Accidental selenium toxicosis in lambs.

Acute selenium toxicosis occurred in 3-week-old lambs after accidental over-supplementation by intramuscular injection and caused dyspnea, cyanosis, and sudden death. Pathological lesions included myocardial necrosis, skeletal muscle necrosis, pulmonary edema, hydrothorax, and hydropericardium.

Toxicose accidentelle au sélénium chez des agneaux. Une toxicose aiguë au sélénium s'est produite chez des agneaux âgés de 3 semaines après une supplémentation excédentaire accidentelle par injection intramusculaire et elle a causé des signes de dyspnée, de cyanose et de mort soudaine. Les lésions pathologiques incluaient une nécrose du myocarde, une nécrose du muscle squelettique, un œdème pulmonaire, de l'hydrothorax et de l'hydropéricarde.(Traduit par Isabelle Vallières).

Acute selenium toxicosis in polo ponies.

Just prior to an international polo event, 21 horses from one team exhibited clinical signs of central nervous system disturbance, hyperexcitability, sweating, ataxia, tachycardia, dyspnea, pyrexia, and rapid death. The suspected cause of this peracute onset of illness and death included intentional contamination of feed or iatrogenic administration of performance-enhancing drugs resulting in a severe adverse reaction. Six horses were submitted to the Bronson Animal Disease Diagnostic Laboratory for necropsy and toxicological examination. The clinical signs and sudden death, the similarity to earlier work by the lead author of selenium toxicosis in calves, as well as published reports, prompted investigators to focus on selenium testing. Sixty-four hours following receipt, the laboratory detected toxic selenium concentrations in the tissues of these animals. Following further investigation of the case by regulatory officials, it was determined that all affected horses had received an intravenous injection of a compounded "vitamin/mineral" supplement just prior to the onset of signs. The compounded supplement contained toxic levels of selenium. The present report illustrates the in-depth laboratory investigation of the cause of acute death in 6 polo ponies due to selenium toxicosis. In addition to solving this high profile case, the toxic levels of selenium found in livers (6.13 ± 0.31 mg/kg wet weight), kidneys (6.25 ± 0.3 mg/kg wet weight), and sera (1.50 ± 0.11 µg/ml) of these affected animals may provide important diagnostic criteria for future interpretations of selenium concentrations in tissues of horses.

Muerte súbita asociada a hipersensibilidad tipo I en un equino pura sangre de carrera / Sudden death associated to type I hypersensitivity in a racing horse

El objetivo de este estudio fue reportar un caso de hipersensibilidad tipo I con muerte súbita en un equino Pura Sangre de Carrera en el Hipódromo “La Rinconada” Caracas, Venezuela. Se tomaron muestras de sangre y orina para estudios toxicológicos mediante la técnica de ELISA competitivo. Se le práctico la técnica de necropsia, fueron colectadas muestras de musculo, tejido pulmonar, hepático, renal, gástrico, esplénico, corazón y sistema nervioso central para estudio histopatológico, las muestras fueron procesados por los métodos convencionales histológicos. Los hallazgos de necropsia fueron flebitis severa en vena yugular derecha, con hematoma en el surco yugular. Edema severo de glotis, edema, congestión y hemorragia pulmonar. Hemorragia petequial subendocardica. Bazo esplenocontraido y con focos de necrosis de coagulación. Hidronefrosis aguda con hematuria. Hígado con patrón lobulillar acentuado. El resto de los órganos con evidente congestión y hemorragia. Los cortes histológicos evidenciaron edema, congestión y hemorragia pulmonar severa. Hemorragia subepicardica marcada. Edema subcapsular esplénico y necrosis centro-folicular. Degeneración hidropica tubular, necrosis tubular aguda. Necrosis de corteza renal. Los estudios toxicológicos permitieron la detección de furosemida y fenilbutazona en las muestras de sangre y orina. En conclusión se reporta un síndrome de hipersensibilidad tipo I asociado a la administración de un producto comercial a base de Vitamina E 80mg, Pangamato sódico (B15) 1 mg, Selenio Sódico 0.6 mg, Antioxidantes y Vehículos Solubles c.s.p. con colapso, shock y muerte aguda en un equino Pura Sangre de Carrera mediante un estudio multidisciplinario clínico, anatomopatologico y toxicológico.

