Hi good morning everyone. So today we're gonna talk about, farm animal toxicology. It's quite a broad, subject, so we're gonna sort of, talk through some of the more general aspects and hopefully alongside the, sort of the, the, the handout that I've supplied, it'll just help you to think about what toxins might be involved in some of these cases that you might see in practise.
So we're gonna go through a, a bit of an introduction, and then what might we do to, approach the investigation? And again, the handout has kind of a flow chart about what you might do for that. Then we're gonna talk about clinical signs and common causes.
So going through the different systems and the clinical signs related to those body systems, and then what some of the causes of those signs might be. And these will be split into plant. Poisons, chemical poisons, metal poisons, microtoxins and other poisons or toxins, and each of those is gonna be highlighted in these colours on the slides so that hopefully when you refer back to it, you'll be able to link, link them together.
We're then gonna talk about some of the common toxins, so the toxins that are in that are within these plants or or or other substances. And then the common poisons. So where these substances would be found.
And both of those sections are gonna include some things about treatment. And then we're gonna finish with a very brief sort of slide about how we can prevent these cases from arising. So there are a number of commonly found substances that can be toxic to farm animals and.
These can occur whether if the animal ingests them, er, they could be inhaled, or they could just have a contact exposure. Depending on how that substance affects the body, er, and the areas that it's going to affect, that will alter the clinical signs and the presenting signs that you will see. We often base our diagnosis on the history and the clinical signs, and then we can do further diagnostics to investigate further.
Treatment is generally supportive care of the animal. There are some specific treatments for some specific toxins, but generally it's supportive care, removing, the substance as much as we can. And then the prognosis is gonna be variable, and this is heavily dependent on what the cause is, er and the severity, and that can be related to the chronicity of the, the, the problem as well.
So why do these poisons or or or or toxins, toxic problems occur? Generally it's because there is a lack of access to appropriate feed and water. Animals won't eat toxic substances, sort of deliberately, but if they don't have, adequate food or water available, they may do.
Sometimes that feed or water can be contaminated and that won't be anything to do with the farmer necessarily, er, particularly if er it's related to poisonings, er when they're out at pasture. Obviously if there's access to poisonous plants, then that will increase the risk of of these problems occurring. But it could also be management issues, so has the farmer stored the feeding correctly, have they mixed the feeding correctly, leading to higher concentrations or moulds are developing.
Might be a buildup of hazardous substances that either the farmer has not disposed of correctly or the general public. We all know that fly tipping is becoming a bigger issue, but there also might be industrial waste that causes a, causes a problem. And then there will be some animals that don't discriminate what they're eating, you know, goats as browsers tend to eat most things that are available to them, .
But there might also be maybe calves that are less discriminate in what they eat. So what's our approach to the investigation gonna be? Generally, as we said, we're gonna diagnose based on the history and then maybe the clinical signs.
So the farmer might tell you, or the owner might tell you that they have seen unexplained illness or deaths, that some of the animals are showing a lost condition, or they've had sudden deaths, or they're seeing clinical signs that they're not used to, used to. At a herd of flock level, you might see just single abortions or multiple abortions. The farmer might report that he's recently changed the, the feed or, or the pasture that the animals are on.
But also the farmer may be aware that certain toxins or certain poisons are a risk on his farm or on certain pastures, but due to availability of pasture, he, he maybe has to use er the same fields. A good example of that would be er any grazing that's on old sort of quarries or mines that can often lead to leaching of of of poisonous substances. So, as I said earlier, they're quite variable clinical signs and will be dependent on the agent that's that's involved.
But they can affect a range of body systems, and we're gonna go through each of these er individually, but as you can see, it's really the full range of body systems that might be affected. So, cardiovascular system, . We can get cardiac glycozides, so these are plant toxins, can be found in oleander or foxglove.
And if there's a moderate intoxication, you'll see bradycardia or depression as a clinical signs. Whereas with severe intoxication, that bradycardia develops into a tachycardia, then into a dysrhythmia, and you will often see death within 24 hours. Another plant toxin is taxine, which is found in you.
Which has a really strongly depressive effect on the heart and will cause sudden death. Selenium toxicity. So we sometimes, in farm animal talk about, selenium deficiencies, causing sort of white muscle disease, but likewise, if there's a toxicity, then that can lead to tachycardia, congestive mucous membranes, and again, we will, we'll see death within 24 hours.
