Farm Animal Toxicology 2021.pdf

Toxicology (Farm Animals) Dr Emma Fishbourne Toxicology • The study of substances (toxicants/ toxins) that produce a detrimental effect on an organism • Toxicosis: a disease state that results from exposure to a poison Recognition that incidence may be an intoxication • Onset of disease associ...

Toxicology (Farm Animals) Dr Emma Fishbourne Toxicology • The study of substances (toxicants/ toxins) that produce a detrimental effect on an organism • Toxicosis: a disease state that results from exposure to a poison Recognition that incidence may be an intoxication • Onset of disease associated with a change in management • Epidemiology not expected of an infectious disease • Clinical / post mortem examination results • The Veterinary Poisons Information Service (VPIS) is available 24 hours a day https://www.vpisglobal.com/ Learning Objectives for Farm Animal Toxicology • Describe the clinical presentations, diagnosis, treatment and prevention of common mineral poisonings seen in farm animals e.g. lead, copper and selenium and were relevant the implications for human health. • Describe the clinical presentations, diagnosis, treatment and prevention of common plant poisonings seen in farm animals. • Describe the clinical presentations, diagnosis, treatment and prevention of common mycotoxins seen in farm animals. • Describe the clinical presentations, diagnosis, treatment and prevention of poisoning from fertiliser, rodenticides and botulism seen in farm animals. Samples for Clinical Pathology • • • • • • • Urine Liver Kidney Blood Stomach contents Feed Bone / hair Treatment - General • Remove source • Limit absorption / hasten elimination • Symptomatic & supportive • A few specific antidotes available* check they can be used in food producing animals (Check on VMD https://www.gov.uk/government/organisations/veterinary-medicines-directorate) https://www.gov.uk/guidance/the-cascade-prescribingunauthorised-medicines#food-producing-species Introduction • Common mineral poisonings • Poisonous Plants • Mycotoxins Common Mineral Poisonings • Latest information on poisonings in sheep and cattle can be found on the government website on chemical food safety in a quarterly report produced by APHA • Common mineral and inorganic poisonings include? Common Mineral Poisonings • Common mineral and inorganic poisonings include: • Lead • Copper • Selenium APHA’s role in toxicology APHA’s role in chemical surveillance is through: Screening programmes An example of this is the Statutory Surveillance Scheme for Veterinary Drug Residues and to which APHA participates on behalf of the Veterinary Medicines Directorate The Wildlife Incident Investigation Scheme (WIIS), which is run by Natural England and Welsh Government on behalf of HSE, detects incidents that might be associated with the misuse or abuse of agrochemicals in relation to wildlife Emergency response Following an incident such as a fire or severe flooding Animal disease outbreaks This forms part of APHA’s scanning surveillance. Food safety • With any poisoning incident which involves food producing animals, it is essential that an assessment of safety in carried out. Under the Food Safety Act 1990 and related legislation, farmers, as primary food producers, and their advisors are required to show due diligence to protect the food chain. As with any surveillance, the key activity is making sure that incidents are detected. The linking up of related incidents can serve as a trigger for action and needs to be co-ordinated as chemical incidents are often complex. Case example on APHA website • The image below shows a lamb with Vitamin A toxicosis. APHA was initially alerted to three affected farms over two days. As a result of a co-ordinated approach, contaminated milk powder was quickly identified, traced and recalled and the speed at which this could be done helped to minimise the impact. Lead Poisoning Aetiology • Ingestion of lead –point sources vs soil ingestion Clinical signs Depend on amount of lead ingested and source • Acute poisoning - typical in young calves • • Found dead or death occurring within 24 hours of sudden onset toxicity with neurological signs including: muscle tremors and twitching (head and neck), hyperthermia, salivation, rolling eyes, bellowing, blindness, stiff gait, convulsions with opisthotonos and pupillary dilation. Subacute – adult cattle and sheep • Animals live for several days. Neurological signs include, dullness, anorexia, salivation, blindness, incoordination, staggering, circling, muscle tremors, colic, ruminal atony, recumbency Lead Poisoning • Chronic – typical in lambs with access to soils high in lead • Nephrosis is common. 