The toxicity to cattle and bufadienolide content of six Bryophyllum species

SUMMARY: Cardiac glycoside poisoning was produced in calves given (in descending order of toxicity) flower heads of the hybrid Bryophyllum (Kalanchoe) daigremontianum x B. tubiflorum, of B. pinnatum, of B. tubiflorum (from previous work), whole plant of B. fedtschenkoi, flower heads of B. daigremontianum and whole plant of B. proliferum. For each plant (except B. tubiflorum), 2 calves were each given a single dose of 20 g wet weight per kg bodyweight. By using high performance liquid chromatography, the bufadienolides (cardiac glycosides) bryotoxin A, B and C were detected and assayed in the flower heads and leaf plus stem of B. tubiflorum and in the roots of B. tubiflorum, the hybrid and B. pinnatum. Only bryotoxins B and C were detected and assayed in the flower heads and leaf plus stem of the hybrid, B. daigremontianum and B. pinnatum. No bryotoxins were detected in B. fedtschenkoi. Bryotoxin A and a mixture of bryotoxins B and C from B. tubiflorum flowers were used as standards in the chromatographic assay. Comparing the results of the calf toxicity experiment with the amounts of bufadienolide measured in the plants suggests that bryotoxins A, B and C probably account for the observed disease, but that B. pinnatum and B. fedtschenkoi contain at least one other cardiac glycoside.     

Prickly paddy melon (Cucumis myriocarpus) poisoning of cattle

Twenty-six Hereford heifers died after eating mostly ripe fruit of Cucumis myriocarpus growing in a fallowed cultivation paddock. Four affected cattle were dehydrated and apparently had abdominal pain. Necropsy of three revealed intense congestion with haemorrhage of the alimentary tract, numerous C. myriocarpus seeds in ruminal contents, pulmonary congestion and oedema and, in two, swollen livers. Midzonal swelling and vacuolation of hepatocytes occurred in these two. C. myriocarpus fruit (83% by weight ripe) were dosed to two calves at 60 g wet weight/kg live weight. Both collapsed with tachycardia and dyspnoea and died within 6 h. Their packed cell volumes just before death had increased to 0.7. They had hydropic degeneration and necrosis of the ruminal mucosa, intense congestion and oedema of the rumen, abomasum and intestines, swollen and vacuolated hepatocytes and foci of myocardial degeneration and necrosis. Two other calves were dosed daily with 20 g fruit/kg for three days, then 40 g/kg for three days. One calf received a further 40 g/kg next day. Both calves developed persistent diarrhoea and neutrophilia, and their plasma gamma glutamyltransferase and bilirubin concentrations increased. Necropsy revealed necrosis and oedema of the rumen and swollen degenerate hepatocytes.     

Curing experimental Bryophyllum tubiflorum poisoning of cattle with activated carbon, electrolyte replacement solution and antiarrhythmic drugs

A slurry of activated carbon (activated charcoal) in electrolyte replacement solution given by stomach tube and antiarrhythmic drugs given parenterally cured 9 of 11 calves dosed 7 to 24 h previously with a lethal amount (20g/kg) of Bryophyllum tubiflorum flower heads. Two of another 4 calves treated 26 to 36 h after dosing with flowers survived. B. tubiflorum toxins are bufadienolides (cardiac glycosides). Activated carbon was effective at a single dose of 5 g/kg. Calves were rehydrated with oral electrolyte replacement solution at 150 ml/kg in divided doses over 24 h. Tachycardia was treated with intravenous lignocaine (200 mg doses) or propranolol (5 mg doses) and atrioventricular block with atropine (0.5 mg/kg).     

Clinical findings in dogs and cats with lead poisoning

Over an 11-year period, 68 cases of lead poisoning were diagnosed in dogs and three in cats, accounting for 58.6% and 21.4% of the accidental poisonings in dogs and cats, respectively, presented at the Small Animal Clinic, University of Queensland. Of the dogs, 94% showed alimentary tract involvement and 67.6% central nervous system signs. Blood lead concentrations above 0.3 ppm were considered to indicate toxicity when associated with alimentary tract or central nervous system abnormalities. The percutaneous absorption of lead in dogs is proposed as a factor for intoxication.     

