Poisoning In Cattle Research Articles

Adjustment of feeding as a way to prevent fodder poisoning in cattle

The publication notes that feeding conditions can contribute to healing or, on the contrary, cause fodder poisoning and specific diseases, weakening of the body's immunity against pathogens of various diseases. The specific diseases caused by the unsatisfactory condition and properties of feed include diseases of insufficient nutrition, which are caused by insufficient supply of vital nutrients to animals and are often accompanied by metabolic disorders, as well as feed poisoning. In infectious and invasive diseases of animals, nutrition plays the role of a powerful factor that determines the body's resistance. Significant damage to animal husbandry from fodder poisoning is expressed primarily in the death of a fairly large number of animals of various species, as well as in significant losses of production or reduced performance of animals. For the effective fight against poisoning and, in particular, for the prevention of the latter, it is necessary for all animal husbandry specialists to orientate themselves in the sources of fodder poisoning, their clinic and diagnosis, as well as know the possibilities and methods of providing assistance to sick animals. Depending on the place of growth, the same plants are poisonous in some cases, and used as fodder in others. Fluctuations and accumulation of poisonous substances take place in the same plants in different phases of vegetation (before and after flowering), in different parts of plants depending on meteorological conditions and in individual months. Many of these plants have a fairly high nutrient content and can be of considerable forage value. One of the causes of fodder poisoning of animals can be fodder affected by various parasitic and saprophytic fungi. Many types of rust, soot, mold and other fungi are widespread in nature. They affect feed (coarse, concentrated, juicy), which causes their harmful properties. Often, animal poisoning is not caused by poisonous plants contained in hay and grain fodder, or by their seeds, but is caused by their spoilage by molds or other fungi. The following factors should be attributed to the causes of poisoning: lack of feed quality control; grazing animals on fields and pastures where fertilizers are used; careless attitude towards animals. In order to reduce the damage caused to cattle by fodder poisoning, it is necessary to carry out appropriate preventive measures, and in case of animal diseases related to poisoning, to provide them with qualified assistance in a timely manner, which is possible only with the ability to recognize poisoning and establish the causes that caused it.

Chronic copper poisoning in cattle: can you have too much of a good thing?

Chronic copper poisoning in cattle: can you have too much of a good thing?

A Feeding Trial to Investigate Strategies to Mitigate the Impacts of Pimelea Poisoning in Australian Cattle.

Pimelea poisoning of cattle causes distinct symptoms and frequently death, attributable to the toxin simplexin. Pimelea poisoning was induced via addition of ground Pimelea trichostachya plant to the daily feed in a three-month trial with Droughtmaster steers. The trial tested four potential mitigation treatments, namely, biochar, activated biochar, bentonite, and a bacterial inoculum, and incorporated negative and positive control groups. All treatments tested were unable to prevent the development of simplexin poisoning effects. However, steers consuming a bentonite adsorbent together with Pimelea showed lesser rates-of-decline for body weight (P < 0.05) and four hematological parameters (P < 0.02), compared to the positive control group fed Pimelea only. Microbiome analysis revealed that despite displaying poisoning symptoms, the rumen microbial populations of animals receiving Pimelea were very resilient, with dominant bacterial populations maintained over time. Unexpectedly, clinical edema developed in some animals up to 2 weeks after Pimelea dosing was ceased.

Salvia reflexa-contaminated hay poisoning in cattle

Salvia reflexa is an annual forb that has recently (2021) been reported to contaminate hay and cause fatal hepatotoxicity in cattle. It is possible that prior poisoning cases may have gone unrecognized due to the lack of information on fatal hepatotoxicity caused by S. reflexa. Two cases are reported. Case 1 occurred in December 2001 in Montana, in which 30 cows died out of 105. Case 2 occurred in 2023 in Wyoming, in which 111 cows out of 155 died. Poisoned cows in both cases had elevated aspartate aminotransferase and alkaline phosphatase activities with microscopic severe acute centrilobular necrosis with hemorrhage. These lesions were similar to those described previously in clinical and experimental S. reflexa trials. Hepatotoxic diterpenes of S. reflexa, salviarin and rhyacophiline, were detected in hay samples in both cases and in rumen contents from animals in Case 2. Plant specimens of S. reflexa were collected from 2 herbaria, representing collections from 12 states, and screened for salviarin and rhyacophiline. The S. reflexa toxins were found in herbarium samples suggesting if S. reflexa is present, it is potentially toxic to cattle.