2 syndromes: ill thrift with gait abnormalities or lameness and paralysis due to fractures (osteoporosis). In pregnant animals – abortion and poor fertility • Subclinical – chronic exposure at low levels – may just be an issue with residues in animal products with no clinical signs! Diagnosis • Clinical signs • Heparin – levels in blood >0.48 µmol/litre diagnostic • Further tests often required to clarify food safety issues – lead can be detected in blood, faces, urine and milk, hair and wool can be used for subclinical and chronic lead poisoning cases • Kidney lead levels provide diagnostic gold standard but liver can also be used (biopsy) - >0.5 parts per million (ppm) Lead Poisoning Treatment • • • • Chelation therapy Thiamine hydrochloride Supportive Therapy Rumenotomy Prevention / Control Measures • • • • Remove animals from source Good waste management on farm Check old buildings for paint, flashing etc More difficult if soil contamination From a human health prospective: • Farmers are obliged to take measures avoid contamination of the food chain – 16 week voluntary withdrawal • Should emergency slaughter of any of the clinically unaffected cattle in the exposed group be required during the 16 weeks then the animal should be accompanied by FCI stating that offal should be discarded • If animals are close to or at finishing weight then the following parameters are followed: • Blood lead analysis < 0.15 µmol/l: no further restrictions required, 0.15 µmol/l to 0.48 µmol/l: provide food chain information (FCI) to the abattoir and ensure offal is discarded • Milk will be permitted to enter the bulk tank provided the blood lead concentration is less than 0.48 µmol/l. However if there are high numbers of milking cows exposed to lead then a risk assessment is required and bulk tank milk will need to be monitored to ensure the lead concentration is below 20 parts per billion. From a human health prospective: • > 0.48 µmol/l in blood: provide food chain information to the abattoir, ensure offal is discarded and make an additional risk assessment as to whether carcase meat requires testing prior to carcase release into the food chain • >1.21 µmol/l: Clinical toxicity is likely. Ideally a further withdrawal period should be observed. If slaughter is essential then provide FCI to the abattoir ensuring offal is discarded and that carcase meat is tested for lead residues prior to carcase release into the food chain. Lead Poisoning • Rare in pigs • Areas where soil is high in lead should not be used for outdoor pigs • Affected animals often present with neurological signs Copper Poisoning Aetiology • More common in sheep • Chronic copper poisoning more common • Variation in breed susceptibility • Cattle tends to occur if have access to pig feed or graze pastures fertilised with pig manure Clinical signs • Sudden onset, depressed, anaemia, jaundice and haemoglobinuria, ataxia, recumbency and eventually death Copper Poisoning Post Mortem Examination • Carcase - pale or jaundiced, dehydrated, liver pale tan or bronze coloured, kidneys dark red or gun metal grey, urine dark red / black, secondary lung consolidation Diagnosis • History, clinical signs and post mortem findings • Kidney copper concentrations used to confirm diagnosis • If other animals in the group can check subclinical liver damage using AST NADIS Copper Poisoning Treatment • Supportive therapy • Copper antagonists – molybdenum or sulphur * care need to monitor to avoid deficiency! Prevention / Control Measures • Remember poisoning is due to a combination of efficiency of absorption and dietary availability • Care copper foot baths Selenium Poisoning Aetiology • Acute toxicosis occurs due to excessive supplementation Clinical signs • Causes toxic damage to the cardiovascular, respiratory and urinary systems and damage to the secondary lymphoid tissue • None specific – staggering gait, dyspnoea, tympany, colic, diarrhoea, recumbency, cyanosis and death Selenium Poisoning Post Mortem Examination • Subcutaneous haemorrhages, straw coloured fluid in the pericardium, severe pulmonary oedema, abomastitis, intestinal and hepatic congestion, brain stem haemorrhages, destruction of the renal cortices Diagnosis • Elevated selenium in the liver, heart and kidneys Treatment • None Prevention / Control Measures • Ensure correct doses when giving selenium supplements • Ensure proper mixing of drenches or wormers containing selenium Case Study Case Study • 2 year old heifer died, had ‘neurological signs’ for 2 days before • Farm had a single barn with a pen housing cattle and another pen for horses. The cattle had access to a small outdoor paddock and the horses to a large pasture. 2 cats and 2 dogs also present on the farm. Farmhouse located across yard from barn. • Liver sample showed lead concentration of 23.1mg/kg DM - high • Tested some of the other animals and owner (pregnant vet) – blood, milk and tissue samples from 2 more cows that subsequently died • Took environmental samples Case Study RESULTS • 5 cows, 2 calves, a dog, a cat and vet had elevated lead levels • Lead found in paint on the barn and paint on the inside of the house! • House undergoing renovation – lead paint dust Rodenticide and Fertiliser Poisoning Anticoagulant Rodenticide Poisoning • Mainly seen in pigs – pet pigs may have more access? Not just poison but also may have eaten poisoned rats! • Often escapees on commercial units! • Human health implications • residues can remain in tissues for along time, affected livestock may never be able to enter the food chain • Clinical signs – anaemic, non-pyrexic, weak, haemorrhages http://www.hse.gov.uk/biocides/eu-bpr/rodenticides.htm Nitrate and Nitrite Poisoning Aetiology • Excessive intake of nitrate • Rumen bugs convert Nitrate  Nitrite  Ammonia  Bacterial Protein BUT if ruminants consume lots of nitrate get accumulation of nitrite which is then absorbed into the bloodstream converts haemoglobin to methemoglobin which cannot transport oxygen Clinical Signs – due to lack of oxygen! • Anoxia, cyanotic mucosae, tachypnoea, weak and rapid pulse – could be mistaken for neurological signs • Can get subacute or chronic forms – signs more vague Nitrate and Nitrite Poisoning Diagnosis • Clinical signs / history • Blood – plasma protein bound nitrite • Chocolate-brown discoloration of blood Treatment • Treatment with Methylene Blue iv Prevention / Control • • • • Usually occurs accidentally Spilt fertiliser on pasture that animals turned out on to graze Run off entering cattle accommodation Carryover to bowsers and equipment used to carry water previously used for fertiliser are not properly washed out Nitrate and Nitrite Poisoning • NB: Can also find high levels in some plants which may result in poisoning. • These include: • • Docks and Sorrels – Poor pasture management Fat Hen – Common waste ground plant and crop contaminator! https://en.wikipedia.org/wiki/Rumex_obtusifolius#/media/File:Rumex-obtusifolius-foliage.JPG Botulism Botulism Aetiology • Often associated with the use of broiler litter as fertiliser (ingestion of pre formed toxin - rotten carcass’s types C and D, rotten plant material type B) Clinical Signs • Often found dead, or if alive often found recumbent with flaccid paralysis or ataxic Diagnosis • Clinical signs / history • PME – botulism toxin test Treatment • None! Botulism Prevention / Control • Take care with broiler litter (Animal By-Products Order) http://apha.defra.gov.uk/documents/surveillance/diseases/botulism-inruminants.pdf From human health prospective: Type B food safety concern. Clinically affected animals should not be presented for slaughter into the food chain and shouldn’t use produce from affected animals. Recovered cases should not be presented into the food chain for 18 days. Mycotoxins Mycotoxins Aetiology • Produced by fungi • Occur in feed routinely but usually at concentrations that do not impact animal health and performance • Around 400 types! Clinical signs • Vary and may be involved in non-specific disease syndromes – may have mix. Feed refusal main effect? Financial Impact to the farm… 1. 