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).     

Tunicamycin and corynetoxin poisoning in sheep

Quantitative toxicity studies were carried out in sheep using corynetoxin, tunicamycin and toxic annual ryegrass (Lolium rigidum). Sheep were very sensitive to these toxins. The lethal dose was about 35 micrograms/kg bodyweight for pure tunicamycin given by subcutaneous injection and 3 to 5 mg/kg for corynetoxin administered orally as slurries of bacterial galls of known corynetoxin content. The total lethal dose was of the same order, whether given as a single dose or as repeated smaller doses, the maximum interval tested being 9 weeks between doses. This finding indicates that a second exposure of animals to toxic rye grass in the one season would present a greater risk than would a first exposure to the same field. It also demonstrates the advisability of the monitoring of pasture levels of gall contamination, as levels below those that produce clinical signs of the disease may still contribute to an accumulating burden of toxicity.     

Staggers induced by consumption of perennial ryegrass in cattle and sheep from northern California

Staggers was diagnosed in sheep and cattle from the northern California coast. The diagnosis was made on the basis of history of ingestion of perennial ryegrass (Lolium perenne) stubble, clinical signs of transient ataxia, which was aggravated by stimulation, and nearly complete recovery after removal of ryegrass as the primary forage. Morbidity was high, but death did not occur in any affected animals. The toxic endophyte, Acremonium lolii, was in most lower leaf sheaths from the ryegrass. Injection of extracts of the ryegrass from affected farms into mice induced signs of toxicosis. Additionally, ryegrass from all 3 farms contained the tremorgenic mycotoxin, lolitrem-B.     

The effect of sporidesmin toxicity on ovine serum vitamin B12 levels

A field outbreak of facial eczema occurred during a vitamin B12 response trial in young growing sheep. Pasture cobalt levels were in the low range for sheep (<0.08 mg/kg, 1.358 micromol/kg) and mean (of 3) liver vitamin B12 levels in the sheep were low (<400 nmol/kg) during the period in which facial eczema occurred. Mean serum vitamin B12 levels of the untreated group were low (<485 pmol/l) for the two months (January and February) preceding the period of facial eczema. However, levels showed an approximate 3.5 fold increase in both cobalt supplemented and unsupplemented groups with the onset of facial eczema in March. From February to March the mean serum vitamin B12 and glutamyl transferase (GGT) activity showed parallel increases with a positive correlation (r = 0.73) between log serum vitamin B12 and log serum GGT activity during the period January to July for both groups. This finding suggested that the increase in serum vitamin B12 was due to sporidesmin induced liver damage. The diagnostic implication is that, in areas where facial eczema is a problem, liver is the sample of choice for determining vitamin B12 status. because sporidesmin toxicity can elevate low serum vitamin B12 levels to diagnostically normal levels.     

The occurrence of Anthrax in New Zealand

A field outbreak of facial eczema occurred during a vitamin B12 response trial in young growing sheep. Pasture cobalt levels were in the low range for sheep <0.08 mg/kg, 1.358 µmol/kg) and mean (of 3) liver vitamin B12 levels in the sheep were low (>100 nmol/kg) during the period in which facial eczema occurred.

Mean serum vitamin B12 levels of the untreated group were low (>185 pmol/1) for the two months (January and February) preceding the period of facial eczema. However, levels showed an approximate 3.5 fold increase in both cobalt supplemented and unsupplemented groups with the onset of facial eczema in March. From February to March the mean serum vitamin B12 and glutamyl transferase (GGT) activity showed parallel increases with a positive correlation (r = 0.73) between log serum vitamin B12 and log serum GGT activity during the period January to July for both groups. This finding suggested that the increase in serum vitamin B12 was due to sporidesmin induced liver damage.

The diagnostic implication is that, in areas where facial eczema is a problem, liver is the sample of choice for determining vitamin B12 status, because sporidesmin toxicity can elevate low serum vitamin B12 levels to diagnostically normal levels.     

Investigation into diagnosis and treatment of cobalt deficiency in lambs.

