Experimental T-2 toxicosis in sheep.

Lambs received T-2 toxin at a rate of 0.6 or 0.3 mg/kg body weight per day in a protein reduced diet for 21 days to study the immunological and pathological effects of T-2 toxin in sheep. Blood was collected before T-2 treatment and on days 7, 14 and 21 of the trial for hematological and biochemical examination and for the separation of peripheral blood lymphocytes for the mitogen assay. Myeloid:erythroid ratios were determined from sternal bone marrow samples taken a day before T-2 treatment began, on day 12 and at death (day 22). Lambs treated with 0.6 mg/kg body weight of T-2 toxin daily were leukopenic on day 7 and lymphopenic on days 7 and 14. Also, on day 7, the mitogenic responses of these lambs to the B-cell mitogen, lipopolysaccharide, were significantly depressed and prothrombin times were prolonged. At necropsy, lymphoid atrophy of mesenteric lymph nodes and spleens was most marked in lambs treated with 0.6 mg/kg body weight of T-2 toxin per day. To the authors' knowledge, this is the first report of leukopenia, lymphopenia and lymphoid depletion in ruminants fed T-2 toxin.     

鸡氨气中毒及其防治对策

鸡氨气中毒包括氨气重度、中度与轻度中毒.一般地,在25 mg/L以下或长期处于低浓度氨气的环境中可导致慢性中毒;在25～50 mg/L导致中度中毒,可诱发难于根除的其它呼吸道疾病;当鸡舍内氨气浓度达50 mg/L或以上时,发病率为100%,导致鸡重度中毒,死亡率为28.1%以上.     

Effects of testosterone on the prevention of T-2 toxin-induced adrenocortical necrosis in mice

To evaluate the effect of exogenous testosterone on the development of T-2 toxin-induced necrosis of adrenal glands, mice were allotted to 3 treatment groups. Each treatment group contained castrated male, and castrated and sexually intact female mice. Each mouse in group 1 was given 0.16 mg testosterone propionate at 48-hour intervals for a total of 12 injections, group-2 mice were given similar injections of only the vehicle, and group-3 mice were given no treatment. Twenty-four hours after the last injection, the mice in all 3 groups were exposed for 10 minutes to an aerosol of T-2 toxin. All mice alive at 24 hours after exposure were euthanatized and the adrenal glands and thymuses were examined histologically. Necrosis of the adrenal cortex was not found in any of the mice given preexposure treatment with exogenous testosterone, whereas all mice given vehicle only or no treatment had T-2 toxin-induced necrosis of the inner portion of the adrenal cortex. Lymphocytolysis in the cortex of the thymus confirmed that each mouse of all 3 treatment groups had experienced systemic mycotoxicosis. The uniform severity of the lesion in all mice suggests that the thymus was not protected by exogenous testosterone administration or by the castration status of the mice. We propose that T-2 toxin-induced adrenal necrosis in mice is prevented by the presence of testosterone.     

Monensin toxicosis in 2 sheep flocks

Several lambs in 2 sheep flocks died suddenly and others were examined for generalized weakness and dyspnea. Postmortem findings were suggestive of degenerative myocardial and skeletal muscle myopathy, which was confirmed histologically. Feed analysis revealed toxic levels of monensin and ionophore toxicosis was diagnosed.     

The pathology of chronic Drechslera campanulata toxicosis in inbred rats

Cultures on autoclaved maize of the phytopathogenic fungus, Drechslera campanulata, were incorporated into diets and fed to male inbred BDIX rats. In a pilot trial, a diet containing 30% D. campanulata culture material killed 5 out of 5 rats in 15-25 days. Lesions included gastric corpus erosions, gastrorrhagia and ulcerative typhlitis. Diets containing 5% or 10% culture material induced erosive to ulcerative typhlitis and oedema and hyperplasia of the ileocaecal lymph nodes in 40 out of 40 rats. Other changes included: mass loss; normocytic, hyperchromic anaemia; leukocytosis with neutrophilia; reductions in plasma proteins, creatinine, calcium and cholesterol; elevated serum enzymes; hepatosis, nephrosis and mycoplasma-like interstitial pneumonia. No lesions were present in control rats, and their profiles were normal. Ulcerative typhlitis induced by D. campanulata in rats resembles that seen in chronic piperonyl butoxide intoxication as well as that due to single treatments of indomethacid, although small intestinal ulcers are more frequent in the latter. Overgrowth of intestinal flora may be involved in ulcer pathogenesis. The pathology of drechsleratoxicosis in rats is compared to that in sheep and goats where necrotic lesions in the forestomach and, to a lesser extent, in the caecum are characteristic findings.     