Overview of Cyanide Poisoning in Cattle from Sorghum halepense and S. bicolor Cultivars in Northwest Italy.

Sorghum plants naturally produce dhurrin, a cyanogenic glycoside that may be hydrolysed to cyanide, resulting in often-lethal toxicoses. Ruminants are particularly sensitive to cyanogenic glycosides due to the active role of rumen microbiota in dhurrin hydrolysis. This work provides an overview of a poisoning outbreak that occurred in 5 farms in Northwest Italy in August 2022; a total of 66 cows died, and many others developed acute toxicosis after being fed on either cultivated (Sorghum bicolor) or wild Sorghum (Sorghum halepense). Clinical signs were recorded, and all cows received antidotal/supportive therapy. Dead animals were subjected to necropsy, and dhurrin content was determined in Sorghum specimens using an LC-MS/MS method. Rapid onset, severe respiratory distress, recumbency and convulsions were the main clinical features; bright red blood, a bitter almond smell and lung emphysema were consistently observed on necropsy. The combined i.v. and oral administration of sodium thiosulphate resulted in a rapid improvement of clinical signs. Dhurrin concentrations corresponding to cyanide levels higher than the tolerated threshold of 200 mg/kg were detected in sorghum specimens from 4 out of 5 involved farms; thereafter, such levels declined, reaching tolerable concentrations in September-October. Feeding cattle with wild or cultivated Sorghum as green fodder is a common practice in Northern Italy, especially in summer. However, care should be taken in case of adverse climatic conditions, such as severe drought and tropical temperatures (characterising summer 2022), which are reported to increase dhurrin synthesis and storage.

Cattle poisoning by Baccharis coridifolia – report of an outbreak and a brief review of the literature

Baccharis coridifolia is a toxic weed from southern Brazil and regions of Argentina, Uruguay, and Paraguay. In Rio Grande do Sul (RS), B. coridifolia occurs mainly in fields bordering Argentina and Uruguay (Campanha). Poisoning by B. coridifolia occurs in cattle, buffalo, sheep, and horses. The disease is often fatal after an acute course characterized by gastrointestinal disturbances. We report here the epidemiology, clinical, and pathological aspects of an outbreak of B. coridifolia poisoning in cattle that occurred in a herd of 70 heifers transported from the municipality of Bossoroca (28° 43' 48" S 54° 54' W), RS (Property 1), to another property in the municipality of Júlio de Castilhos (29° 13' 37 " S 53° 40' 55" W), here referred as Property 2, 180 km away from Property 1. Upon arriving at Property 1, the heifers were placed in a paddock of native pasture, which had a shortage of forage and a moderate amount of B. coridifolia. The next day, three heifers were found dead, and the others were transferred to an oat pasture, where 36 died, many without showing evident clinical signs. Out of 70 heifers, 39 died, and three were necropsied. The main gross changes were in the gastrointestinal tract. The ruminal contents were abundant and liquid; microscopically, there were degeneration and necrosis of the epithelium of the pre-stomachs and abomasum; these changes were more pronounced in the omasum. The final diagnosis was based on epidemiological data and pathology. Although B. coridifolia is found mainly in the Campanha region of RS, this outbreak indicates that it should also be considered in the differential diagnosis of acute death in cattle in the midwestern region of the State.