Our first mycotoxin, er ergots, so from Clavicep species. This causes vasoconstriction due to a direct action on the muscles of the vessels. And repeat doses will injure the vascular endothelium, so causing leakage.
So we initially get reduced blood flow, but then that leads to complete stasis and this sort of dry gangrene, so terminal necrosis of extremities. Moving on to some toxins that can affect the GI system, grayanotoxin or dromedotoxin, which we find in rhododendron, so in plants, and we'll see excessive salivation, or we might see green froth at the mouth and the nose, and the animal may attempt to vomit, remembering that ruminants shouldn't vomit. And they can often be in severe abdominal pain, so you might see signs of colic.
Then tannins from oak trees, especially from unripe acorns, this can lead to anorexia or constipation, but it can also lead to persistent diarrhoea and dysentery. Arsenic, so acute will see severe watery diarrhoea, severe abdominal pain, and then sudden death. Subacute we'll see a watery diarrhoea, possibly some sort of evidence of blood, so Melina.
Molybdenum poisoning, that can be a severe persistent diarrhoea with the presence of a green liquid faeces and it's often very bubbly. And thenganophosphates can lead to increased peristalsis and salivation. We can also have bacterial toxins, so botulinum toxin er will lead to flaccid paralysis of the tongue, so there's difficulty in prevention of food and swallowing, and there's often drooling in chronic cases.
Then we can also get brain overload, which leads to a lactic acidosis, so we'll get an enlarged, distended rumen and abdominal pain. We may get reduced room and contractions. Cattle don't want to eat but are quite bright and alert, and diarrhoea is quite common.
Then sapponyms, which are amphipathic glycosides, so these are found in common ivy. And can cause emesiss and diarrhoea. And some of you may have seen some small ruminant owners will talk about using ivy as a natural wormer, and I think that's because it causes these sort of spasms in the gut to, to, to push the worms out.
But it isn't something that I would necessarily er advise myself. The hemapoietic system, so we have an aplastic anaemia factor in. And what we would see if we take bloods would be a thrombocytopenia, leukopenia, and anaemia.
We on postmortem might see internal haemorrhage or pale bone marrow. But clinically, what we're probably gonna see is just hematuria. Brassica species can have Smethyl cystine sfoxide contained within them, which causes a hemolytic anaemia.
And organic sulphur compounds in alium species, so onion species, will also show signs of hemolytic anaemia. Dicuarin, which is contained in sweet clover, this can cause clotting problems, so we'll see, multiple haemorrhages and pale mucous membranes. And fairly similarly, warfarin and similar congenas of warfarin, which are found in anticoagulant rodenticides, they'll lead to clotting problems, haemorrhages and pale mucous membranes as well.
So the hepatic system, so pyrolazidine, alkaloids, which we find in ragwort, so the clinical signs would be with see with because of the effects on the liver, would be chronic wasting, ill thrift, and jaundice. Blue-green algae, hepatotoxic peptides, again, will lead to the same chronic wasting, ill thrift, and jaundice due to their effects on the liver. Copper poisoning, the clinical signs would be jaundice, we also might see haemoglobin, urea, anaemia, methemoglobin production, and progressing to recumbency and death.
Mycotoxins, aflatoxin and aspergillus er can lead to hepatocellular necrosis. So again, ill thrift and reduced growth rates would be the clinical sign. What's gonna affect the skin, so pyrolazadine, alkaloids in ragwort, or hypericin in Saint John's Wort or chlorophyll in lush pasture will all cause photosensitization, which can lead to .
Problems in the skin, redness, sloughing of the skin. We've mentioned ergots and lavats that will lead to sort of dry gangrene, so you'll see sloughing of the skin of the extremities. Trichothecines infusarium species can lead to dermal irritation and blistering.
And then molybdenum, due to an increased molybdenum, will lead to copper deficiency. So we'll see that discoloration of hair around the eyes, that sort of classical, spectacles of, related to copper deficiency. Neurological toxins, so anotoxin in blue-green algae, will cause muscle fasciculations and then decrease movement, then convulsions and then death.
