Selenium toxicosis in feeder pigs.

Selenium toxicosis was diagnosed in feeder pigs on a central Michigan farm. Use of a commercial supplement, found to contain approximately 20 times the intended Se concentration, resulted in a Se concentration of 8.1 mg/kg of the complete feed. This was fed for 34 days during which daily feed consumption decreased approximately 35%, several pigs developed weakness and forelimb paresis, and 1 pig died. The highest serum Se concentration measured was 1,550 ng/ml (normal range, 140 to 190 ng/ml). Normal feed consumption returned when an alternative feed was provided. Mean serum Se concentrations of representative pigs, monitored over the subsequent 26 days, decreased from 905 to 258 ng/ml. Histologic examination of a recovering pig revealed skeletal and cardiac myopathy and bilaterally symmetric malacia of the gray matter of the ventral horns of the spinal cord. During the developing toxicosis, the pigs consumed an estimated 11.4 mg of Se/pig/d.     

Selenium toxicosis in swine

Selenium toxicosis was diagnosed as the cause of fatal paralytic disease in a group of feeder pigs. Lumbar poliomyelomalacia and coronary band necrosis were the principal lesions. High selenium concentrations were detected in liver and kidney. Excessive selenium was traced to the premix added to the complete ration.     

Clinical, pathological and toxicological findings of a iatrogenic selenium toxicosis case in feeder pigs

Histopathological and toxicological analyses confirmed a clinical diagnosis of selenium (Se) intoxication in pigs from a farm in Spain. After an initial episode of diarrhoea, animals presented both dermatological and neurological signs; the most obvious sign was a marked hind limb paresis. Cutaneous lesions consisted on diffuse alopecia, multifocal skin necrosis and coronary band necrosis of the hooves. Central nervous system lesions involved the cervical and lumbar intumescences of the spinal cord and consisted of a severe, bilateral symmetrical poliomyelomalacia of the ventral horns; pons and medulla oblongata also presented lesions of polioencephalomalacia. Analyses of feed and sera from clinically affected pigs revealed a marked increase in Se concentration. Clinical investigations indicated that a failure in Se dosage in feed was the cause of the toxicosis.     

Experimental polychlorinated biphenyl toxicosis in germfree pigs.

The effects of polychlorinated biphenyls were studied in eight germfree pigs. Beginning at fourteen days of age, two pigs each were fed daily 12.5, 25, 50 and 100 mg/kg body weight of polychlorinated biphenyls as Aroclor 1254. Three germfree pigs were negative controls. Clinically the treated pigs had inappetance, a hemorrhagic diarrhea, erythema of the nose and the anus, retarded growth, distended abdomen and at the higher dose levels, incoordination and coma followed by death. Deaths occurred in 11 to 35 days after exposure. At necropsy, the piglets exhibited grossly enlarged mottled liver, erosions of the gastric mucosa, hemorrhages through the mesentery and the intestinal wall, a fibrinous pericarditis, a hypoplastic thymus and congested swollen thyroid glands. The histopathological lesions included hepatic centrolobular necrosis, interstitial myocarditis, endocarditis, myopathy of the muscles, gastric erosions and colitis. All of the organs examined for polychlorinated biphenyls had elevated residue levels which were particularly high in the fat, liver, psoas muscle, brain and kidney and were higher than has been reported in conventional pigs fed approximately equal concentrations of polychlorinated biphenyls. The severity of clinical signs, pathological changes and tissue concentrations were directly related to the dose administered and were more pronounced in the germfree pigs than has been described in conventional pigs.     

Acute selenium toxicosis in a dog

A toxic dose of selenium administered by IM injection to a 3-year-old Chihuahua resulted in pulmonary edema and death. The compound had been dispensed to the owner inadvertently in combination with a vitamin E preparation. Vitamin and mineral products often are considered safe for use in megadoses by the uninformed public. The potential danger of selenium overdosage should not be underestimated.     

