Clinical presentations of non-lethal toxicoses in New Zealand ruminants

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1 Clinical presentations of non-lethal toxicoses in New Zealand ruminants Geoff Orbell Registered Specialist in Veterinary Anatomic Pathology, New Zealand Veterinary Pathology, Massey University, Palmerston North Sudden death is the most common syndrome associated with toxicoses in production animals. However, a definitive diagnosis can be difficult without demonstrated access to toxic agents or the offending material identified on gross post mortem examination. Sometimes histological lesions will also be non-existent e.g. Yew toxicity; or they will be non-specific. In some cases of sudden death, sublethally affected animals may demonstrate characteristic clinical signs which may assist the clinician in determining the aetiology. These clinical signs may not be evident for some time after the toxic insult occurred e.g. ataxia and urinary incontinence in cattle with chronic cyanide toxicity. This aim of this article is to review some toxicological agents from a practical perspective based on clinical signs or major findings revealed during a thorough clinical examination of sublethally affected sheep or cattle. The majority of the toxins listed can also present with sudden death. There is some overlap between the clinical presentations described; some due to multiple clinical signs from one aetiology e.g. Acorn toxicity and some which can mimic other clinical presentations e.g. due to hypoxia rather than neurological toxicosis. Investigation of supect toxicoses When investigating suspect toxicoses, a thorough history and clinical examination of live animals with post mortems of any dead animals is mandatory. Case history should be retrospective for up to two months as some toxicities are cumulative or present with clinical signs late in the disease course. These should include discussion of: stock movements drenching vaccination, trace element supplementation prescription animal remedies fertiliser history water sources and access feed type and quality change in diet and forage crops feed supplements resown pasture and cultivars If a definitive diagnosis cannot be made clinically or from post mortem examination, samples for clinical pathology should be taken from live affected animals and any normal cohorts for comparison if required. These samples should include peripheral blood in EDTA, Lithium Heparin and serum blood tubes. Fresh blood smears Proceedings of ther Society of Sheep & Beef Cattle Veterinarians of the NZVA,

2 taken at the time of collection can be invaluable in cases of lead toxicity and haemolytic disease. A full range of post mortem tissues including the brain should be fixed for histology. In addition, fresh brain, liver, kidney, rumen contents, aqueous humor and fat should be taken for future toxicology if required. A farm walk to identify potential sources of toxins should be undertaken at this stage paying close attention plant species other than pasture which may have evidence of grazing/browsing. Plant and water samples can also be collected at this time if deemed necessary for future identification and analysis if required. Plant associated toxins A significant number of toxicological agents listed are of plant origin or are plant associated (e.g. endophyte). Toxic plants frequently increase in toxicity when stressed due to: environmental factors e.g. Drought. dense sowing. physical damage. damage from insect infestation. A significant proportion of unpalatable toxic plants can also become more palatable with herbicide application resulting in toxicity e.g. ragwort. Plant identification Identification of suspect toxic plants can be difficult for veterinarians and in cases where quick identification is paramount, consider consulting botanists or herbariums available through local councils and some universities. Plant specimens can be scanned using a flatbed scanner and ed. When selecting specimens for identification including scanning, specimens with flowers and or fruit/seeds are usually required. New Zealand virtual herbarium This is a database available online that gives geographic locations for specific toxic plants in New Zealand. Visit for more details. It also lists a number of participating herbariums and facilities throughout New Zealand that can be consulted for accurate plant identification. References Black A. Turnips can be toxic. Vetscript 29, 2010 Carbery JT. A case of onion poisoning in a cow. New Zealand Veterinary Journal 47, Ellison RS. Poisoning in ruminants grazing pasture and fodder crops. Surveillance 21, 2, 23-26, 1994 Galey FD. Diagnostic toxicology for the food animal practitioner. Veterinary Clinics of North America; Food Animal Practice 16, , 2000 Hill BD, Wright HF. Acute interstitial pneumonia in cattle associated with consumption of moulddamaged sweet potatoes (Ipomoea batatas). Australian Veterinary Journal 69, 36-7, 1992 Hill F. Laboratory diagnosis of poisonings in production animals. Proceedings of the NZVA association of Sheep and Beef Cattle Veterinarians, 1-17, 2002 McKenzie RA. Plant poisoning NZ: An exploration plants, syndromes, toxicants, pathogenesis, pathology. Proceedings of the New Zealand Society for Veterinary Pathology, 2012 Parton K, Bruere AN, Chambers JP. Veterinary Clinical Toxicology 3 rd Edition, 2006 Parton K, Bruere AN. Plant poisoning of livestock in New Zealand. New Zealand Veterinary Journal 50, S3, 22-27, 2002 Abamectin toxicity in calves. Surveillance 39 (1), 18, 2012 Amaranthus retroflexus (red root) toxicity in cattle. Surveillance 32 (2), 28, 2005 Arsenic poisoning in cattle. Surveillance 39 (1), 27, 2012 Copper toxicity in cattle and sheep. Surveillance 32 (2), 25, 2005 Fluorine toxicity in sheep and DAP. Surveillance 29 (4), 21, 2002 Lead poisoning in calves. Surveillance 30 (1), 22, 2003 Nitrate poisoning in cattle. Surveillance 29 (3), 24, 2002 Selenium toxicity in cattle. Surveillance 32 (4), 16, 2005 Selenium toxicity lambs. Surveillance 38 (4), 20, 2011 Urea poisoning in cattle. Surveillance 38 (4), 16, Proceedings of ther Society of Sheep & Beef Cattle Veterinarians of the NZVA, 2012