Greyanotoxins in rhododendron, a staggering gait, sternal recumbency and then convulsions, alkaloids, which we find in a lot of plants, so lupins, ragwort, hemlock, ewe, will lead to dilation or constriction of the pupils, in coordination, and then convulsions, coma and then death. Ammonia and urea poisoning, so again this could be related to incorrect feeding or incorrect storage of feed. We might see muscle and skin tremors, ataxia, weakness, dullness, the animals might be restless or excitable, or show signs of hy prosthesia.
They may hypersalivate, have abdominal pain, excessive vocalisation, bloat ruminatory, and then that will progress to recumbency, convulsions, and death. Arsenic, we talked about sort of the gastro signs, but they would also lead to convulsions. And lead can lead to hyperesthesia, so overreacting to stimulus, depression and death as well.
Organophosphates, hyperesthesia, with a delayed ataxia and potentially an ascending paralysis. Salt toxicity, er, has these GI signs, but it will also lead to generalised weakness. Fumonicins, another mycotoxin, will lead to weakness and recumbency which progresses to death.
And then botulinum, which we talked about leads this flaccid paralysis, and can then also lead to death. What can affect the renal system, so tannins in in oak will lead to nephrosis, so we may on a blood see elevated urea and creatinine. Tequilaide in Brackener leads to haemorrhages, so an enzootic hematuria, .
Cos it will lead to papillomas forming in the bladder which will bleed. Copper poisoning can lead to nephrosis and we'll also see haemoglobin urea. And then oxalate, which we find in sugar beet, rhubarb and sorrel, can lead to nephrosis, but also can lead to urolethiasis due to the buildup of oxalate crystals.
What can affect the reproductive system? Xeralanone causes signs of hyper estrogenism, so . We may see development of precocious udders, we may see signs of estrus, and it can cause infertility in young male animals due to atrophy of the testicles.
Fumonacin can cause abortion, nitrate poisoning can cause abortion, warfarin and it's congenas can cause abortion, as can lead poisoning. Now, I think a lot of poisonings and toxins could relate in abortion . End up with abortion, but more due to the stress that the body's put under.
The respiratory system, what toxins are gonna affect this, soumonicin will lead to pulmonary edoema and is recorded in pigs quite not commonly, but more seen in pigs with acute dysmia and sciotic mucous membranes. Ipermenols in sweet potatoes can cause severe respiratory distress, so dyspnea, abdominal breathing, extended lowered head, flared nostrils, and also emphysema. Cyanogenic glycosides, as the name suggests, we can find these in laurel and pruna species will lead to dyspnea, and then sort of discoloured membranes.
And then selenium can also lead to pulmonary edoema. So that's a bit of a whistle stop tour about the systems that are involved. And sort of highlights the range of some of those toxins on working on multiple systems, but also sort of the key clinical signs related to those systems.
What we're gonna do now is talk about in more detail some of those common toxins. So all of the ones that have been mentioned, we can go into a bit more detail about. So alkaloids, so these are plant poisons.
I will just say now as well, er, all of the pictures er of the plants are are taken from er just the internet searches, . Rather than me trying to find good examples of pictures of, of these. So generally the plant tastes bitter.
The alkaloid content can be modified by various things including climate, soil, and the environment. Most alkaloid poisonings are fatal. So what plants contain these, we can have you, laburnum.
Ragwort, hemlock, Lupins. So in an acute poisoning, the poi the the toxin has a similar structure to acetylcholine, dopamine and serotonin, so it mimics or blocks neurotransmitters. So we see excessive salivation, dilation or constriction of the pupils, vomiting, abdominal pain, in coordination, leading to convulsions and coma.
Another plant poison, glycosides, so these are widely distributed in the plants, but most are non-toxic. And we get four different types, cyogenic, goitergenic, cardiac, and saponins. Cyogenic glycosides contain enzymes which convert glycosides to hydrocyanic acid.
But actually in the plant, these enzymes are kept separate to the glycoside, so it doesn't cause a problem. However, when, those plants are processed or eaten, the enzymes can, react. Hydrocyanic acid, er it inactivates the cytochrome oxidase system which starves cells of oxygen, so it'll affect the brain and myocardium first.
Oxygen transfer in tissues is blocked, so we see very bright red venous blood. And our clinical signs will be dyspnea, convulsions, muscle tremors, and death. And plants that are cytogenic, er would be things like linseed and cherry laurel.