Clinico-Pathological Alterations and Therapeutic Management of Thiram Poisoning in Cattle

As there is very scarce literature on fungicide poisoning in livestock animals and in view of reporting fungicide poisoning in cattle in the study area, the present study was conducted to study the clinico-pathology of thiram poisoning in cattle and to standardize the therapeutic regime for the poisoning cases. Clinical cases suspected for Thiram poisoning on the basis of confirm evidence from animal owner were subjected to clinical examination, hematology and therapeutic management. Cases died of severe poisoning were subjected to post-mortem examination. A total of 17 cattle suspected for Thiram poisoning on the basis of history and evidence showed clinical signs of sudden onset of anorexia, salivation, shivering, teeth grinding, restlessness, prolonged sitting, tympany, colic, dyspnea and constipation or diarrhea in few cases. Significant increase in heart rate and respiration rate was observed while hematological analysis showed non-significant changes compared to healthy counterparts. Post-mortem and histopathological examination of cattle died of thiram poisoning showed mild hepatocellular degeneration, tubular necrosis in kidneys with focal infiltrates while marked edema and congestion was evident in lung tissues. The ailing cattle were treated with fluid therapy, anti-inflammatory drugs, vitamin B complex, atropine sulphate, antihistaminics along with laxative and prebiotics-probiotics showed good response to treatment with complete clinical recovery in 4-5 days of treatment. Being there is no specific antidote, the cases of fungicide like Thiram poisoning could be managed with symptomatic treatment and regular clinical assessment of the severity of the poisoning.

No Body, No Crime? Vicariously Imagining Africa’s Arsenic Century: Bovines, Arsenic Poisoning and Multi-Species Toxic Histories in Southern Rhodesia (Colonial Zimbabwe), 1900–1940s

During the first half of the twentieth century, white settler farmers in colonial Zimbabwe raised incessant complaints and alarm over ‘mysterious’ and inexplicably frequent incidences of cattle mortalities. These mortalities were attributed to poisoning from careless handling of arsenical dips, ingestion of arsenic sprayed grass and grazing in veld impregnated with arsenic trioxide. The arsenic question occupied the attention of experts from the colonial Branch of Chemistry, toxicologists, bacteriologists, veterinary officials and white settler farmers in contested cattle-centred narratives. Within the framing of colonial toxic politics, cattle poisoning disproportionately received more elaborate scrutiny and attention than that of humans and other species. The colonial archive only affords limited and vague visibility to the toxic encounters of humans and non-bovine species. This paper seeks to transcend and interrogate bovine-centric poisoning discourses with which colonial sources are replete and to use existing cattle poisoning records to amplify and construct multi-species toxic histories connecting cattle, humans, landscapes and other species in a co-constituted narrative of arsenic toxicities. The paper employs vicarious imagination of experiences to reframe Africa’s ‘arsenic century’ and colonial toxic histories outside the body-centric script, and examines the intricate and complex chemical relations enmeshing cattle, humans and other species in ecosystems of mutual toxic vulnerabilities and slow chemical violence. The paper uses archival sources, toxicological reports from the Branch of Chemistry and veterinary records of cattle poisoning in colonial Zimbabwe.

Spontaneous poisoning of cattle by onion (Allium cepa) in Brazil

Spontaneous poisoning of cattle by onion (Allium cepa) in Brazil

Binding of the plant-derived toxin simplexin to bovine protein kinase C: insights from molecular dynamics.

Pimelea poisoning of cattle is toxicologically linked to the activation of bovine protein kinase C (PKC) by the plant-derived toxin simplexin. To understand the affinity of PKC for simplexin, we performed molecular dynamics (MD) studies of simplexin, simplexin analogues, and several other activators of PKC. Binding enthalpy calculations indicated that simplexin had the strongest affinity for PKCα-C1B among the activators studied. Key to simplexin's affinity is its ability to form more hydrogen bonds to PKC, compared to the other activators. The C-3 carbonyl group and C-20 hydroxyl group of simplexin were identified as especially important for stabilizing the PKC binding interaction. The hydrophobic alkyl chain of simplexin induces deep membrane embedding of the PKC-simplexin complex, enhancing the protein-ligand hydrogen bonding. Our findings align with previous experiments on structure-activity relationships (SAR) for simplexin analogues, and provide insights that may guide the development of interventions or treatments for Pimelea poisoning.

