modified in vitro cytotoxicity bioassay, using the murine fibrosarcoma cell line, WEHI 164 clone 13. The TNF activity after 6 and 24 hours' incubation was greater in culture media of macrophages exposed to endotoxin than in media from control macrophages. For macrophages cultured in media that contained endotoxin, neither the concentration of endotoxin nor incubation time had any effect on TNF activity. Endotoxin-induced macrophage production of TNF, as determined by measurement of TNF activity, was significantly less after horses were fed the alpha-linolenic acid-rich ration for 8 weeks.

Phenotypic characteristics of 12 paired, Salmonella serotypes isolated from healthy and ill chickens were compared. Variables compared included antibiotic resistance profiles, production of colicins and siderophores, mannose-sensitive hemagglutination of erythrocytes, resistance to serum complement, carbon source utilization, presence and transmissibility of R plasmids, and invasiveness in primary chicken kidney cell culture. Differences were found between pairs for utilization of carbon sources, mannose-sensitive hemagglutination of erythrocytes, and invasiveness in cell culture.

The in vivo effects of a single prophylactic dose of recombinant bovine interferon (rBoIFN)-alphaI1 in calves with salmonellosis were investigated, using a Salmonella typhimurium infection model. Treatment with rBoIFN-alphaI1 reduced the degree of septicemia compared with that in control groups, and, in one experiment, using disease of reduced severity, body temperature was lower in treated calves than in controls.

The breaking strength (stress at failure) of equine third metacarpal bones, with and without clustered drill holes, was determined in vitro. Paired ossa metacarpalia II-IV of 39 horses (n = 39) between 2 and 7 years old were tested in palmarodorsal 3-point bending. Four treatments were compared. Clustered 2.7- or 3.5-mm drill holes, in a 4- or 7-hole pattern, were made in the dorsal cortex of the distal diaphysis of the left third metacarpal bone. Undrilled right third metacarpi were used as controls. Bones with clustered drill holes failed by an oblique fracture through 1 or more drill holes, whereas undrilled bones failed with a middiaphyseal transverse fracture. Clustered drill holes acted as a stress concentrator and significantly (P < 0.05) decreased the stress required for failure. However, differences in breaking strength between treatment groups were not significant (P > 0.05).