Cestrum parqui (green cestrum) poisoning in cattle

SUMMARY Naturally occurring cases of poisoning of cattle by Cestrum parqui were characterised by ataxia, depression, recumbency, convulsions and death. Three cattle were dosed experimentally by intrarumenal administration of fresh plant material. One calf died 48 h after receiving 30 g (wet weight) of plant /kg body weight. Doses of 11 and 17 g/kg caused only mild intoxication, with dullness and anorexia lasting 2 days. In natural and experimental cases the main lesion was hepatic periacinar necrosis. Elevated levels of plasma aspartate transaminase and prolonged prothrombin times were demonstrated in experimental cases. Haemorrhage beneath the serosa and into the intestinal lumen occurred in field cases, but not in the experimental. It is concluded that C. parqui poisoning in cattle is a primary hepatotoxicity.     

A review of insecticide poisonings among domestic livestock in southern Ontario, Canada, 1982-1989

From 1982 to 1989, inclusive, 20 poisonings were investigated by the Ontario Ministry of Agriculture and Food following ingestion by domestic livestock of granular insecticides including terbufos (13 poisonings), disulfoton (two poisonings), fonofos (two poisonings), phorate (two poisonings), and carbofuran (one poisoning); all are used for rootworm (Diabrotica spp.) control in corn. A further three poisonings of livestock occurred following the ingestion of the foliar insecticide, endosulfan (two poisonings), and the seed protectant insecticides diazinon plus lindane (one poisoning). There were six poisoning cases as a result of excessive topical applications of the three insecticides coumpahos, fenthion, and lindane as dusts or sprays to control external parasites. Together, these events caused the deaths of 258 domestic animals of which 200 were cattle, 23 were swine, and 35 were sheep. Not all deaths are reported to the Ministry and the cases reported here may only represent 30-50% of the actual deaths over the period. Based on total populations of livestock, the percent losses were very small but they represent serious losses to individual growers. The economic loss is estimated at $160,000 over the eight years, or $20,000 per annum, and this does not include veterinary costs.

Some of the poisoned animals died within as little as three to four hours of ingestion while others were sick but survived for several days. Lethal doses of insecticide were found in the rumen, abomasum, or stomach of dead animals. Signs typical of cholinesterase inhibition caused by organophosphorus poisoning were observed in most cases. Cholinesterase readings were found to be zero in dying animals. Necropsy findings were rarely more than pulmonary edema or myocardial hemorrhage. Where organochlorine insecticides were ingested, convulsions were the major manifestation.

Contamination of feed was most often accidental, and chemical analysis was most helpful in identifying both potent and minor sources, thus facilitating cleanup procedures.

     

Correlation of Serum Cardiac Troponin I and Myocardial Damage in Cattle with Monensin Toxicosis

Background: Cardiac troponin I (cTnI) is used as a biomarker of myocardial injury in people and small animals. Little is known about the diagnostic use of cTnI in cattle.
Hypothesis: Serum cTnI correlates to myocardial function and histopathologic lesions in cattle with monensin-induced myocardial injury.
Animals: Ten healthy cows.
Methods: Experimental study. Animals received 1 dose of monensin PO; 30 mg/kg (n = 1) or 40 mg/kg (n = 1) (Group A) or 50 mg/kg monensin (n = 8) (Group B) of body weight. Repeated measurements were performed of serum cTnI, biochemistry, and ECG and echocardiography until study termination at 80 (Group A) and 144 hours (Group B) after dosing. Semiquantitative histopathologic examinations of the heart were performed in each cow. A scoring system with regard to the magnitude of myocardial injury was established and a total heart score was compared with maximum cTnI concentration measured after monensin administration. Five hearts from healthy cows served as controls.
Results: Increased cTnI (>0.07 ng/mL) was found in 9/10 cows. cTnI was significantly associated with left ventricular shortening fraction ( r ²= 0.51; P = .02) and myocardial histopathologic lesion score ( r ²= 0.49; P = .021). All cows (n = 7) with evidence of myocardial necrosis had a cTnI concentration ≥ 1.04 ng/mL.
Conclusion and Clinical Importance: cTnI is related to myocardial necrosis and severity of myocardial damage in cattle with monensin toxicosis. cTnI could become a useful diagnostic tool in the noninvasive assessment of myocardial injury in cattle with naturally occurring cardiac disease.     

Disseminated mycoses in cattle. A study on nine autopsy cases.