In, pregnant ewes, prolonged exposure can also have a goitergenic effect on lambs. How do we diagnose this? Gonna be based on the feeding history and those clinical signs.
But on postmortem, pretty non-specific, bright red mucosa, but you will get that, smell of bitter almonds, sort of cyanide smell in the rumen. We can also do HCN content of liver or muscle. Treatment of these cases is rarely practical, but large doses of vitamin B12 may allow cobalt to bind to bind to the cyanide.
Goitergenic glycozides or glucosinolates, er, these are found in brassica crops, so, you know, pictures here that will include rape seed, but also turnip, broccoli, things like that. The highest concentration of this toxin is in the seeds of the mature plant. We have two toxins, glucosinolate and thiocyanate.
Glucosinolate interferes with thyroid hormone synthesis, whereas thiocyanate impairs the uptake of iodine. So the clinical signs that we're gonna see will be goitre, we'll see reduced growth rates, we'll see diarrhoea and sudden onset blindness. If it's a glucosinolate induced goitre, that can't be treated, whereas if it's thiocyanate, it can be managed with iodine supplementation.
So again, how would you know which it is, you would probably treat them with iodine and see if they respond. Cardiac glycosides, so we can find these in foxgloves, lily of the valley and oleander. They don't lose their toxicity when they're dried or boiled, so they're still toxic.
And the toxins within them are digitoxin and digitalin, where some of our cardiac drugs are derived from. And they have a specific action on the myocardium, which increases contractility and, and reduces the heart rate. So clinically, we'll see with a moderate intoxication, this bradycardia, depression, regurgitation, diarrhoea, progressing if it's severe to tachycardia and dysrhythmia, and deaths if they're going to occur, normally occur within 12 to 24 hours.
Treatment is gonna be supportive fluid therapy, atrine and propranolol, as far as I'm aware, are not licenced in food er producing animals. So what else can we do? We could give oral administration of activated charcoal to bind those toxins, or we could do a ruinostomy, and sort of dump the contents of the rumen.
And, you know, if we suspect a toxin, those two. Treatment methods are not a bad starting point, you know, oral supportive fluid therapy, or administration of charcoal to try and bind the toxins, or a ruinotomy to remove, the toxins that are present. Saponins, so our antipathic glycosides.
These have the physical properties of soap, have a very bitter taste, and are absorbed very slowly. And large quantities can cause this irritation of the gut lining, so they're emetic and purgative. And as I said, there will be, you might come across some small ruminant owners who will swear by, Ivy as a, as a natural wormer.
But this will be because of the, the, the gastroenteritis, being caused. Nitrates and nitrites, so common substances, er, plants absorb nitrates from the soil, and generally they rapidly convert them to other nitrogenous compounds, but they can accumulate during dry periods. Overcast conditions will favour the plant to store, nitrates, and some plants can get very high concentrations, so clovers in Nebraska species.
Obviously if we're gonna use nitrogenous fertilisers, that will increase the plant concentrations and generally the roots and the stems contain more nitrate than the leaves. Ingestion of large amounts of nitrates itself can cause gastroenteritis. However, nitrates are much more important as a source of nitrites.
Nitrates are formed in the rumen, and nitrates combined with haemoglobin to form methemoglobin, which cannot transport oxygen. And if that happens, we're gonna see dyspnea, tachytardia, muscle tremors, weakness, and probably the most obvious one, these brown coloured mucous membranes. And we'll often see death within a few hours.
Treatment, we would remove from the source of nitrates. We would provide carbohydrate-rich feed. Carbohydrates will encourage the rumen to change, nitrates into harmless ammonium products rather than nitrites.
So we do need to be really careful, particularly during those risk periods. So, following, a dry period where the plants will take up more, nitrates or if we've used fertilisers. Treatment would be intravenous infusion of methylene blue, so 4.4 migs per gig, and you may need to repeat that every 6 to 8 hours and that will reconvert methemoglobin to haemoglobin.
Now, as far as I know, methylene blue does not have a residue, a limit set, so this will have implications on er the animal entering the food chain. Plant oxalates, so most plants will contain oxalates in different quantities and some plants will have large amounts. So ones with large amounts would include things like sugar beet, rhubarb and sorrel.
Sheep tend to be more susceptible than horses, which are more susceptible than cattle. