Objective: To determine the impact of a free-choice diet on nutritional intake and body condition of feral horses. Animals: Cadavers of 41 feral horses from 5 Australian locations. Procedures: Body condition score (BCS) was determined (scale of 1 to 9), and the stomach was removed from horses during postmortem examination. Stomach contents were analyzed for nutritional variables and macroelement and microelement concentrations. Data were compared among the locations and also compared with recommended daily intakes for horses. Results: Mean BCS varied by location; all horses were judged to be moderately thin. The BCS for males was 1 to 3 points higher than that of females. Amount of protein in the stomach contents varied from 4.3% to 14.9% and was significantly associated with BCS. Amounts of water-soluble carbohydrate and ethanol-soluble carbohydrate in stomach contents of feral horses from all 5 locations were higher than those expected for horses eating high-quality forage. Some macroelement and microelement concentrations were grossly excessive, whereas others were grossly deficient. There was no evidence of ill health among the horses. Conclusions and Clinical Relevance: Results suggested that the diet for several populations of feral horses in Australia appeared less than optimal. However, neither low BCS nor trace mineral deficiency appeared to affect survival of the horses. Additional studies on food sources in these regions, including analysis of water-soluble carbohydrate, ethanol-soluble carbohydrate, and mineral concentrations, are warranted to determine the provenance of such rich sources of nutrients. Determination of the optimal diet for horses may need revision.

Intrareticularly placed sustained-release selenium boluses were administered to 1 group of selenium-deficient heifer calves (n = 16), and a second group (n = 16) was left as nontreated controls. Age range for all calves was 83 to 156 days. These boluses release 3 mg of selenium each day, as sodium selenite. Measurements of blood selenium concentration, plasma copper concentration, hepatic copper concentration, and body weight were made over a 188-day day study. The treated group of calves had significantly higher mean blood selenium concentration at posttreatment days 68 (P < .0001), 112 (P < 0.0001), and 188 (P < 0.005) than did the control group. Mean blood selenium concentration in the treated calves was > 0.10 micrograms/ml for 188 days. These boluses were observed to be clinically safe; signs of selenium toxicosis were not detected and untoward effects were not seen in the selenium-treated calves. There were no differences between control and treatment groups with respect to mean hepatic copper concentration or mean plasma copper concentration. There were no observed differences between the control and treatment groups with respect to weight gain during the study.

The effect of dietary copper deficiency on T-cell mitogenic responsiveness and phenotypic profile of blood mononuclear cells (MNC) in weaned pigs was examined. Outbred, weaned pigs were fed a semipurified diet containing adequate (6.4 mg/kg of body weight) or deficient (0.8 mg(kg) amounts of Cu. Pigs fed the low Cu diet for 10 weeks had markedly decreased concentrations of Cu in liver and plasma, and hypertrophic hearts. In vitro reactivity of MNC from Cu-deficient pigs to phytohemagglutinin and concanavalin A was significantly suppressed. This functional impairment was not associated with a decrease in the percentages of T cells, CD4 or CD8 cell subsets, or B cells. Expression of SLA-DQ and SLA-DR class II major histocompatibility complex (MHC) antigens was increased by Cu deficiency, the former significantly. Unlike rodents, in which inadequate Cu nutriture induces functional T cell deficiency that is associated with a decrease in the CD4 T-cell subset, swine fed inadequate Cu diets for 10 weeks had no changes in MNC subsets yet clearly manifested functional impairment of T-cell responses.

Although low plasma taurine concentrations have been associated with congestive cardiomyopathy in cats, the cause of taurine depletion in cats consuming adequate quantities of taurine is unknown. Taurine depletion and cardiovascular disease (cardiomyopathy and thromboembolism) developed unexpectedly in 3 of 6 healthy adult cats during a potassium-depletion study. Plasma taurine concentration decreased significantly (P < 0.05) and rapidly over an 8-week period (from 98 to 36 nmol/ml) in 6 cats that consumed a potassium-deficient diet (0.20% potassium, dry matter basis) that was acidified with 0.8% ammonium chloride, despite containing dietary taurine concentrations (0.12% dry matter basis) in excess of amounts currently recommended. Taurine concentrations were significantly lower in cats fed the acidified diet than in 6 cats fed a potassium-deficient diet that was not acidified (36 nmol/ml vs 75 nmol/ml) after 8 weeks. In addition, plasma taurine concentrations did not decrease over a 6-month period in 8 cats that were fed a potassium-replete diet with acidifier. Plasma taurine concentrations were lowest in 3 cats that died of cardiovascular disease in the group receiving potassium-deficient, acidified diets. These data indicated an association between taurine and potassium balance in cats and suggested that development of taurine depletion and cardiovascular disease may be linked to concurrent potassium depletion.