The toxicosis of Embellisia fungi from locoweed (Oxytropis lambertii) is similar to locoweed toxicosis in rats

Locoweeds cause significant livestock poisoning and economic loss in the western United States. The toxicity of Embellisia sp. fungi isolated from locoweed was compared with locoweed toxicity using the rat as a model. Rats were fed diets containing locoweed, fungus and alfalfa, or alfalfa. Locoweed- and fungus-fed rats consumed swainsonine-containing food at approximately 1.3 mg x kg(-1) x d(-1), gained less weight (P = 0.001) and ate less than controls. Swainsonine is the principal agent responsible for inducing locoism in animals. The concentrations of alkaline phosphatase and aspartate aminotransferase enzymes were greater (P < 0.05) in serum of locoweed- and fungus-fed rats compared with control rats. Similar intracellular vacuolation was observed in renal, pancreatic, and hepatic tissues of rats that consumed either locoweed or fungus. Rats that ate locoweed or Embellisia fungi displayed indistinguishable toxicity symptoms. The Embellisia fungi from locoweed can induce toxicity without the plants. Locoism management strategies need to involve management of the Embellisia fungi.     

Effect of T-2 toxin on brain biogenic monoamines in rats and chickens.

Two experiments were conducted to determine the effect of T-2 toxin on brain biogenic monoamines and their metabolites. Male rats (180 g) and cockerels (28 day, 300 g) were orally dosed with T-2 toxin at 2.5 mg kg-1 body weight. In the first experiment, whole brains were collected 2, 6, 12, 24 and 48 h postdosing and analyzed for monoamines by high performance liquid chromatography with electro-chemical detection. T-2 toxin did not influence whole brain concentrations of monoamines in either species. In the second experiment, brains were collected 24 h postdosing, dissected into five brain regions, and analyzed for monoamines. T-2 toxin treatment resulted in increased serotonin and 5-hydroxy-3-indoleacetic acid in all brain regions of the rat. However, this was not seen in poultry where T-2 toxin treatment resulted in an increase in 5-hydroxy-3-indoleacetic acid, no alteration in serotonin concentration and a decrease in regional norepinephrine and dopamine concentrations. These results suggest that T-2 toxin influences brain biogenic amine metabolism and that there is an intraspecies difference in the central effects of this mycotoxin.     

Swainsonine toxicosis suppresses appetite and retards growth in weanling rats

Two groups of weanling rats were treated with swainsonine, the toxin responsible for 'pea-struck' and locoism in grazing animals, for 21 days. The initial dose rate was 46 mg kg-1 d-1 in one group, and 7.6 mg kg-1 d-1 in the other. Food and water intake, urinary volume and bodyweight gain were recorded for each rat and compared with those for pair-fed and ad libitum fed control individuals. At both dose rates, swainsonine caused marked retardation of growth consequent to profound suppression of appetite. In intoxicated rats, intake of water was also diminished.     