2. 3. 4. Reduced crop yields Product rejection Reduced animal performance Increased Health Issues Mycotoxins Diagnosis • Can be difficult to diagnose due to lack of tests to determine the presence of mycotoxins in feed or in the animal! Treatment • Depends on source of mycotoxin Prevention / Control Measures • Reduce exposure to mycotoxin • Prevent production of mycotoxins – influenced by temperature, carbon dioxide and water levels – most likely to be an issue in warm, wet conditions Taken from beefandlamb.ahdb.org.uk Mycotoxins – control measures • Ensure grain is dried to correct moisture content • Prevent exposure of silage to oxygen by ensuring adequately compacted and covered • With big bale silage handle with care to avoid damaging the wrap • Keep straw dry • Avoid feed, forage or bedding with visual mould or spoilage! • Clean crop storage areas between batches • Consider adding a mycotoxin binder to ration – monitor impact on stock Mycotoxins – Aflatoxins (best known – carcinogenic) Aetiology • Aspergillus fungi • Occur in field prior to harvest or postharvest if drying delayed, insect or rodent infestation • Highest risk of contamination – corn (peanuts, cottonseed) Clinical signs • • • • Primarily a hepatic disease Decreased feed intake Decreased milk yields Recurrent infection – immune suppression Treatment • None, remove source! Mycotoxins – Deoxynivalenol (DON) (also known as vomitoxin!) Aetiology • Recent study showed high prevalence in UK cereals (corn, wheat, barley, oats) • Caused by Fusarium fungi Clinical Signs • • • • Lower feed intake Lower milk production Diarrhoea Immune alterations Treatment • None, remove source! Mycotoxins – Zearalenone Aetiology • Fusarium fungi • Production of this toxin enhanced by high temperatures • Pigs more susceptible but can see in other species Clinical Signs • • • • Signs of hyperestrogenism Hyperemia and swelling of the vulva, mammary glands Nymphomania Other signs - Rectal and vaginal prolapses, poor libido in boars Diagnosis • Clinical signs , history Treatment • None, remove source! Mycotoxins – Facial Eczema Aetiology • Ingestion of sporidesmin, produced by the fungus Pithomyces chartarum found in the mat of leaf litter in shaded pasture • Occurs in humid, warm weather • Toxin concentrates in the liver causing epithelial necrosis of the bile ducts Clinical Signs • Ill thrift, reduced fertility • Severely affected animals develop photosensitisation. Signs include: photophobia, swelling of the face and ears https://en.wikipedia.org/wiki/Facial_eczema Mycotoxins – Facial Eczema Diagnosis • History • Serum gamma glutamyltransferase (GGT) concentration can be used to diagnose subclinical disease • Can measure pasture spore counts Treatment • No specific treatment available Prevention / Control Measures • Oral administration of zinc salts prior to exposure • Feed hay, or brassica crops during high risk periods and avoid close grazing. • Remove stock from high risk areas • Breed for resistance Mycotoxins – Ryegrass Staggers Aetiology • Ingestion of the mycotoxin Lolittrem produced by Acremonium loliae found on perennial ryegrass Clinical Signs • Neurological signs 1-2 weeks after the introduction to toxic pasture and include: • Fine tremors of the head and neck at rest, head nodding, jerky movements of the neck and limbs, alteration in stance. Severely affected animals can collapse head first before rolling into lateral recumbency, with their necks arched back and limbs extended. Tetanic spasma can persist for several minutes before apparent recovery Diagnosis • History Mycotoxins – Ryegrass Staggers Treatment • No specific treatment available Prevention / Control Measures • Remove from affected pasture • Avoid close grazing, consider feeding supplementary hay / reseeding Mycotoxins – Ergotism Aetiology • Ingestion