Microcytosis is a common laboratory finding in dogs with congenital portosystemic shunt (PSS), although its pathogenesis is not yet understood. Because the most common cause of microcytosis in dogs is absolute or relative iron deficiency, iron status was evaluated in 12 young dogs with PSS. Complete blood counting was done before surgical correction in all dogs, and in 5 dogs after surgery, by use of an automated hematology analyzer. Serum iron concentration and total iron-binding capacity (TIBC) were determined colorimetrically, and percentage of transferrin saturation was calculated. Erythrocyte protoporphyrin content was quantified by use of front-face fluorometry. Serum ferritin concentration was measured by use of ELISA. Serum ceruloplasmin content was determined colorimetrically (with p-phenylenediamine dihydrochloride as substrate) as an indirect indicator of subclinical inflammation, which may result in impaired iron utilization. Special stains were applied to liver (10 dogs; Gomori's) and bone marrow aspiration biopsy (7 dogs; Prussian blue) specimens for qualitative assessment of tissue iron content. Nonpaired Student's t-tests were used to compare serum iron concentration, TIBC, percentage of transferrin saturation, and erythrocyte protoporphyrin, ferritin, and ceruloplasmin concentrations in dogs with PSS with those in clinically normal dogs. All dogs had microcytosis before surgery; microcytosis resolved in 3 dogs after surgical correction. Serum iron concentration and TIBC were significantly lower, in PSS-affected dogs than in clinically normal dogs. Erythrocyte protoporphyrin, ferritin, and ceruloplasmin concentrations in PSS-affected dogs were not significantly different from those in healthy dogs. Excess iron was not detected consistently in liver or bone marrow samples. These results suggest that relative iron deficiency, perhaps associated with altered iron transport and not absolute iron deficiency, is related to microcytosis in dogs with PSS.

Six primiparous Holstein cows were fed a Se-deficient diet, beginning at least 90 days before their first calving, and 6 other primiparous cows were given the same diet plus a supplement of 2 mg of Se/cow/d as sodium selenite. All cows were fed their diets for the duration of the experimental period. One uninfected quarter of each cow was injected with 25 microgram of Escherichia coli endotoxin at postpartum week 5. Leukocytes were isolated by centrifugation from milk collected at postinjection hour 16. Isolated cells were 92 +/- 3% neutrophils and were incubated with Staphylococcus aureus or E coli in a 1:300 ratio. Phagocytosis and intracellular killing by neutrophils were assessed after 0, 30, 60, and 90 minutes by a fluorochrome assay, using acridine orange. Viability of neutrophils was assessed by use of trypan blue. Superoxide anion production and hydrogen peroxide production by neutrophils also were determined. Cows fed Se-deficient diets had significantly (P < 0.05) lower blood Se concentration and blood glutathione peroxidase activity than cows fed Se-supplemented diets. Selenium status had no effect on the phagocytic capacity of neutrophils. Neutrophils obtained from cows fed Se-supplemented diets killed a significantly (P < 0.05) higher percentage of ingested bacteria than did neutrophils from cows fed the Se-deficient diet. Viability was significantly (P < 0.05) reduced by incubation with S aureus in neutrophils from both groups of cows, with neutrophils from Se-deficient cows having lower viability. Superoxide anion production did not differ significantly between neutrophils from the 2 groups, but extracellular hydrogen peroxide concentration was significantly (P < 0.05) higher in neutrophils harvested from milk of cows fed the Se-deficient diet.

Muscle damage attributable to selenium (Se)/vitamin E deficiencies is known to develop at birth or later in lambs. The purpose of this study was to determine whether and when muscle damage develops in utero. Thirty pregnant ewes maintained on Se-deficient forages from birth were allotted to 3 equal groups. Half of each group was given a single IM injection of 0.056 mg of Se/kg of body weight, 1 month before parturition. At 3 weeks before parturition, cesarean section-derived fetuses from Se-deficient ewes did not have evidence of muscle damage. At 2 weeks before parturition, fetuses from Se-deficient ewes had biochemical evidence of congenital nutritional myopathy, as evidenced by low blood Se concentration (P < 0.05) and by increased plasma creatine kinase (P < 0.001) and lactate dehydrogenase (P < 0.01) activities, compared with fetuses from Se-treated ewes. Thus, for optimal protection of fetuses and newborn lambs in Se-deficient areas, Se should be administered to ewes at least 1 month before parturition.

Effects of selenium (Se) deficiency and supplementation on production of colostral immunoglobulins by beef cows and transfer of antigen-specific and nonspecific immunoglobulins to their calves were examined. Eighty beef cows, with marginal to deficient Se status (blood Se concentration, 50 micrograms/L), were allotted by breed and age to 1 of 4 Se treatment groups (n = 20/group): no supplemental Se; parenteral administration of 0.1 mg of Se and 1 mg of vitamin E/kg of body weight; ad libitum consumption of 120 mg of Se/kg of salt-mineral mix (SMM); and parenteral administration of 0.1 mg of Se and 1 mg of vitamin E/kg plus ad libitum consumption of 120 mg of Se/kg of SMM. All cows were inoculated IM with lysozyme. Cows consumed Se-deficient pastures or hay (21 to 62 micrograms/kg) during the study that began at mid-gestation and ended at postpartum hour 24. Although the concentration of specific lysozyme antibodies was not affected, cows given 120 mg of Se/kg of SMM (treatments 3 and 4) had higher colostral IgG concentration (P < 0.002) than did Se-deficient cows (treatments 1 and 2). Calves from cows in treatments 3 and 4 had higher postsuckle serum concentrations of IgG (P < 0.01) than did calves from cows in treatments 1 and 2. Colostral IgM and calf serum IgM concentrations did not differ among treatments.