Nine cases affected with disseminated mucormycosis (1.3% of all autopsy cases and 20.0% of systemic mycosis) were found among bovine systemic mycosis examined from 1975 to 1985. The disseminated lesions were found in the lungs (3 cattle), heart (2 cattle), liver (2 cattle), spleen (1 beef cattle), kidneys (1 cattle), central nervous system (1 cattle) and lymph node (1 cattle). Histological examination revealed granulomatous lesions, necrotic foci including infarcts, and thromboangiitis with the hyphae of a member of the Zygomycetes and neutrophil reaction. Granulomatous lesions with asteroid bodies were found in the liver. Metastatic foci were established from the primary lesions found in the alimentary organ (4 from the forestomach or abomasum and 1 from the tongue). One case resulted from uterine mucormycosis, and no primary lesion was found in the other 3 cattle. Complicated infection with respiratory aspergillosis occurred in 4 cases with alimentary mucormycosis. All of the 9 cattle had predisposing disorders. Six cattle had been manifested with prolonged debilitating conditions. Anemia was present in 4, leukopenia in 2 and lymphopenia in 1 cattle.     

Pimelea trichostachya poisoning (St George disease) in horses

A dense population of Pimelea trichostachya plants (Family Thymelaeaceae) in pasture poisoned a horse herd in southern inland Queensland in October-November 2005. Plant density was 2 to 45 g wet weight/m(2) (mean 16 g/m(2)) from 5 to 69 plants/m(2) (mean 38 plants/m(2)) representing 3 to 20% (mean 9%) of the volume of pasture on offer. Ten of 35 mares, fillies and geldings were affected. Clinical signs were loss of body weight, profound lethargy, serous nasal discharge, severe watery diarrhoea and subcutaneous oedema of the intermandibular space, chest and ventral midline. Pathological findings were anaemia, leucocytopenia, hypoproteinaemia, dilatation of the right ventricle of the heart, dilated hepatic portal veins and periportal hepatic sinusoids (peliosis hepatis), alimentary mucosal hyperaemia and oedema of mesenteric lymph nodes. Cattle grazing the same pasture were affected by Pimelea poisoning simultaneously. Removal of the horses to Pimelea-free pasture initiated recovery. The one other incident of this syndrome, previously only recognised in cattle in Australia, occurred in horses, in South Australia in 2002, with access to a dense Pimelea simplex population.     

Pyrrolizidine alkaloids and seneciosis in farm animals. Part 2: clinical signs, species-specific sensitivity, food residues, feed contamination, limit values

At the forefront of pyrrolizidine alkaloid (PA) poisoning is the chronic ingestion of contaminated hay, which causes liver damage resulting in an ongoing fatal liver cirrhosis or in the veno-occlusive disease in liver or lung, respectively. The symptomatology of PA-poisoning is not identical for all animal species, and also includes central nervous symptoms. In affected horses significantly elevated levels of hepatogenic serum enzymes and an increase of the retention time for bromosulfophthalein indicates the fatal outcome of the intoxication. Chronic seneciosis of horses is incurable. Rabbits, Japanese quails, and guinea pigs are regarded as poison-resistant species. Sheep and in particular goats are insensitive unless extremely high amounts of plants which exceed the animal's body weight by several-fold are ingested. In contrast, pigs, cattle, and horses as well as chicken and likewise man are very sensitive to poisonings by PA-containing plants. In sensitive animal species a very small amount of contaminated dry hay is needed to exceed the daily dose of 1μg/kg body weight PA which is taken as harmless for man by health authorities. Therefore, all feed with visible pieces of Senecio jacobaea plants are not acceptable as animal fodder and should be destroyed.     