Experimentally induced phenylbutazone toxicosis in ponies: description of the syndrome and its prevention with synthetic prostaglandin E2

Phenylbutazone (PBZ) toxicosis was induced in 9 ponies to further define the clinical and pathologic changes occurring with this syndrome. Six additional ponies were treated with PBZ and a synthetic prostaglandin E2 to determine the role of prostaglandins in the pathogenesis of PBZ toxicosis. Ponies given only PBZ exhibited CNS depression, anorexia, weight loss, diarrhea, cyanotic mucous membranes, and oral ulcers. Total serum protein concentration gradually decreased during the 10-day treatment period. Marked mucosal atrophy, focal erosions, and ulcers characterized the lesions in the alimentary tract. Ponies given PBZ and prostaglandin E2 remained clinically healthy and did not develop hypoproteinemia or mucosal atrophy. A few erosions were seen, but ulcers were not observed. The results of the present study indicate that mucosal atrophy is a characteristic lesion of PBZ toxicosis. It is also evident that inhibition of prostaglandin synthesis has an important role in the development of this syndrome.     

T-2毒素毒性作用研究进展

T-2是A类单端孢霉烯族化合物中毒性最强的一种,对动物机体具有较强的危害,可造成多个系统出现中毒效应。作者主要对T-2毒素对动物的广泛毒性作用进行论述,且对下一步的研究方向进行了展望。     

Suspected toxicosis after topical administration of minoxidil in 2 cats

Objective: To discuss the clinical presentation and necropsy findings of 2 cats after topical administration of a minoxidil solution. Additionally, a potential management plan is offered for future cases. Case summary: Two cats with dermal exposure to topical minoxidil solution were identified from the ASPCA Animal Poison Control Center (APCC) files. Both cats were presented with lethargy and dyspnea within 36 hours of exposure. The cats were hypothermic, and had pulmonary edema and pleural effusion present on thoracic radiography. Both cats died despite supportive care. Necropsy of both cats confirmed pleural effusion and pulmonary edema and indicated cardiac compromise. New or unique information provided: Topical administration of minoxidil solution may cause life‐threatening pulmonary edema, pleural effusion, and cardiac dysfunction in the cat.     

Arsenic toxicosis and suspected chromium toxicosis in a herd of cattle

Arsenic toxicosis and suspected chromium toxicosis were diagnosed in a herd of cattle that ingested ashes from lumber treated with copper, chromium, and arsenic. Findings included peracute death, depression, ataxia, weakness, recumbency, and watery diarrhea. Chemical analyses of liver, kidney, abomasal contents, rumen contents, and ashes revealed high concentrations of arsenic and chromium. Histologically, specimens of abomasum and duodenum had diffuse mucosal degeneration and engorged capillaries. Epithelial cells of the proximal convoluted tubules and distal collecting tubules of the kidney were swollen and had mild granular cytoplasmic degeneration. Burning lumber treated with copper, chromium, and arsenic does not remove the heavy metals from them, and ingestion of the ashes from the wood constitutes a hazard to livestock health.     

T-2毒素研究进展

T-2毒素是污染我国饲料的主要霉菌毒素,主要危害动物的造血组织和免疫器官,引起出血性综合征,出现白细胞减少、贫血,使胃肠道功能受损等,对畜禽健康和畜牧业生产的危害很大.本文主要从T-2毒素的一般性质、产毒菌株、毒性效应、毒性机制及预防控制等方面作了论述.     

Methionine toxicosis in cats

Cats given DL-methionine (1 g/kg of body weight/day) developed severe hemolytic anemia with marked increase of methemoglobin (MetHb) concentration and Heinz-body formation at treatment-day 6 to 10. Cats fed 0.5 g of methionine/kg for 52 days had a moderate Heinz-body hemolytic anemia with methemoglobinemia at treatment days 17 to 31, but thereafter recovered from the anemia despite continuation of methionine feeding, indicating an adaptation of the cats. In vitro, significant (P less than 0.01) increases of MetHb concentration and Heinz-body formation were observed when RBC were incubated with plasma from cats fed (1 g of methionine/kg) or with 10 mM 3-methylthiopropionate, a product of methionine catabolism. However, these increases were not observed when RBC were incubated with 10 mM methionine. Seemingly, excessive methionine intake leads to production of an intermediate of the methionine catabolism that may affect RBC directly as an intensive oxidizing agent, resulting in an excessive oxidation of hemoglobin to MetHb and Heinz-body formation.