Vitamin and Trace Element Nutrition of Stocker Cattle on Small Grain and Winter Annual Pastures.

This article reviews the trace mineral and macro mineral content of small grain forages and the potential role in the health of cattle grazing the forages. Reasons for the variability of trace mineral content in small grain forages are discussed, as well as the role of antagonists, such as sulfur and molybdenum, in creating trace mineral deficiencies. The sampling of cattle for the determination of trace mineral statues is described, including which samples to collect for analysis, as well as sample handling. The authors offer a useful discussion on the vitamin content of small grain forages, and conclude that vitamin supplementation is not necessary.

The comparative toxicity of a reduced, crude comfrey (Symphytum officinale) alkaloid extract and the pure, comfrey-derived pyrrolizidine alkaloids, lycopsamine and intermedine in chicks (Gallus gallus domesticus).

Comfrey (Symphytum officinale), a commonly used herb, contains dehydropyrrolizidine alkaloids that, as a group of bioactive metabolites, are potentially hepatotoxic, pneumotoxic, genotoxic and carcinogenic. Consequently, regulatory agencies and international health organizations have recommended comfrey be used for external use only. However, in many locations comfrey continues to be ingested as a tisane or as a leafy vegetable. The objective of this work was to compare the toxicity of a crude, reduced comfrey alkaloid extract to purified lycopsamine and intermedine that are major constituents of S. officinale. Male, California White chicks were orally exposed to daily doses of 0.04, 0.13, 0.26, 0.52 and 1.04 mmol lycopsamine, intermedine or reduced comfrey extract per kg bodyweight (BW) for 10 days. After another 7 days chicks were euthanized. Based on clinical signs of poisoning, serum biochemistry, and histopathological analysis the reduced comfrey extract was more toxic than lycopsamine and intermedine. This work suggests a greater than additive effect of the individual alkaloids and/or a more potent toxicity of the acetylated derivatives in the reduced comfrey extract. It also suggests that safety recommendations based on purified compounds may underestimate the potential toxicity of comfrey.

Reduced neophobia: a potential mechanism explaining the emergence of self-medicative behavior in sheep.

Gastrointestinal helminths challenge ruminants in ways that reduce their fitness. In turn, ruminants have evolved physiological and behavioral adaptations that counteract this challenge. For instance, emerging behavioral evidence suggests that ruminants self-select medicinal compounds and foods that reduce parasitic burdens. However, the mechanism/s leading to self-medicative behaviors in sick animals is still unknown. We hypothesized that when homeostasis is disturbed by a parasitic infection, consumers should respond by increasing the acceptability of novel foods relative to healthy individuals. Three groups of lambs (N=10) were dosed with 0 (Control-C), 5000 (Medium-M) and 15000 (High-H) L3 stage larvae of Haemonchus contortus. When parasites had reached the adult stage, all animals were offered novel foods and flavors in pens and then novel forages at pasture. Ingestive responses by parasitized lambs were different from non-parasitized Control animals and they varied with the type of food and flavor on offer. Parasitized lambs consumed initially more novel beet pulp and less novel beet pulp mixed with tannins than Control lambs, but the pattern reversed after 9d of exposure to these foods. Parasitized lambs ingested more novel umami-flavored food and less novel bitter-flavored food than Control lambs. When offered choices of novel unflavored and bitter-flavored foods or different forage species to graze, parasitized lambs selected a more diverse array of foods than Control lambs. Reductions in food neophobia or selection of a more diverse diet may enhance the likelihood of sick herbivores encountering novel medicinal plants and nutritious forages that contribute to restore health.

Analysis in horse hair as a means of evaluating selenium toxicoses and long-term exposures.

Horses are very susceptible to chronic selenosis if grazed on seleniferous forages for a prolonged period. In this study, mane and tail samples from horses that exhibited classical hoof lesions of chronic selenosis were analyzed by inductively coupled plasma mass spectrometry for selenium (Se) content. The horses had grazed for 6 months, from approximately May 15 until November 15, each year for three grazing seasons in a pasture containing seleniferous forages and water sources with elevated Se concentrations. The segmented hair samples showed a cyclic pattern in Se concentrations in the mane and tail, which corresponded to entering and exiting the contaminated pasture. The Se concentration in the tail of one horse could be traced for three grazing seasons. These results demonstrate that in some cases hair samples can be used to determine Se exposure in horses for up to 3 years postexposure.

Dermatopathy in juvenile Angus cattle due to vitamin A deficiency.