The development of cobalt deficiency was studied in 30 Scottish Blackface lambs grazing pasture on a soil containing 0-17 ppm cobalt. By the end of an eight-week period 50 per cent of lambs were subjectively appraised as showing signs of cobalt deficiency. After a further period lasting four weeks, during which three groups of lambs were studied (one group, least affected by cobalt deficiency, acted as control, the second received a single cobalt bullet and the third received oral doses of 200 mg cobalt chloride at the beginning of the period and three weeks later). Mean urinary formiminoglutamic acid (FIGLU) concentrations were inversely related to serum vitamin B12 concentrations and increased from 0-08 to 0-20 mumole per ml in group 1, and decreased to virtually zero within one week of treatment in groups 2 and 3. The use of serum vitamin B12 and urinary FIGLU concentrations in the diagnosis of cobalt deficiency in sheep are discussed.     

An assessment of the efficacy and safety of selenium and cobalt included in an anthelmintic for sheep

A trial was devised to assess whether the administration of selenium and cobalt together with the anthelmintic mebendazole (Ovitelmin S&C) was safe and could improve the supplies of selenium and cobalt for adult sheep fed a whole grain diet, low in both elements, which produced a steady decrease in blood glutathione peroxidase (GSHPx) and plasma vitamin B12 concentrations. Ovitelmin S&C, when given orally in a single dose as a suspension containing 0.34 mg selenium/ml, and 0.44 mg cobalt/ml (to provide 0.11 mg selenium and 0.15 mg cobalt/kg liveweight) significantly increased the GSHPx activity in blood. After a second dose given 28 days later the rate of change increased from 2.5 to 3.5 u/g haemoglobin/day. The responses in GSHPx were similar for a preparation which contained twice the concentration of selenium. Ovitelmin S&C increased the concentration of vitamin B12 in the plasma by about 1000 pg/ml for four to seven days after each dose and the increases were similar to those observed in sheep treated with an Ovitelmin preparation containing 45 times more cobalt (providing 6.7 mg cobalt/kg liveweight). After 63 days, liver vitamin B12 concentrations were 43 per cent higher in the cobalt treated than in the untreated groups (P less than 0.01) with no differences among the groups given cobalt. Neither adverse reactions nor signs of toxicity followed the administration of Ovitelmin S&C or Ovitelmin containing the higher concentrations of selenium and cobalt.     

铝胁迫对多花黑麦草生长和生理的影响

选取5个多花黑麦草(Lolium multiflorum)品种为受体材料,在水培条件下分析了不同浓度的铝胁迫对5个多花黑麦草品种种子萌发、幼苗生长及生理特性的影响。结果表明:(1)铝胁迫对多花黑麦草种子萌发及幼苗生长的影响表现为"低促高抑"。与对照相比,25mg/L低浓度铝胁迫下多花黑麦草的发芽率、根长、株高、单株鲜重增加;当铝浓度增加为50 mg/L时,多花黑麦草幼苗生长受到抑制;当铝浓度500mg/L时,多花黑麦草种子萌发和幼苗生长受到显著抑制;当铝浓度1 000mg/L时,多花黑麦草幼苗生长受到严重抑制,根系停止生长,株高、单株鲜重显著下降。(2)低浓度铝胁迫下(0~50mg/L),多花黑麦草叶绿素含量、可溶性糖含量、丙二醛、过氧化物酶和超氧化物歧化酶活性变化不大;中等浓度铝胁迫下(100mg/L),多花黑麦草叶绿素含量显著降低,可溶性糖和丙二醛含量显著增加,过氧化物酶和超氧化物歧化酶活性显著增强(P0.05);高浓度铝胁迫下(500mg/L),多花黑麦草叶绿素、可溶性糖和丙二醛含量降低,过氧化物酶和超氧化物歧化酶活性降低。多花黑麦草的铝胁迫阈值为100mg/L。     

Association of Hepatic Necrosis With Trimethoprim Sulfonamide Administration in 4 Dogs

Hepatic necrosis in association with trimethoprim-sulfonamide (TMS) combination therapy was diagnosed in 4 dogs based on history, clinical presentation, and examination of histopathologic specimens collected postmortem. Duration of TMS therapy prior to onset of clinical signs ranged from 4 to 30 days. The dose of TMS ranged from 18 mg/kg to 53 mg/kg bid. Despite supportive medical therapy, all dogs died or were euthanized due to hepatic failure. This report highlights the potential for hepatotoxicity during TMS therapy. Duration of therapy, type of TMS combination, and dose did not appear related to the development of toxicity. The low number of dogs affected suggests an idiosyncratic drug reaction.     