No Body, No Crime? Vicariously Imagining Africa’s Arsenic Century: Bovines, Arsenic Poisoning and Multi-Species Toxic Histories in Southern Rhodesia (Colonial Zimbabwe), 1900–1940s

During the first half of the twentieth century, white settler farmers in colonial Zimbabwe raised incessant complaints and alarm over ‘mysterious’ and inexplicably frequent incidences of cattle mortalities. These mortalities were attributed to poisoning from careless handling of arsenical dips, ingestion of arsenic sprayed grass and grazing in veld impregnated with arsenic trioxide. The arsenic question occupied the attention of experts from the colonial Branch of Chemistry, toxicologists, bacteriologists, veterinary officials and white settler farmers in contested cattle-centred narratives. Within the framing of colonial toxic politics, cattle poisoning disproportionately received more elaborate scrutiny and attention than that of humans and other species. The colonial archive only affords limited and vague visibility to the toxic encounters of humans and non-bovine species. This paper seeks to transcend and interrogate bovine-centric poisoning discourses with which colonial sources are replete and to use existing cattle poisoning records to amplify and construct multi-species toxic histories connecting cattle, humans, landscapes and other species in a co-constituted narrative of arsenic toxicities. The paper employs vicarious imagination of experiences to reframe Africa’s ‘arsenic century’ and colonial toxic histories outside the body-centric script, and examines the intricate and complex chemical relations enmeshing cattle, humans and other species in ecosystems of mutual toxic vulnerabilities and slow chemical violence. The paper uses archival sources, toxicological reports from the Branch of Chemistry and veterinary records of cattle poisoning in colonial Zimbabwe.

Identification of Acid Hydrolysis Metabolites of the Pimelea Toxin Simplexin for Targeted UPLC-MS/MS Analysis.

Pimelea poisoning of cattle is a unique Australian toxic condition caused by the daphnane orthoester simplexin present in native Pimelea pasture plants. Rumen microorganisms have been proposed to metabolise simplexin by enzymatic reactions, likely at the orthoester and epoxide moieties of simplexin, but a metabolic pathway has not been confirmed. This study aimed to investigate this metabolic pathway through the analysis of putative simplexin metabolites. Purified simplexin was hydrolysed with aqueous hydrochloric acid and sulfuric acid to produce target metabolites for UPLC-MS/MS analysis of fermentation fluid samples, bacterial isolate samples, and other biological samples. UPLC-MS/MS analysis identified predicted hydrolysed products from both acid hydrolysis procedures with MS breakdown of these putative products sharing high-resolution accurate mass (HRAM) fragmentation ions with simplexin. However, targeted UPLC-MS/MS analysis of the biological samples failed to detect the H2SO4 degradation products, suggesting that the rumen microorganisms were unable to produce similar simplexin degradation products at detectable levels, or that metabolites, once formed, were further metabolised. Overall, in vitro acid hydrolysis was able to hydrolyse simplexin at the orthoester and epoxide functionalities, but targeted UPLC-MS/MS analysis of biological samples did not detect any of the identified simplexin hydrolysis products.

Oak Acorn Poisoning in Cattle during Autumn 2022: A Case Series and Review of the Current Knowledge.

Oak poisoning is a known intoxication in grazing animals, but is slightly described in the literature. This case report describes 7 cattle from 3 different farms admitted to the clinic for ruminants of the University of Liège for suspected acorn poisoning in the autumn of 2022. The clinical signs were, anorexia, apathy with polyuria with low density. Further investigations led to the diagnosis of renal failure (blood urea 162 ± 88 mg/dL; blood creatinine 12 ± 4 mg/L). Supportive treatment, based on infusions (NaCl 0.9%) and electrolyte rebalancing, was administered and renal values were assessed every 24-48 h. Of these animals, 5/7 were euthanized. At necropsy, digestive erosions and ulcerations, oedema and renal hemorrhages, between the pyloric/caliceal cavity and the medulla were observed. Histopathological examination revealed necrosis of the renal tubules. The renal values of the two remaining animals were reduced, their general condition improved, and they were discharged. Acorn poisoning is a serious disease with no specific antidote or characteristic symptoms. Animals are identified as sick too late, when renal failure is already established. Farmers should be made more aware in order to prevent exposure, especially in years when acorns are abundant. Furthermore, there is no antidote for this intoxication.