Selenium toxicosis in a white-tailed deer herd

Chronic selenium (Se) toxicosis was found in a herd of white-tailed deer showing signs of anorexia, weight loss, and lameness. Concentration of Se in the liver ranged from 2.7 to 8.97 mg/kg wet weight. Myocardial necrosis, mineralization, and fibroplasia were seen histologically. This is the first report of this toxicosis in white-tailed deer.     

Observations on an outbreak of anthrax in pigs in north Wales.

Nineteen pigs in a 500 sow herd died from anthrax over a period of 95 days. This paper describes some of the problems encountered and how they were dealt with, including the risks to public health, the disposal of slurry and the cleansing and disinfection of the premises after the herd was slaughtered.     

Selenium and vitamin E deficiency in pigs. II. Influence on plasma selenium, vitamin E, ASAT and ALAT and on tissue selenium.

The effect of dietary selenium (Se) and vitamin E (Vit. E) in pigs on Se and Vit. E in plasma and on Se in tissue from liver, heart, m. long, dorsi and m. psoas major was studied; and furthermore was the influence on the enzymes ASAT and ALAT studied.Two levels of Se were used, 0.03 and 0.06 mg Se per kg feed. Within each Se level 2 levels of Vit. E were used, 15 and 45 i. u. per kg feed. This resulted in 4 groups: 1. low Se and low Vit. E; 2. low Se and high Vit. E; 3. high Se and low Vit. E; 4. high Se and high Vit. E.Ten% of all pigs fed low Se, and 4% of the pigs fed low Se and high Vit. E diet died with severe symptoms of Se deficiency. None of the pigs fed the high Se diet died with such symptoms. Plasma Se determinations have been shown to indicate the Se status in pigs almost as accurately as liver Se determination. ASAT and ALAT enzyme determinations were not of any diagnostic value.There was a good agreement between dietary Vit. E level and the corresponding levels in plasma. Oxidized herring oil seems to enhance the Vit. E need.     

Selenium toxicosis in a flock of Katahdin hair sheep

Selenium supplementation by injection is a common practice. Acute toxicosis from dosaging errors may occur. In this report, 23 of 56 ewes and all 24 lambs injected with selenium died. Tissue, whole blood, and serum concentrations aided in the diagnosis. Caution should be taken when supplementing selenium by injection.     

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).     

Blue-green algae (Anabaena spiroides) toxicosis in pigs

Toxicosis caused by Anabaena spiroides was diagnosed in 7 of 26 finishing hogs in a farrow-to-finish operation in Kentucky. Several sick pigs in the herd had the following clinical signs: vomiting, dull appearance, lethargy, anorexia, muscle tremors, frothing at the mouth, coughing, sneezing, dyspnea, and bloody diarrhea. Of the 7 dead pigs, 2 were necropsied. Tissue speciments and stomach contents were obtained for microscopic, microbiologic, and toxicologic evaluations. In addition, vomitus from sick pigs and pond water samples were collected for laboratory analysis. Direct microscopic examination of pond water, vomitus, and stomach contents revealed nearly pure A spiroides, a toxic blue-green algae. The possible involvement of bacterial toxins in these pigs was not established; however, the laboratory and field data suggested that the clinical signs and death losses were attributable to the consumption of pond water mixed with the bloom of the alga, A spiroides.     

Experimental 3-nitro-4-hydroxyphenylarsonic acid toxicosis in pigs

Five times the recommended dose of 3-nitro-4-hydroxyphenylarsonic acid (187.5 mg kg-1) induces a pathognomonic clinical syndrome in pigs. The main clinical features are not continually present but are inducible only by exercise. From day 11 on the experimental diet a nervous syndrome was inducible. This manifested as muscle tremors and clonic convulsive episodes. Paraparesis developed by day 22 and paraplegia by day 33. Liver arsenic levels plateaued at 5.4 +/- 1.3 mg kg-1. The experiment confirms field observations that 3-nitro produces a characteristic toxicological syndrome, which is distinct from that of arsanilic acid. It also confirms that 3-nitro has a higher absolute toxicity than arsanilic acid in pigs as well as a lower margin of safety.