The aim of this study was to report a case of type I hypersensitivity to sudden death in a Thoroughbred race horses at the Hippodrome “La Rinconada” Caracas, Venezuela. Samples of blood and urine for toxicology studies using competitive ELISA. He practiced the technique of necropsy, samples were collected from muscle, lung tissue, liver, kidney, stomach, spleen, heart and central nervous system for histopathological examination, samples were processed by conventional histological methods. Autopsy findings were severe phlebitis right jugular vein, with hematoma in the jugular groove. Severe edema of glottis edema, pulmonary congestion and hemorrhage. Subendocardial petechial hemorrhage. Esplenocontraido Spleen foci of necrosis and coagulation. Hydronephrosis with acute hematuria. Liver accentuated lobular pattern. The rest of the organs with obvious congestion and hemorrhage. The histological sections showed edema, severe pulmonary congestion and hemorrhage. Marked subepicardial hemorrhage. Edema and necrosis subcapsular splenic follicular center. Tubular hydropic degeneration, acute tubular necrosis. Necrosis of renal cortex. Toxicological studies allowed the detection of furosemide and phenylbutazone in samples of blood and urine. In conclusion we report type I hypersensitivity syndrome associated with the administration of a commercial product based Vitamin E 80mg, sodium pangamate (B15) 1 mg, 0.6 mg; Sodium Selenium, Soluble Antioxidants and Vehicle qs with collapse, shock and acute death in a race Thoroughbred horses by a multidisciplinary clinical, pathological and toxicological.

Sudden death associated with myocardial contraction band necrosis in Boer goat kids.

Parenteral selenium (Se) and vitamin E (Vit E) were administered to all newborn kids at a Boer goat farm where there was previous high neonatal mortality assumed to be due to nutritional myopathy. All treated kids were affected by severe respiratory distress and died within 8 hours of Se/Vit E administration. Gross lesions included severe pulmonary edema, hydrothorax, and hydropericardium. The primary histopathologic finding was severe, acute, and monophasic myocardial contraction band necrosis. The diagnosis was accidental acute selenosis based on trace mineral analysis of the liver. This case highlights an important differential diagnosis in cases of acute myocardial contraction band necrosis and sudden death in goats and emphasizes the need for caution when administering parenteral Se/Vit E preparations.

Peracute selenium toxicosis followed by sudden death in growing and finishing pigs.

Fattening pigs (n = 751) showed progressive apathy, paralysis, and sudden death after accidental ingestion of excessive concentrations of selenium in mineral feed. Selenium concentrations of 1.09 to 1.32 mg/L in the serum confirmed the diagnosis. Within 3 d all pigs had died spontaneously or were euthanized due to the grave prognosis and on welfare grounds.

[Nutrition disorders in fattening pigs in an "organic" facility]. / Ernährungsschäden bei Mastschweinen in einem "Bio"-Betrieb.

In a herd of fattening pigs under an organic system of management, the following problems were observed: sudden deaths, skin diseases, diarrhea, increased restlessness and cannibalism. The diet consisted of cereals (barley, wheat, rye), field beans, lime stone and deteriorated, raw potatoes without addition of a mineral mixture. Deficiencies of sodium, zinc and selenium were found in the diet and in the animals (blood samples, autopsy). The vitamin E status in the pigs was also below normal.

The effect of taurine transport antagonists on cardiac taurine concentration and the incidence of sudden death syndrome in male broiler chickens.

Two experiments were conducted in which 540 day-old male broiler chickens were raised in heated battery brooders to 4 wk of age. Diets contained taurine antagonists to test effects on cardiac taurine content and the incidence of Sudden Death Syndrome (SDS). In Experiment 1 treatments during Weeks 2 to 4 were A) basal diet; B) basal diet supplemented with .25% guanidinoethyl sulfonate (GES) in Week 2 and 1.5% GES in Weeks 3 and 4; and C) basal diet supplemented with .5% GES in Weeks 2 to 4. The taurine content of heart was significantly reduced (P less than .05) with GES supplementation, but no effects on SDS mortality rates were noted. In Experiment 2 birds received diets containing 0. 2.5, or 5% beta-alanine. Supplementation with this compound decreased cardiac taurine concentration to extremely low levels (P less than .05). No significant effects on SDS mortality rates were noted. The results are interpreted as suggesting that taurine does not play a major role in the etiology of SDS.

Lack of an effect of taurine supplementation on the incidence of sudden death syndrome in male broiler chicks.

Two experiments were conducted to study the effect of taurine supplementation on growth and the incidence of Sudden Death Syndrome (SDS) in male broiler chickens. The 4,650 birds were day-old male broiler chickens raised in floor pens to 9 wk of age. In Experiment 1, the birds received diets containing 0, 250, 500, or 1,000 mg taurine/kg. In Experiment 2, the treatments were no added taurine, 500 mg taurine/kg feed, 1,000 mg taurine/kg feed, 250 mg taurine/L water, and 500 mg taurine/L water. Taurine supplementation did not have any significant influence on growth performance although supplementation of the feed at 250 mg/kg reduced the feed:gain ratio from 1.67 to 1.63 in Experiment 1, which was significant (P less than .05). In general, mortality was unaffected by treatment with a few exceptions: in Experiment 2, SDS deaths were reduced significantly (P less than .01) by supplementation of the feed with 500 mg taurine/kg, and at 3 and 6 wk of age, SDS deaths as a percentage of total deaths were reduced significantly with this treatment. The results are interpreted as suggesting that taurine does not play a major role in the etiology of SDS.