Oleander Poisoning in Cattle in Devghat, Nepal- a Case Report

Oleander poisoning, though widely seen in the Mediterranean region, is rarely seen in Nepal. The poisonous effect of the fodder is due to the accidental ingestion of the different parts of ‘oleandrin’ which contains cardiac glycosides called cardenolides causing mortality in animals. In our study, 8 lactating cows were affected after oleander leaves were accidentally mixed and chopped with Napier. After the ingestion of the mixed fodder, out of 8 cows, 5 died instantly and the remaining 3 were showing severe clinical signs such as severe depression, anorexia, ruminal atony, diarrhea, serous nasal discharge, tachycardia, and irregular heartbeat. The diagnosis of the poisoning was made by finding the chopped leaves of oleander in the feed and ruminal content. The visual observation of the oleander leaves along with gross lesions specifically in the heart causing coagulative necrosis- as it acts as cardiac glycosides- we came to diagnose the oleandrin poisoning. As there was not the availability of digoxin-specific antibodies for the therapy, symptomatic and supportive treatment was done, and the good prognosis was seen on morbid animals within a week.

O35 | Recent outbreaks of cyanide poisoning of cattle in North‐Western Italy after ingestion of Sorghum ssp. grown under severe climatic conditions

Journal of Veterinary Pharmacology and TherapeuticsVolume 46, Issue S1 p. 44-45 ORAL PRESENTATIONS O35 | Recent outbreaks of cyanide poisoning of cattle in North-Western Italy after ingestion of Sorghum ssp. grown under severe climatic conditions First published: 11 June 2023 https://doi.org/10.1111/jvp.13201Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. Volume46, IssueS1Special Issue: 15th International Congress of the European Association for Veterinary Pharmacology and Toxicology held Bruges, Belgium, July 2–5, 2023June 2023Pages 44-45 RelatedInformation

Lantana camara poisoning in cattle that took refuge during a storm in a forest invaded by this plant

An outbreak of poisoning by Lantana camara occurred in cattle when a herd sought refuge in a Eucalyptus forest heavily infested by this plant. The animals showed apathy, elevated serum activities of hepatic enzymes, severe photosensitivity, jaundice, hepatomegaly and nephrosis. After a clinical manifestation period of 2–15 days, 74 out of 170 heifers died. The main histological changes were random hepatocellular necrosis, cholestasis, biliary proliferation and, in one animal, centrilobular necrosis. Immunostaining for Caspase 3 detected scattered apoptotic hepatocytes.

Gastric Perforation Due to Yellow Oleander Poisoning: First Case Report in Humans

Yellow oleander (Thevetia peruviana) is a commonly found shrub in India which produces multiple alkaloidswhich are cardiotoxic. Numerous cases of yellow oleander poisoning have been reported in humans. The spectrumof toxicity due to this plant ranges from nausea, vomiting, diarrhoea, electrolyte abnormalities and arrhythmiasin humans. No case of bowel necrosis due to yellow oleander has been reported in humans to the best of ourknowledge.We present a case of 45-year-old female with suicidal consumption of crushed yellow oleander seeds. The patientwas admitted and observed for arrhythmias. On day 2 of admission, she developed bloody stools, hematemesisand abdominal pain. Abdominal examination showed rigidity and per rectal examination showed blood-stainedmucoid stools. A CECT was done which showed findings suggestive of gastric necrosis with perforation. Thepatient was taken up for surgery and stomach was found to be gangrenous with a perforation at the greatercurvature. Total gastrectomy was performed. The post operative biopsy showed extensive transmural coagulativenecrosis of the stomach and lymphoplasmacytic infiltration of the submucosa.Necrosis of bowel has been reported in experimental settings in animals and in cattle poisoning but no reportedcase of stomach necrosis and perforation due to yellow oleander has been reported in humans. As yellow oleanderis a commonly used suicidal poison in Southern Asia, an eye needs to be kept out for gastrointestinal symptoms.We conclude with recommendations on management of yellow oleander poisoning in the light of these newmanifestations.