Reassessment of the toxicity of Hypericum perforatum (St John's wort) for cattle

OBJECTIVE: To investigate the clinical effect of administering sufficient Hypericum perforatum to cattle to deliver quadruple the reported oral toxic dose. ANIMALS: Thirty-six yearling Hereford (n = 18) and Angus (n = 18) steers. DESIGN: A series of six experiments was conducted, each using 12 animals in a 2 x 2 factorial design, with two breeds of cattle (Hereford, Angus) and two dose levels of hypericin, 1.5 mg/kg (treated group) and 0 mg/kg (control group). Each set of 12 steers was used in duplicate experiments, with all animals alternated between treated and control groups. PROCEDURES: Treated groups received finely milled H. perforatum administered orally in gelatin capsules to provide 1.5 mg hypericin/kg body weight. All cattle were then exposed to direct sunlight for 5 h per day for 5 successive days. Rectal temperatures were measured immediately before and at the end of each sunlight exposure session. Rectal temperature above 40 degrees C, together with some other clinical sign of hypericin poisoning, was considered indicative of intoxication. RESULTS: No animals developed a rectal temperature above 40 degrees C or other clinical signs of hypericin poisoning. CONCLUSIONS: While the reported bovine oral toxic dose of 3 g dried plant/kg body weight, for flowering stage, presumed narrow leaved biotype, H. perforatum, is probably correct, the corresponding dose for hypericin of 0.37 mg/kg is incorrect. Based on its known concentration in this plant the toxic dose of hypericin for partially pigmented Hereford-cross cattle is estimated at about 10.5 mg/kg body weight and more than this for fully pigmented cattle. This would imply that cattle of the former type should be about three and a half times better protected against H. perforatum toxicity than are unpigmented, wool protected, Merino sheep. Cattle, particularly if fully pigmented, may have a role in grazing management to control H. perforatum.     

白苏提取物的毒性研究

瘤胃分别注射白苏挥发油及水煎液，观察中毒山羊的临床病理特征，研究白苏提取物的毒性。结果表明，瘤胃注射20mL白苏挥发油（相当于4．167kg新鲜白苏茎叶），山羊出现明显的中毒反应；而瘤胃注射500mL白苏水煎液（相当于5kg新鲜白苏茎叶）对其无影响。中毒山羊的心、肺血流量先上升后下降，主要临床病理特征为：颈静脉怒张，胸腔积液，心脏扩张、心壁变薄、心肌有出血点，肺水肿，支气管、细支气管内有大量的泡沫。试验进一步证实，白苏挥发油是动物白苏中毒的主要致病因子，其病理演变过程为急性心衰，导致肺水肿。     

贯叶连翘引种驯化过程中生理生化特性、活性物质含量及抗氧化能力的变化

为了探明贯叶连翘引种驯化过程中生长适应能力以及活性物质的变化,以野生和栽培盛花期植株为材料,分别对生理生化特性、活性物质含量以及抗氧化能力进行了测定与分析,结果表明,栽培贯叶连翘的净光合速率、蒸腾速率、气孔导度、叶绿素含量和根系活力均高于野生植株,尤其是其盛花期和地上部分干重分别较野生植株提前了7 d和提高了16.67%。总黄酮和金丝桃素含量在栽培和野生植株同一器官中无显著差异;总酚类在野生花中的含量显著高于栽培花,而叶中的含量则相反;野生和栽培植株各器官中,总黄酮和酚类化合物含量在叶和花中的含量显著大于茎,而金丝桃素的含量表现为花>叶>茎。野生和栽培各器官抗氧化能力为叶>花>茎,其中,野生和栽培叶、茎提取液的抗氧化能力无显著差异,而栽培花的抗氧化能力显著大于野生花。以上研究结果表明,贯叶连翘野生转栽培后,不仅具有较好的生长适应能力,而且主要活性物质的积累量及抗氧化能力并未显著降低。该研究结果将对贯叶连翘种植栽培以及保护野生资源具有重要的参考价值和实践意义。     

Toxicologic disease of the digestive tract.

There is a diverse and long list of toxicants that can affect the digestive system of food-producing animals. The plants and other natural toxicants discussed in this article are those primarily affecting the GI system. A number of other plants may also affect the digestive tract, but the effects from these are considered secondary and less pronounced. Often, plant poisonings affecting the digestive tract present with similar clinical signs, and a good thorough history is necessary to help differentiate between them. Moreover, a careful walk through the pasture with a keen eye to note plants that have been browsed or grazed may greatly assist the history. In cases where toxins are suspected as the cause of a GI disorder, consultation with a veterinary toxicologist at a diagnostic laboratory may be indicated. These professionals are knowledgeable about a wide variety of natural and other toxicants that may be present in your area. They can help with developing a differential diagnosis and the selection of appropriate samples to confirm the diagnosis.     