Cats with cardiomyopathy, especially dilated cardiomyopathy associated with taurine deficiency, often develop systemic thrombi. To investigate the relation of taurine deficiency to formation and persistence of thrombi, cats were made taurine-deficient by consumption of a casein-based taurine-deficient diet, then were evaluated for anticoagulant and pro-fibrinolytic activities and platelet function. The cats served as their own controls in the taurine-replete state; then, values were compared for the taurine-deficient state. Plasma (P < 0.01), blood (P < 0.05), and platelet (P < 0.05) taurine concentrations were decreased markedly after cats consumed the taurine-deficient diet for 6 weeks, compared with baseline concentrations before diet. Compared with the taurine-replete state, taurine deficiency induced significantly (P < 0.05) increased mean antithrombin III activity, no significant change in plasminogen and fibrinolytic activities, and similar clot retraction/lysis test results. Decreased (P < 0.01) adenosine diphosphate (ADP)-induced platelet aggregation and [14C]serotonin release, and slightly increased (P < 0.05) collagen-induced platelet [14C]serotonin release, but unchanged collagen-induced platelet aggregation were observed in taurine-deficient cats, compared with taurine-replete cats. Changes in antithrombin III activity most likely reflected hepatocellular acute-phase reaction, which indicates that taurine deficiency may induce a stress-responsive state. Results of platelet function testing indicate that taurine may modulate platelet responsiveness to physiologic agonists, but not in a consistent manner. That platelets from the taurine-deficient cats had decreased responsiveness to ADP, but increased responsiveness to collagen is surprising, because irreversible aggregation is mediated by release of granule-associated ADP after sufficient initial stimulus. All cats had normal clot retraction in dilute blood, which indicated adequate platelet numbers and function; however, clots failed to lyse in vitro. To the authors knowledge, this observation, at present, lacks adequate explanation. Development of marked taurine deficiency and altered in vitro results of anticoagulant activities and some platelet function tests did not result in clinical manifestations in our cats. Results of our study do not conclusively document a pathophysiologic role of taurine depletion in the formation or persistence of thrombi.

Monensin is an ionophoretic antibiotic, which selectively transports alkali metal cations across biological membranes. In growing swine, monensin toxicosis causes acute, degenerative cardiac and skeletal myopathy resembling vitamin E-selenium deficiency. Selenium is an essential trace element incorporated in glutathione peroxidase (GSH-Px), an antioxidant enzyme system that protects subcellular membranes. In our study, we examined the effects of monensin on body weight, Se balance, antioxidant status, and serum concentrations of selected minerals in growing pigs that were genetically hypo- or hyperselenemic (hypo-Se and hyper-Se, respectively). Three groups of eight 8-week-old pigs, each comprised of 4 hypo-Se and 4 hyper-Se pigs (76.4 +/- 3.0 and 106.3 +/- 10.3 ng of Se/ml of serum, respectively), were fed standard diets containing 0.1 mg of supplemental Se/kg of body weight, and either 0, 200, or 400 mg of monensin/kg for a 77-day period, followed by a 28-day monensin withdrawal period. On days 0, 7, 28, 56, 70, and 98, all pigs were weighed and blood was collected for determination of serum GSH-Px, creatine phosphokinase, and aspartate transaminase values, as well as serum concentrations of vitamin E, Se, Ca, Cu, Fe, K, Mg, Na, P, and Zn. Significance of main effects of monensin treatment, genetic Se status, and their interactions was tested by Fisher's variance ratio test, followed by conditional comparison of treatment means with a Bonferroni test. Signs of monensin toxicosis were not observed and monensin consumption had no effect on body weight, or serum creatine phosphokinase, aspartate transaminase, or Se values. However, pigs consuming monensin had consistently higher serum GSH-Px activities, possibly because of increased synthesis of this adaptive antioxidant enzyme. Interactions were not found between monensin and genetic Se status. Hyperselenemic pigs were heavier and had higher serum Se and GSH-Px values than hypo-Se pigs. Furthermore, hypo-Se and hyper-Se pigs were hypo- and hypercupremic, respectively, suggesting genetic regulation of copper status. It is likely that pigs with inadequate antioxidant status (hyposelenemia, hypocupremia) are more susceptible to diseases associated with cellular membrane damage, such as vitamin E-Se deficiency disease and monensin toxicosis.