Effects of social stress on the toxicity of malathion in young chickens

Thirty-eight 7-week-old white leghorn chickens of two strains (high and low antibody response to sheep erythrocytes) were divided into groups for exposure to high and low levels of social stress. They were then challenged orally with a toxic dose of the organophosphate insecticide malathion (250 mg/kg body weight) and evaluated 60 min later for muscarinic signs (diarrhea, lacrimation, respiratory secretions), nicotinic signs (muscle weakness), plasma cholinesterase activity, and brain acetylcholinesterase activity. A significant correlation was shown between clinical and biochemical indices of organophosphate toxicity. The correlation between social stress and malathion toxicity was less well defined. Chickens with low antibody response preexposed to high social stress were most resistant to organophosphate toxicity.     

Synchronization of estrus in dairy goats given norgestomet and estradiol valerate at various stages of the estrous cycle.

Dairy goats were given subcutaneous implants with 3 mg of norgestomet (NOR) and IM injections of 0.625 mg of estradiol valerate and 0.375 mg of norgestomet on day 0 of the estrous cycle (estrus; NOR 0, n = 18), on postestrus day 4 (NOR 4, n = 18), or on postestrus day 11 (NOR 11, n = 15). Ear implants were removed after 9 days. Mean (+/- SE) hours from removal of ear implants to onset of estrus and proportion of goats responding were 36 +/- 3.8 and 83%, 33 +/- 4.0 and 61%, and 36 +/- 2.7 and 93% for groups NOR 0, NOR 4, and NOR 11, respectively. There were no significant differences between treatment groups in time to onset of estrus. The percentage of goats in group NOR 11 that had signs of estrus was significantly greater than the percentage of goats in group NOR 4. Of the goats in groups NOR 0, NOR 4, and NOR 11 that had signs of estrus, 53, 55, and 86%, respectively, had onset of behavioral estrus between 24 and 48 hours after implant removal. All goats that had signs of estrus had onset of behavioral estrus between 12 and 72 hours after implant removal. Mean (+/- SE) hours from removal of ear implants to time of peak concentrations of luteinizing hormone (LH) were 49 +/- 4.1, 49 +/- 3.8, and 49 +/- 4.0 for groups NOR 0, NOR 4, NOR 11, respectively (not different). The percentage of goats in group NOR 11 that had LH peaks was significantly greater than the percentage of goats in group NOR 4.(ABSTRACT TRUNCATED AT 250 WORDS)     

The clinical differentiation of nervous and muscular locomotor disorders of sheep in Australia