Suspected botulism in cattle associated with poultry litter

Botulism was diagnosed clinically in grazing cattle on three closely sited dairy farms. The evidence suggests that the source of the toxin was poultry carcases containing types C and D Clostridium botulinum. These organism were also found in the alimentary tract of affected animals. Silage is suspected as having acted as a vehicle for the organisms and, or, toxins in cases which occurred later in housed cattle on one of the farms.     

Toxic feed constituents in the horse.

Poisoning cases in horses associated with dietary exposures can encompass a wide variety of etiologies that can be caused by natural or man-made components. Feed mixing errors and ingestion of feed formulated for other species are the most common means by which poisonings from man-made materials occur. Ionophore feed additives and antibacterial agents are especially toxogenic to horses. Effects of ionophores in horses include clinical, clinicopathologic, and pathologic changes associated with cardiac, muscular, and neurologic tissues involvement. The acute effects of ionophores, however, can result in long-term cardiac dysfunction. Antibacterial effects are associated with changed microbial populations in the digestive tract that results in bacterial toxin liberation. These bacterial toxins damage the mucosa, and they result in systemic effects. For either type of feed-associated poisoning, it is critical that samples be analyzed for an accurate diagnosis.     

二倍体菘蓝开花习性及传粉特性研究

菘蓝是药材板蓝根和大青叶的基原植物,依赖种子繁殖。通过田间观测和人工授粉实验,对民乐县栽培菘蓝开花时序和传粉生物学系统进行研究,旨在为其种子繁育和杂种优势利用提供科学和技术依据。研究表明,菘蓝为无限花序,单株表现异向开花习性,花序从植株顶部向下,单花从花序基部向上依次开放。花两性,雄蕊6,4枚长,2枚短,花萼和花瓣均为4,花萼绿色,花瓣黄色,子房上位,1室。单花寿命6~7 d,异常气候可缩短至3~4 d,群体开花期30 d左右。即将开放的花蕾柱头已成熟,花瓣刚露出花萼后开花当天,花粉鲜黄而散,末花期子房膨大,花粉干枯。短角果结种子0~2粒。自然结籽率95.0%,不去雄和去雄套纸袋均不结实,同株异花去雄授粉结籽率仅4.0%,去雄套纸袋异株异花授粉结籽率72.0%,去雄不套袋结籽率53.3%,自交不亲和指数为0.96~1.00。不去雄套网袋结籽率5.0%,去雄后提高至13.7%,访花者主要有食蚜蝇、黑蜂等。说明菘蓝具有较强的自交不亲和性,不存在无融合生殖现象,属典型的异花授粉类型,需传粉者,传粉媒介以虫媒为主,风媒为辅。     

Supplementary report on experimental autumn crocus (Colchicum autumnale L.) poisoning in cattle: morphological evidence of apoptosis.

Previously we reported that tissue destruction characterized by the presence of karyopyknotic, karyorrhectic and mitotically arrested cells was seen in alimentary epithelial cells and lymphocytes in the lymphoid and hemopoietic systems of cattle experimentally administered with autumn crocus (Colchicum autumnale L.). This report deals with the mechanism of acute cellular injury following experimental autumn crocus poisoning in cattle as demonstrated by the in situ DNA strand break analysis and electron microscopy. The analyses revealed that cellular injury caused by autumn crocus was closely associated with apoptosis.     

The efficacy of acetamide for the treatment of experimental Dichapetalum cymosum (gifblaar) poisoning in sheep

High mortality of livestock is caused annually by the plant, Dichapetalum cymosum (gifblaar), in the Northern Transvaal. So far no therapeutic measures have been developed for the prevention or treatment of this poisoning. In this presentation, the efficacy of acetamide as therapy for experimental gifblaar poisoning was tested in 18 sheep. When 2.5-5 g/kg of acetamide was dosed to sheep at various intervals before and sometimes after the administration of 5 g/kg of gifblaar, 1 out of 5 survived, compared with 0 out of 2 controls. Dosing of 2 g/kg of acetamide before and/or simultaneously with or after 1 g/kg gifblaar prevented mortality as 5 out of 5 treated sheep survived compared with none of the 5 controls. The experiments indicate that acetamide has demonstrable therapeutic value as an antidote for the prevention of experimental gifblaar poisoning in sheep. Further investigations should determine the feasibility and applicability of these findings under field conditions in sheep and cattle.