Mass Acorn Poisoning of Japanese Black Breeding Cattle

2019年10月，肉用牛飼養施設において，黒毛和種繁殖雌牛10頭が元気消失，食欲低下及び下痢等の症状を呈し，その後約3週間で9頭が死亡した．血清生化学検査でBUNとCreが高度に上昇，腎臓の病理組織学的検査を実施した5頭全頭で急性尿細管壊死が認められた．放牧場の糞便及び死亡牛の第一胃内容物中からクヌギのドングリの果皮が見つかった．比色法により定量したところ，クヌギドングリには6.08％（乾燥重量％）と高濃度の総ポリフェノールが含まれていた．また，第一胃内容の検査を実施した死亡牛全4頭からもポリフェノールが検出された．以上の結果から，本事例をドングリ中毒の集団発生と診断した．牧草の少ない時期に，大型台風により大量のドングリが放牧地に落下しており，放牧牛が短期間に大量に摂取したことが，発生要因と推測された．

Investigation and management of nitrate poisoning in cattle: a case study

Nitrate poisoning is generally caused by ingestion of high levels of nitrate containing fodder and it usually occurs in late autumn in Bangladesh, mainly during a flush growth of green grasses after a dry period. This case report was based on a suspected nitrate poisoning in two Holstein Friesian (2 years age, pregnant; 3.5 years age milking) cows in a commercial dairy farm at Hathazari, Chattogram. The cows had a history of feeding German grass from grassland that was flooded by a nearby fertilizer company’s wastewater and after 6 hours of feeding of that grass the animals were showing clinical signs of inappetite, diarrhoea, mild dyspnea and distended abdomen. The suspected fodder samples were brought to the Department of Physiology, Biochemistry and Pharmacology laboratory, Chattogram Veterinary and Animal Sciences University, Chattogram for toxicological testing. In diphenylamine test, we detected a high concentration of nitrate in the supplied fodder. However, we could not measure the plasma nitrate concentration of affected animals. The affected cows were treated with slow intravenous administration of 1% methylene blue (20mg/kg body weight) and ascorbic acid (15mg/kg body weight) for every 8 hours until completely remission of all clinical signs. In addition, cattle were medicated liver tonic (15 ml per animals) for a period of one week. Feeding of nitrate containing grass was restricted. After three days of treatment, the animals were recovered.

Mineral-salt supplementation to ameliorate larkspur poisoning in cattle.

Larkspurs (Delphinium spp.) are native forbs that are poisonous to cattle and cost livestock producers millions of dollars in losses each year. Macro and micro minerals are required for normal functioning of essentially all metabolic processes in ruminants. The role that mineral status may play in larkspur poisoning in cattle is not clear. In this study, we seek to determine the effects a mineral-salt supplement, commonly used by cattle producers, to potentially reduce cattle losses to larkspur. The ability of mineral-salt supplementation to alter susceptibility to larkspur toxicosis was evaluated in a pen study. Animals supplemented with mineral-salt were found to be less susceptible to larkspur poisoning than the non-supplemented animals. A separate group of animals were then grazed on larkspur infested rangelands. One group was supplemented with a mineral-salt mix and the other group did not receive any mineral-salt. Supplementing cattle with the mineral-salt mix did not alter larkspur consumption (P > 0.05). However, overall larkspur consumption was low and averaged 3 ± 1.0% and 2 ± 1.1% for cattle supplemented with mineral and non-supplemented, respectively. Serum was collected from animals once a week during the grazing study. Average and maximum serum concentrations of toxic larkspur alkaloids were numerically higher in mineral-salt supplemented cattle compared with the non-supplemented animals. Results from the pen study suggest that a good mineral supplementation program will provide a protective effect for animals grazing in larkspur-infested ranges. The mineral-salt supplemented steers, in the grazing study, were not observed to consume less larkspur than the non-supplemented animals; however, the mineral-salt supplemented animals had higher concentrations of larkspur alkaloids in their serum indicating they may be able to tolerate higher larkspur consumption. The data also indicate that mineral-salt supplementation must be continuous throughout the time the animals are grazing these rangelands as the positive effects can be lost within 30 d post supplementation.