SUMMARY Many of the nervous and muscular locomotor disorders that affect sheep throughout Australia are commonly referred to as ‘staggers’ syndromes. The range of clinical signs displayed by sheep suffering these disorders is sufficiently diverse to enable each syndrome to be graded into one of 5 progressive clinical groups. The first group, the limb paresis syndromes, includes the primary myopathies associated with the ingestion of Ixiolaena brevicompta, Malva parviflora, and Trachymene ochracea, as well as selenium and vitamin E disorders, Paroo virus staggers, congenital progressive muscular dystrophy, humpy back, hypocalcaemic muscle weakness, Tribulus terrestris staggers and tetanus . The second group is characterised by limb paresis with knuckling of the fetlocks, and includes the plant-associated toxicities of Romulea rosea, Stachys arvensis, Trachyandra divaricata, and Tribulus micrococcus, together with haloxon toxicity, enzootic ataxia (copper deficiency), and the probably genetic disorders of segmental axonopathy, neuroaxonal dystrophy, and degenerative thoracic myelopathy. Other locomotor disorders that fit more loosely into this group are listerial myelitis (post-dipping staggers), vitamin A deficiency, cervico-thoracic vertebral subluxation, Stypandra glauca toxicity, Ipomoea spp toxicity, ivermectin toxicity, and botulism . The third group, the falling syndromes, includes the probably genetic disorders of thalamic cerebellar neuropathy, cerebellar abiotrophy, and globoid cell leucodystrophy, together with Swainsona spp toxicity . The fourth group, the falling-with-tremors syndromes, includes the plant-associated toxicities of phalaris staggers, perennial rye grass staggers and nervous ergotism (Claviceps paspali) . The fifth group, the convulsive syndromes, includes the polioencephalomalacic entity nardoo fern (Marsilea drummondii) staggers, outbreaks of focal symmetrical encephalomalacia and the tunicaminyluracil toxicities known as annual ryegrass (Lolium rigidum) toxicity, annual beard grass (Polypogon monspeliensis) toxicity, blow away grass (Agrostis avenaceae) toxicity, and water damaged wheat (Triticum aestivum) toxicity . A dichotomous system is presented for the differential diagnosis of these groups of conditions .     

Experimental evidence that tryptamine alkaloids do not cause Phalaris aquatica sudden death syndrome in sheep

The acute toxicity for sheep of 3 alkaloids that occur in Phalaris acquatica was examined by intravenous and oral administration. The lowest tested dose rates that produced clinically observed signs were, for 5-methoxy dimethyltryptamine, 0.1 mg/kg body weight intravenously and 40 mg/kg orally; for gramine, 10 mg/kg intravenously and 500 mg/kg orally; and for hordenine, 20 mg/kg intravenously and 800 mg/kg orally. All induced the clinical signs observed in the nervous form of phalaris toxicity, but none induced the cardiac, sudden death, syndrome.     

Ovarian cyclicity in thyroid-suppressed ewes treated with propylthiouracil immediately before onset of seasonal anestrus

Two experiments were conducted to determine if propylthiouracil (PTU)-induced thyroid suppression immediately before onset of anestrus would extend the breeding season in mature ewes. In Exp. 1, twice-weekly serum concentrations of progesterone indicated that all ewes were cyclic before initiation of treatment. Beginning on d 0 (January 17), ewes received 0 (n = 4), 20 (n = 5), or 40 (n = 5) mg of PTU x kg(-1) of body weight (BW) x (-1) for 35 d. Blood samples were collected regularly throughout the trial and serum thyroxine and progesterone were quantified. Ewe BW were similar (P > 0.90) among treatments before the experiment began (mean = 78.2 +/- 4.5 kg). Likewise, serum concentrations of thyroxine averaged 86.5 +/- 8.0 ng/mL on d 0. After 11 d of PTU treatment, serum thyroxine was 90.2,75.2, and 44.2 +/- 14.0 ng/mL in ewes receiving 0, 20, and 40 mg of PTU/kg BW, respectively (linear effect, P = 0.04). On d 20, thyroxine values in the three respective groups were 73.0, 51.1, and 16.1 +/- 12.9 ng/mL (linear effect, P < 0.01). Fourteen days after PTU treatment ended, serum thyroxine did not differ (P = 0.53) among the three respective groups (71.4,73.3, and 57.5 +/- 11.8 ng/mL). Ewes receiving PTU tended to weigh less on d 42 (84.2, 78.2, and 71.8 +/- 5.1 kg for ewes treated with 0, 20, and 40 mg PTU/kg, respectively; linear effect, P = 0.10). Day of onset of anestrus was designated as the day on which serum progesterone decreased and remained below 1 ng/mL. Ewes treated with 0, 20, or 40 mg of PTU/kg BW became anestrous on d 16,40, and 81 (+/- 12) of the experiment, respectively (linear effect, P < 0.01). At the time the 35-d treatment period ended, 25, 60, and 100% of ewes receiving 0, 20, or 40 mg of PTU/kg exhibited normal estrous cycles. In Exp. 2, ewes received 0, 20, or 40 mg of PTU/kg BW for 14 d. The dose was then decreased to 0, 10, and 20 mg of PTU/kg BW for the remaining 21 d. Serum thyroxine decreased to concentrations below 20 ng/mL by d 9 after initiation of PTU treatment. Ewe weights did not differ throughout the trial and no BW loss was observed. The average day that each group entered anestrus was similar to those in Exp 1. Large doses of PTU dramatically lower serum thyroxine and this effect appears to inhibit onset of anestrus in ewes.     

TREATMENT OF OVINE ANNUAL RYEGRASS TOXICITY WITH CHLORDIAZEPOXIDE

The results of pen trials indicate that sheep affected by annual ryegrass toxicity can be treated successfully with chlordiazepoxide. In the first experiment, 87% of chlordiazepoxide-treated animals survived a lethal dose of toxic ryegrass. In the second experiment, 90% of chlordiazepoxide treated animals survived compared with a 10% recovery of control animals.     

Caprine hepatic lipidosis induced through the intake of low levels of dietary cobalt

Forty-one, 10-week-old newly weaned goats were randomly allocated into two groups, namely control (n=22) and treated (n=19). Kids in both groups were fed Rhodegrass hay ad libitum that contained < 0.1 mg/kg DM cobalt and 150 g/day of a commercially prepared ruminant concentrate that contained approximately 0.12 mg/kg DM cobalt. This diet provided the minimum daily requirement of cobalt as specified for sheep. The treated goats were supplemented with bi-monthly subcutaneous injections of 2000 microg of hydroxycobalamin. All goats were weighed and blood samples collected monthly for haematological, clinical biochemical and serum vitamin B12 analysis. After a 10-month experimental period the goats were slaughtered. The control animals exhibited significantly (P<0.05) lower weight gains, and had dry scruffy hair coats. In addition, there was a decline in erythrocyte counts, mean haemoglobin, packed cell volume, mean corpuscular volume, mean corpuscular haemoglobin and mean corpuscular haemoglobin concentration. Controls also exhibited significantly (P<0.05) lower levels of total serum proteins and elevated levels of serum alkaline phosphatase compared to treated goats. Fourteen (63.6%) of the control goats developed pathology consistent with reported field cases of hepatic lipidosis associated with low liver levels of cobalt. Only one (5.3%) of the treated goats developed hepatic lipidosis. Contrary to previous reports that suggested that goats are less sensitive to low levels of dietary cobalt than sheep, it is apparent that this is not the case with Omani goats. This is the first report of the induction of hepatic lipidosis in goats due to feeding low levels of cobalt in their diet.     

The toxicity of Senecio inaequidens DC

This study was designed to confirm the toxicity of a plant implicated in an outbreak of poisoning of stock in Frankfort, Free State Province, South Africa. Cows died acutely after being introduced into a camp, where an abundant, green shrublet was noted to be heavily grazed. This plant was subsequently identified as Senecio inaequidens DC. (Asteraceae) by the South African National Biodiversity Institute (SANBI). Extraction and chemical analyses for pyrrolizidine alkaloids (PAs) in Senecio inaequidens revealed the presence of 4 different compounds, namely retrorsine and senecionine (known to be hepatotoxic) and 2 unidentified compounds. The average total PA (free base plus N-oxide) concentration in plant parts of S. inaequidens collected at Frankfort during the outbreak was 0.81%, compared with the total alkaloid content in the dried, milled S. inaequidens plant material, collected 7 weeks after the outbreak, of only 0.18%. Male Sprague-Dawley rats (n = 4), aged 8-9 weeks, were dosed per os. Each rat received a different dose of the crude Senecio inaequidens extract, ranging from 0.049 mg/g body weight (b.w.) to 0.25 mg/g b.w. No clinical signs were observed in the rat receiving the lowest dose. Rats receiving higher doses showed depression, an unsteady gait, pilo-erection and jaundice, which was particularly noticeable in the ears. Clinical chemistry evaluation revealed an increase in the activities of ALP (except Rat 4), AST and GGT in all animals. Total serum bilirubin, creatinine and urea concentrations were also elevated. All rats had low serum globulin concentrations with an A/G ratio above 1.2. Post mortem examination of the rats revealed marked hepatic lesions. Histopathologically, these changes were characterised by necrosis (variable in extent) of the centrilobular and midzonal hepatocytes (but sparing the portal hepatocytes), with extensive haemorrhage and congestion. Proliferation of the bile ducts, fibrosis and oedema were also present. Ultrastructural changes in affected rats were characterised by margination of chromatin, the presence of numerous autolysosomes in necrotic hepatocytes, intramitochondrial woolly inclusions and changes in the endoplasmic reticulum. A sheep, also dosed with the crude extract, failed to exhibit clinical signs, clinical chemistry aberrations or macroscopic lesions; however, examination of the liver of this sheep revealed histopathological and ultrastructural changes similar, though milder, to those displayed by the rats. Pyrrolizidine alkaloids were extracted from the liver and kidneys of the rats and the sheep. In the case of the sheep, retrorsine was also detected in the lungs, urine and bile.     