Sudden death syndrome in broilers: dietary fat supplementation and its effect on tissue composition.

The effects of dietary fat sources on the general performance of broiler chickens and the incidence of sudden death syndrome (SDS) were investigated in two experiments. In Experiment 1, a wheat-soy diet supplemented with sunflower oil was found to improve significantly (P less than .05) performance characteristics and reduce the mortality attributed to SDS as compared with the same diet supplemented with tallow. The blood lipid parameters--total lipids, triglycerides, and cholesterol at 4 and 7 weeks of age--were not affected (P greater than .05) by the type of fat used in the diet. In Experiment 2, wheat-soy diets were supplemented with either tallow or sunflower oil at the same dietary levels and two stocking densities (.09 m2/bird or .08 m2/bird). The sunflower oil diet significantly (P less than .05) improved the general performance of the birds and reduced mortality from SDS. Bird density had no significant effect. Fatty acid composition of the heart and liver tissues from SDS birds showed differences when compared with culled birds (leg problems) from the same experimental period. In the heart tissue, increased palmitic (16:0) and oleic (18:1) acids were observed, while linoleic (18:2) and arachidonic (20:4) acids were lower. Liver tissue showed increased 18:1 and lower 18:2 and 20:4. Analysis for copper and zinc in heart tissue did not indicate significant (P greater than .05) treatment effects, but calcium concentration was significantly (P greater than .05) higher in SDS than culled birds. Analysis performed on the liver tissue showed significant (P lesser than .05) differences in copper and zinc between these two groups of birds.

Abdominal fat deposition and sudden death syndrome in broilers: the effects of restricted intake, early life caloric (fat) restriction, and calorie: protein ratio.

The effects of feed restriction, early life fat restriction, and calorie:protein ratio on abdominal fat pad development and sudden death syndrome (SDS) in the broiler chicken were studied in two experiments. In Experiment 1, restricting feed intake to 90% of ad libitum intake was found to reduce significantly (P less than .01) both 49-day body weights and abdominal fat pad size while feed efficiency was significantly (P less than .01) improved compared to groups fed a wheat diet ad libitum. Corn-fed birds tended to outperform wheat fed groups. Reduced growth rate or supplementation of the diet with additional vitamins and minerals did not effect the incidence of SDS. In Experiment 2, fat restriction in the diet from 0 to 7 days initially reduced growth rate and increased feed:gain ratios. By 49 days, no effect of fat restriction on these parameters was observed. Dietary fat restriction tended to increase abdominal fat measured at 49 days of age. Lowering the calorie: protein ratio of the finishing diet significantly (P less than .05) improved feed:gain ratios measured from 29 to 49 days and tended to reduce fat pad size. Incidence of SDS was significantly (P less than .05) lower from 29 to 56 days in groups fed the 24% protein finisher diet as compared to birds fed a 19% finisher diet.

Dietary induction of sudden death syndrome in broiler breeders.

Sudden death syndrome in broiler breeders at the point of lay was a serious problem in Australia for 18 months. This condition was reproduced by a combination of dietary and management practices. Chickens fed a diet low in potassium, phosphorus, protein, and energy had plasma potassium and phosphorus levels significantly lower than the levels seen in the controls. The plasma values of the test breeders were similar to levels seen in field cases. There was a significant difference (P less than 0.01) in the venous acid-base balance between the test chickens and controls. Test chickens were alkalotic and had a 6% mortality rate between 18 and 30 weeks of age.

Interrelationships between biotin, choline and other B-vitamins and the occurrence of fatty liver and kidney syndrome and sudden death syndrome in broiler chickens.

1. Addition of supplemental choline to a biotin-deficient diet decreased the biotin status of chicks and increased mortality from fatty liver and kidney syndrome (FLKS). 2. Mortality was also increased by dietary supplementation with a mixture of other B-vitamins, excluding biotin, and was highest when the choline and B-vitamin supplements were combined. 3. The occurrence of sudden death syndrome (SDS) was unaffected by dietary biotin concentration. 4. A previously unreported condition was observed in which birds died showing post-mortem signs characteristic of both FLKS and SDS and whose occurrence was related to the biotin status of the chicks.

Effect of biotin supplementation on incidence of acute death syndrome in broiler chickens.

This study examined the effect of supplementary biotin on the incidence of acute death syndrome (ADS) and total mortality in a commercial flock of 64,000 broiler chickens. Biotin supplementation via the drinking water at 20 and 100 micrograms/day supplied 1.2 to 5 times or 6 to 25 times the level recommended by the National Research Council for different stages of growth from day-old to slaughter. Uptake of biotin was confirmed by radioisotopic analysis of liver biotin content of both ADS-affected birds and clinically normal birds. Treatment groups did not differ significantly from the control group with respect to total mortality, ADS mortality, feed conversion ratio, or slaughter weight. High levels of biotin supplementation neither prevented ADS nor reduced total mortalities in the flock.