of ergot alkaloids produced by Claviceps purpurea a parasitic fungus of rye and other small grain crops. • Ergots are the resting stage of the fungus and can be seen as dark horn like structures which replace grass seeds Mycotoxins – Ergotism Clinical Signs • Capillary damage with extremities of affected animals appearing painful, inflamed then cold with numbness and the development of dry gangrenous lesion’s in the lower legs, ears and tail. Affected animals may loose weight, have reduced milk yields and painful udders. Irritation of the digestive tract can also occur with abdominal pain and vomiting. Diagnosis • History and clinical signs Treatment • No specific treatment available Prevention / Control Measures • Remove from affected pasture Taken from www.canadiancattlemen.ca Common Plant Poisonings Common Plant Poisonings Why do you think livestock might eat poisonous plants? What could make them more palatable? How are you going to treat them? Common Plant Poisonings Often associated with:• • • • • Poor pasture availability i.e. heavy snow Overgrazing Incorporation into conserved forages Use of herbicides Increased accessibility i.e. dumping of hedge cuttings and garden waste, clearing ditches and leaving plants to wilt • Transportation – hungry on arrival!! Diagnosis of plant poisoning Commonly relies on plant identification, but plant alone not diagnostic! Need to consider: • • • • Evidence of potential exposure Believable time frame Risk factors that may have contributed i.e. overgrazing Clinical signs *important to consider that diagnosis may be in support of an insurance claim or litigation Treatment Few specific treatments available - check they can be used in food producing animals (Check on VMD https://www.gov.uk/government/organisations/veterinarymedicines-directorate) General advice: • Remove stock from suspected source • Give access to good quality forage – may dilute • Eliminate poison – rumenotomy or adsorption with activated charcoal • Treat symptomatically NOW FOR THE QUIZ WITH PRIZES!!! PLANT IDENTIFICATION….. Ragwort Aetiology • • Ingestion over a prolonged period of time of Pyrrolizidine alkaloids: hepatotoxic Rarely acute poisoning Clinical Signs • • • Weight loss, oedema, straining diarrhoea Photosensitisation Pigs quite resistant to ragwort toxicity Diagnosis • Liver Biopsy: fibrosis, vein occlusion, bile duct proliferation Ragwort • Pyrrolizidine alkaloids is probably the most common cause of plant poisoning in wildlife and livestock and can also affect people. Pyrrolizidine alkaloids can cause hepatotoxicity and pulmonary toxicity and some of them are carcinogens. As a result of food animal exposure poisoning of people and an increased long-term cancer risk may arise from food (eg, milk or honey) contamination. Rape and Kale (Brassica crops) Aetiology • Ingestion of a variety of substances found in common feed associated plants (fodder beets, kale, rape, turnips) including S-methylcysteine sulfoxide (SMCO), nitrate / nitrites, goitrogens, oxalates • Some evidence for inherited predisposition e.g. Zwarbles to oxalate deposition Clinical Signs • SMCO – causes haemolysis, anaemia, haemoglobinuria, pallor, jaundice, tachycardia • Nitrates (see below) • Hypothyroidism, goitre and hypocalcaemia Rape and Kale (Brassica crops) Diagnosis • Clinical signs and history • Bloods – depends! • Can measure nitrate levels • Haematology – red blood cell inclusions on smears Other feed associated plants that can cause poisoning include…. Clovers • Grown for forage and to fix nitrogen • Toxins include oestrogens, cyanogenic glycosides, goitrogens and nitrates • Clinically see frothy bloat, laminitis, photosensitisation, infertility, goitre, abortions Linseed • Cyanogenic glycosides • Clinically see sudden death, salivation, sleepiness, staggering, convulsions Potatoes • Glycoalkaloids, phenolic compounds (all parts of the plant can be toxic) • Clinically see death, nervous signs, GI signs https://www.wildlifetrusts.org/ Plants causing photosensitisation Aetiology • Ingestion of St John’s wort (Hypericin) (fresh plant) • Other plants that cause this include Ragwort, Bog asphodel causing