3 Presentation Source Toxin Mechanism Other clinical signs Perennial Ryegrass Diagnosis Endophyte Mycotoxins Tremors Paspalum Ergot alkaloids Mycotoxins Tremors Phalaris Indole alkaloids Serotonin receptor stimulation Dips Insecticides Industrial additives Poa aquatica Sorghum Sudan grass/ hay Reed sweet grass Spasms Arrhythmias (Acute) Tachycardia Organophosphates Cholinesterase inhibitors Salivation Urination Miosis Muscle fasciculation Chronic cyanide Cyanogenic glycosides Bright red blood Urinary Incontinence Tutu Tutin GABA Antagonist Tremors/ Convulsions Mydriasis Bloat/ Regurgitation Histology brain Cholinesterase (EDTA, Brain) Organophosphate (Fat) Picric acid test on leaves Skeletal muscle cyanide Histology spinal cord Leaves in rumen Anthelmintics Abamectin GABA Antagonist Recent anthelmintics Monogastric ruminants Levamisole Nicotinic (± muscarinic) stimulation Muscle fasciculation Hypersalivation Urination Recent anthelmintics Can mimic organophosphate toxicity See also: Blindness Pestcides Water Paint Batteries Poorly mixed feed Monofluoroacetate (1080) Sulphur/sulphates Lead Salt toxicity Kreb cycle inhibition Table 2) Respiratory* Table 5) Recumbency* Cerebral oedema (Polioencephalomalacia) Cerebral oedema (Polioencephalomalacia) Cerebral oedema (Polioencephalomalacia) Anthelmintics Closantel Optic nerve/retinal degeneration Parsley Celery - Microbes Parsnip Microbes Figs Citrus Cardiac arrhythmia Opisthotonous Convulsions Opisthotonous Convulsions Opisthotonous Convulsions Furanocoumarins Corneal oedema* Skin irritation and vesicles * Denotes a condition resembling neurological disease with a different pathogenesis. Rumen content analysis Histology Brain Whole blood/ Urine Haematology Histology Kidney, Brain Serum electrolytes Histology brain Recent drenching Histology eye/ optic nerves/ brainstem Photosensitivity without elevated liver enzymes or jaundice CONTINUED... Proceedings of ther Society of Sheep & Beef Cattle Veterinarians of the NZVA,

4 Presentation Source Toxin Mechanism Other clinical signs Depression Hepatotoxins Hyperammonemia Hepatic encephalopathy Head pressing Jaundice Feed additives Fertiliser Urea Hepatic encephalopathy Head pressing Marijuana Tetrahydrocannibinol Unknown Somnolescence Excitement Table 1. Toxicites presenting with neurological signs Diagnosis Serum biochemistry Histology brain Serum biochemistry Rumen ph Histology brain Exposure Presentation Source Toxin Mechanism Other findings Diagnosis Dyspnoea Goats Rue Galegine Pulmonary oedema Hydrothorax Fibrin-rich hydrothorax Tachypnoea Pasture Mouldy kumara Tryptophan 4-Ipomeanol Pulmonary oedema Frothing at mouth and nose Pasture tryptophan Lung Histology Herbicide Paraquat Pulmonary oedema Recumbency Histology lung Calf/Pig/ Poultry feed Oleander Fox glove Helleborus Rhododendron Azalea Annual Ryegrass/Hay Sorghum Green oats Maize Amaranthus Copper Onion Zinc Bracken fern Aflatoxicosis Mouldy Sweet Clover Mouldy Sweet Vernal Ionophores Cardiac dysfunction Arrhythmia Cardiac glycosides CK and AST Cardiac dysfunction Hematochezia History of access Cardiac arrhythmia Histology myocardium Grayanotoxins Aspiration pneumonia Regurgitation Arrhythmias Aspiration pneumonia Nitrate toxicity Methaemoglobinemia Muddy Mucous membranes Brown blood Haemolysis Anaemia Haemoglobinuria Jaundice Haemorrhage Anaemia Haematochezia Petechiae Echymoses Haemorrhage Anaemia Widespread haemorrhage Table 2. Toxicities presenting with respiratory signs Nitrate - Serum Aqueous humour Plant nitrates Kidney/Liver Copper Heinz bodies Liver/serum Zinc Thrombocytopenia Bladder neoplasia Bone marrow histology Dicoumarol in feed or blood Coagulation profile 4 Proceedings of ther Society of Sheep & Beef Cattle Veterinarians of the NZVA, 2012