Safety and effectiveness of cupric oxide particles for increasing liver copper stores in sheep

Five groups of four, housed Cheviot ewes (mean live-weight 50 kg) were given single doses of 0, 2.5, 5, 10 or 20 g cupric oxide particles in gelatin capsules while receiving a diet of marginal copper content based on pelleted oats. After 65 days liver copper concentrations had increased curvilinearly in relation to dose and all ewes given 10 or 20 g cupric oxide particles showed increases of at least 13.4 mmol kg-1 dry matter (850 ppm). Liver copper concentrations had generally declined after 85 days but biochemical and histological evidence of copper toxicity was recorded in one ewe which had received 20 g cupric oxide particles. Despite marked variations between individual sheep a dose of 0.1 g kg-1 liveweight (5 g) was considered to be safe and did not induce clinical copper toxicity in five sheep of the susceptible North Ronaldsay breed given the same basal diet.     

钴和铜对肉用绵羊维生素B_(12)合成、瘤胃发酵及造血机能的影响

为研究不同水平的钴和铜对肉用绵羊维生素B12合成、瘤胃发酵及造血机能的影响,试验选20只体重相近(28.9±1.1)kg、装有永久瘤胃瘘管的杂交一代羯羊,随机均分为5组,定量饲喂对照组日粮,4种不同水平的钴铜(0.3:10、0.3:20、0.6:10和0.6:20)日粮。结果表明:瘤胃维生素B12合成主要取决于钴的摄入量,日粮中同时添加钴、铜及其不同的配比对维生素B12合成未显协同效应和影响。钴与铜合用可增加瘤胃挥发性脂肪酸的浓度,并改变乙酸、丙酸和丁酸比例,用量越多其影响越大。随肉羊日粮中钴与铜合用及其用量增加,可更有效地促进铁的吸收和利用,从而更加明显地改善机体的造血机能。     

国产赛福丁对绵羊的毒性及治疗绵羊痒螨病的效果

应用国产赛福丁对3组绵羊(每组3只)分别以10、20、40 mg/kg剂量进行了毒性试验。结果,10、20 mg/kg剂量的绵羊,药后临床未出现任何毒性反应;40 mg/kg剂量的绵羊,均于药后40～60 min出现了典型的有机磷中毒症状。全血胆碱酯酶对赛福丁非常敏感,但其抑制程度与中毒靠状的出现并无直接关系。中毒后血清GOT和GPT无变化。以50、100、200、250 ppm浓度的赛福丁溶液分别药浴患痒螨绵羊,均可迅速地治愈患羊,浴后24 h即可杀灭全部螨虫,24～72 h痒觉消失,2周后脱痂,长毛。近期疗效同于倍特和林丹.而远期疗效优于倍特和林丹。证明国产赛福丁是一种高效、低毒的杀螨剂。