liver damage (secondary photesensitisation) Clinical Signs • Photosensitisation - erythema, swelling, skin necrosis in white areas (sunburn on hairless and un-pigmented skin, especially on the dorsal aspect. Diagnosis • Clinical signs and history Treatment and Management • Move affected animals into shade, anti-inflammatories and antibiotics if required. Supportive therapy for liver Cattle Medicine 19 Courtesy of Dr. Karin Mueller Rhododenrdon (Pieris species and Rhododendron species) Aetiology • • Grayanotoxins bind sodium channels in excitable cells, thereby exerting their main effect on cardiac and skeletal musculature and the nervous system. Access to woodland or ornamental shrubs Clinical Signs • Abdominal pain, vomiting (pathognomonic), tremors, staggering, recumbency, paddling, death Diagnosis • Clinical signs and presence of plant in rumen https://www.woodlands.co.uk/blog/tree-identification/oak/ Acorns and oak Aetiology • Ingestion of phenols and tannins following windy conditions in the autumn Clinical Signs • Alimentary signs: colic, anorexia, weight loss, ascites, oedema, constipation replaced by black tarry faeces. Haematuria • On PME – gastrointestinal ulceration and haemorrhage, nephritis, liver degeneration • Bloods – raised urea and creatinine, raised liver enzymes *Pigs are more resistant, can be used to clear acorns Bracken (Pteridium spp) Aetiology • Cyanogenic glycoside, thiaminases Clinical Signs • Vary! Different toxins affect species differently • Enzootic haematuria in cattle • Depression, weakness, anorexia, haemorrhagic syndrome (blood in faeces, urine and haemorrhages on mousuc membranes). Pancytopenia with agranulocytosis leucopenia and thrombopenia • Tumours of the bladder wall • Thiamine deficiency in pigs – heart enlargement • Bright blindness in sheep (retinal degeneration) Diagnosis • History, clinical signs, blood results Bracken (Pteridium spp) • Bracken contains some genotoxic or possibly genotoxic substances, including ptaquiloside, kaempferol and shikimic acid. Ptaquiloside from bracken ingested by food-producing animals (eg, dairy cows) can be passed into milk that might be consumed by people. Available data suggest a withdrawal period of at least four days for ptaquiloside in milk. For meat, the withdrawal is likely to be longer and currently a withdrawal period of 15 days is recommended. Yew (Taxus spp) Aetiology • Yew contains the alkaloid and the heterocide taxicatoside, toxicity is considered maximal in winter. • The lethal oral dose of fresh plant material per • kg of bodyweight is reported to be 1 to 10 grams. • Very acute! Ingestion of yew Clinical Signs • Sudden death • Cardiac depression, dyspnoea, abdominal pain, muscle tremor, weakness Diagnosis • Presence of plant in rumen or mouth! Hemlock water dropwort Aetiology • Oenanthotoxin Clinical Signs • Sudden death • Nervous signs: salivation, dilated pupils, convulsions • Diarrhoea occurs with sublethal exposures Diagnosis • Grows in ditches – history of access to exposed tubers, which often occur after ditching or following flooding • Presence of plant in rumen Summary…. In a lot of suspected poisoning cases for a diagnosis you are looking at • • • • Evidence of potential exposure Believable time frame Risk factors that may have contributed i.e. overgrazing Clinical signs Few specific treatments available General advice: • Remove stock from suspected source • Give access to good quality forage – may dilute • Eliminate poison – rumenotomy or adsorption with activated charcoal • Treat symptomatically Remember…. • Have poisonous plants but also there are some common feed associated plants that can cause poisoning! • Some of these can pose an issue if products from affected animals enters the food chain – Bracken (genotoxic) and Ragwort (potential increased long term cancer risk) Further reading Plant poisoning in farm animals. Payne & Murphy. In Practice 2014; 36(9): 455-465. Bovine Medicine (Andrews). Chapter 54 Diseases of sheep (Aitken). Chapter 56 The veterinary clinics of North America. 2011. Ruminant toxicosis A colour atlas of poisonous plants (Frohne Pfander) Clinical Veterinary Toxicology