In juvenile cattle, vitamin A deficiency is reported most commonly as a neurological condition; only rarely are there dermatologic manifestations. In the current study, alopecia, severe epidermal and follicular orthokeratosis, and acanthosis due to hypovitaminosis A are reported in 2 of 32 Angus calves, with a third animal suspected. Affected animals responded to vitamin A supplementation, and no additional calves displayed signs. Vitamin A acts on skin by regulating DNA transcription in keratinocytes, reducing the number of tonofilaments and desmosomes, both involved in cell-to-cell adhesion. Hence, adequate levels of dietary vitamin A are necessary for normal keratinocyte turnover, and deficiencies result in retention of keratinized cells (orthokeratosis). The present report reminds diagnosticians to consider vitamin A deficiency in cases of orthokeratotic dermatopathy in cattle.

Toxicokinetics and pathology of plant-associated acute selenium toxicosis in steers.

Sixteen of approximately 500 yearling steers died of acute selenium (Se) toxicosis after grazing on a Se-contaminated range for only a few days. Field studies and chemical analyses identified the predominant toxic plant as western aster (Symphyotrichum ascendens, previously Aster ascendens), which contained over 4,000 ppm Se (dry weight). Several dead animals that were necropsied had acute severe myocardial necrosis characterized by edema and myocyte swelling, with hypereosinophilia, clumping, and coagulation of myocardial proteins. Whole blood from 36 surviving steers was collected and analyzed, and 10 steers with elevated Se concentrations were selected for close monitoring and clinical evaluations. Each steer was weighed, and serum, blood, liver, skeletal muscle, and hair were regularly collected after removal from the Se-contaminated range. One animal that died 18 days after exposure was necropsied and exhibited severe multifocal myocardial fibrosis with extensive hepatic congestion, degeneration, and hemosiderosis. At 180 days postexposure, 2 of the 10 steers were euthanized, and tissue samples were collected. Both steers had rare, small fibrotic foci in their hearts. The Se elimination half-lives from serum, whole blood, liver, and muscle of the recovering steers were 40.5 ± 8.2, 115.6 ± 25.1, 38.2 ± 5.0, and 98.5 ± 19.1 days, respectively. The Se concentration in hair reached a peak of 11.5 ± 5.3 ppm at 22 days postexposure. The findings indicate that cattle are sensitive to acute Se toxicosis caused by ingestion of Se-accumulator plants, with myocardial necrosis as the primary lesion. Some poisoned animals may develop congestive heart failure weeks after the toxic exposure, and in the current study, Se was slowly excreted requiring a relatively long withdrawal time.

Tannins and self-medication: Implications for sustainable parasite control in herbivores.

Animals adapt to the variability of the external environment and to their changing internal needs not only by generating homeostatic physiological responses, but also by operating in the external environment. In this study, we determined whether sheep with a gastrointestinal parasite infection increased intake of a low-quality food containing a natural antiparasitic agent (tannins) relative to non-parasitized sheep. Four groups of lambs (n=8 lambs/group) were assigned to a 2 x 2 factorial design with parasitic burden (P=parasites; NP=no parasites) and the offer of a supplement containing tannins (yes, no) as the main factors. Parasitized lambs ate more of the tannin-containing food than non-parasitized lambs for the first 12 days of the study, when parasite burdens were high, but differences became smaller and disappeared toward the end of the study when parasite burdens decreased. This result suggests the lambs detected the presence of internal parasites or associated symptoms and modified their ingestion of an antiparasitic agent as a function of need.

Defining limits of treatment with humanized neutralizing monoclonal antibody for West Nile virus neurological infection in a hamster model.

A potent anti-West Nile virus (anti-WNV)-neutralizing humanized monoclonal antibody, hE16, was previously shown to improve the survival of WNV-infected hamsters when it was administered intraperitoneally (i.p.), even after the virus had infected neurons in the brain. In this study, we evaluated the therapeutic limit of hE16 for the treatment of WNV infection in hamsters by comparing single-dose peripheral (i.p.) therapy with direct administration into the pons through a convection-enhanced delivery (CED) system. At day 5 after infection, treatments with hE16 by the peripheral and the CED routes were equally effective at reducing morbidity and mortality. In contrast, at day 6 only the treatment by the CED route protected the hamsters from lethal infection. These experiments suggest that hE16 can directly control WNV infection in the central nervous system. In support of this, hE16 administered i.p. was detected in a time-dependent manner in the serum, cerebrospinal fluid (CSF), cerebral cortex, brain stem, and spinal cord in CSF. A linear relationship between the hE16 dose and the concentration in serum was observed, and maximal therapeutic activity occurred at doses of 0.32 mg/kg of body weight or higher, which produced serum hE16 concentrations of 1.3 microg/ml or higher. Overall, these data suggest that in hamsters hE16 can ameliorate neurological disease after significant viral replication has occurred, although there is a time window that limits therapeutic efficacy.