5 Pathogenesis Source Mechanism Other clinical signs Diagnosis Prehepatic Hepatic Posthepatic Onions Zinc Copper (chronic) Blue green algae Ngaio Cestrum parqui Aflatoxin Xanthium Cycad (Palm) seeds Copper (acute) Crystalloid associated hepatopathy (Inkweed?) Pyrrolizidine Alkaloids Haemolysis Hepatic necrosis Cholestatic Anaemia Haemoglobinuria Hepatic encephalopathy Photosensitivity Ill thrift Table 3. Toxicities presenting with jaundice Heinz body anaemia Serum/Pancreas zinc Serum/Liver copper Serum biochemistry GLDH GGT Serum biochemistry GLDH GGT Pathogenesis Source Toxin Diagnosis Primary Secondary (Hepatogenous) Unknown St Johns Wort Parsley Celery Wild Parsnip Pithomyces chartarum Lantana Panicum/Inkweed? Rape Spring Excema Hypericin Furanocoumarins (Corneal Oedema) Sporodesmin Glucosinolate Lantadene Saponins Unknown Table 4. Toxicities presenting with photosensitivity Rule out hepatogenous photosensitivity GGT Time of year Spore counts Rule out hepatogenous photosensitivity Time of year. ± GLDH/GGT elevations Proceedings of ther Society of Sheep & Beef Cattle Veterinarians of the NZVA,

6 Pathogenesis Source Toxin Mechanism Other clinical signs Metabolic Fat Hen Sorrel Diagnosis Oxalate Hypocalcemia Hypocalcemia Musculoskeletal Ionophores Myopathy Arrhythmia Vascular Ergotism Fescue foot See also: Table 1) Neurological* Table 2) Respiratory* * Denotes other conditions that can present with recumbency. Ergot alkaloids Ischaemia Cool distal limbs Line of demarcation Table 5. Toxicities presenting with recumbency Ergot alkaloids in blood and feed. Ergots in seedheads Presentation Source Toxin Mechanism Other clinical signs Polyuria/Oliguria Acorns Tannins Nephrosis Haematochezia Incontinence Retained placenta Superphosphate DAP Rhubarb Dock Sorrel Amaranthus Fluorosis Phosphate Oxalates Weakness Thirst Weakness Recumbency Diagnosis High Phosphate Azotemia Azotemia Hypocalcemia Cestrum diurnum Vit D analogue Dyspnoea serum calcium ± phosphate Histology lung, kidney, stomach Sorghum Sudan grass including hay Reed sweet grass Macrocarpa Ponderosa pine Cyanide Isocupressic acid Spinal Cord Neuropathy Unknown Bright red blood (Acute) Abortion Metritis Table 6. Toxicities presenting with urogenital clinical signs Picric acid test on leaves Skeletal muscle cyanide Histology spinal cord 6 Proceedings of ther Society of Sheep & Beef Cattle Veterinarians of the NZVA, 2012

7 Presentation Source Toxin Other clinical signs Diagnosis Regurgitation Rhododendron Azalea Grayanotoxin Regurgitation Arrhythmias Aspiration pneumonia Tutu Tutin Tremors Convulsions Drenches/Vaccines Selenium Myopathy/Bloat Blood/Liver selenium Haematochezia/ Melena Hypersalivation Boluses/fungicides Palm kernel extract Slag Nightshades Potatoes Poroporo Buttercup Clematis Helleborus Tanalised timber Pig/Poultry feed Daphne Jatropha (biofuel) Oleander Acorn Bracken fern Mixed rations Sweet clover Insecticides Anthelmintics Copper Glycoalkaloids Colic ± Haemolysis ± Depression ± Cardiac arrhythmia ± Haemolysis Serum/kidney copper Protoanemonin Vesicular stomatitis Arsenic Diterpenoids Cardiac glycoside Tannins Ptaquiloside Aflatoxicosis Dicoumarol Organophosphates Levamisole Haematochezia Haematuria Arrhythmia Nephrosis Haemorrhage Jaundice Haemorrhage Miosis Bloat Kikuyu Suspected Mycotoxin Dehydration Sham drinking Blood Urine Liver Histology kidney Anaemia, Thrombocytopenia Cholinesterase (EDTA, Brain) Organophosphate (Fat) Omasal perforation Rumenitis Tutu Tutin Tremors Leaves in rumen Fat Hen Sorrel Oxalates Weakness Table 7. Toxicities presenting as gastrointestinal disease Hypocalcemia Source Toxin Mechanism Other clinical signs Diagnosis Senecio (Ragwort) Borage Pyrrolizidine alkaloids Cytotoxic Antimitotic Pithomyces chartarum in ryegrass pasture Poorly stored feed Grains Sporidesmin Aflatoxicosis Biliary epithelial necrosis Cholestasis RNA and protein synthesis inhibition Photosensitivity Jaundice Haemorrhage Anaemia Autumn Feed analysis Table 8. Toxicities presenting as ill thrift Proceedings of ther Society of Sheep & Beef Cattle Veterinarians of the NZVA,

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