The effect of copper deficiency on the formation of hemosiderin in sprague-dawley rats.

We demonstrated previously that loading iron into ferritin via its own ferroxidase activity resulted in damage to the ferritin while ferritin loaded by ceruloplasmin, a copper-containing ferroxidase, was not damaged and had similar characteristics to native ferritin (Welch et al. (2001) Free Radic Biol Med 31:999-1006). Interestingly, it has been suggested that the formation of hemosiderin, a proposed degradation product of ferritin, is increased in animals deficient in copper. In this study, groups of rats were fed normal diets, copper deficient diets, iron supplemented diets, or copper deficient-iron supplemented diets for 60 days. Rats fed copper-deficient diets had no detectable active serum ceruloplasmin, which indicates that they were functionally copper deficient. There was a significant increase in the amount of iron in isolated hemosiderin fractions from the livers of copper-deficient rats, even more than that found in rats fed only an iron-supplemented diet. Histological analysis showed that copper-deficient rats had iron deposits (which are indicative of hemosiderin) in their hepatocytes and Kupffer cells, whereas rats fed diets sufficient in copper only had iron deposits in their Kupffer cells. Histologic evidence of iron deposition was more pronounced in rats fed diets that were deficient in copper. Additionally, sucrose density-gradient sedimentation profiles of ferritin loaded with iron in vitro via its own ferroxidase activity was found to have similarities to that of the sedimentation profile of the hemosiderin fraction from rat livers. The implications of these data for the possible mechanism of hemosiderin formation are discussed.

Comparative toxicosis of sodium selenite and selenomethionine in lambs.

Excess consumption of selenium (Se) accumulator plants can result in selenium intoxication. The objective of the study reported here was to compare the acute toxicosis caused by organic selenium (selenomethionine) found in plants with that caused by the supplemental, inorganic form of selenium (sodium selenite). Lambs were orally administered a single dose of selenium as either sodium selenite or selenomethionine and were monitored for 7 days, after which they were euthanized and necropsied. Twelve randomly assigned treatment groups consisted of animals given 0, 1, 2, 3, or 4 mg of Se/kg of body weight as sodium selenite, or 0, 1, 2, 3, 4, 6, or 8 mg of Se/kg as selenomethionine. Sodium selenite at dosages of 2, 3, and 4 mg/kg, as well as selenomethionine at dosages of 4, 6, and 8 mg/kg resulted in tachypnea and/or respiratory distress following minimal exercise. Severity and time to recovery varied, and were dose dependent. Major histopathologic findings in animals of the high-dose groups included multifocal myocardial necrosis and pulmonary alveolar vasculitis with pulmonary edema and hemorrhage. Analysis of liver, kidney cortex, heart, blood, and serum revealed linear, dose-dependent increases in selenium concentration. However, tissue selenium concentration in selenomethionine-treated lambs were significantly greater than that in lambs treated with equivalent doses of sodium selenite. To estimate the oxidative effects of these selenium compounds in vivo, liver vitamin E concentration also was measured. Sodium selenite, but not selenomethionine administration resulted in decreased liver vitamin E concentration. Results of this study indicate that the chemical form of the ingested Se must be known to adequately interpret tissue, blood, and serum Se concentrations.

Evaluation of the respiratory elimination kinetics of selenium after oral administration in sheep.

OBJECTIVE: To evaluate the respiratory excretion and elimination kinetics of organic and inorganic selenium after oral administration in sheep. ANIMALS: 38 crossbred sheep. PROCEDURES: Selenium was administered PO to sheep as a single dose of 0, 1, 2, 3, or 4 mg/kg as sodium selenite or selenomethionine. Expired air was collected and analyzed from all sheep at 4, 8, and 16 hours after administration. RESULTS: Clinical signs consistent with selenium intoxication were seen in treatment groups given sodium selenite but not in treatment groups given the equivalent amount of selenium as selenomethionine. However, a distinct garlic-like odor was evident in the breath of all sheep receiving 2 to 4 mg of selenium/kg. The intensity of odor in the breath did not correlate with clinical signs in affected animals receiving sodium selenite treatment. CONCLUSIONS AND CLINICAL RELEVANCE: The concentration of selenium in expired air was greater in sheep receiving selenium as selenomethionine than sodium selenite. The concentration of selenium in expired air from sheep receiving high doses of selenium (3 and 4 mg of selenium/kg) was larger and selenium was expired for a longer duration than the concentration of selenium in expired air from sheep receiving low doses of selenium (1 and 2 mg of selenium/kg).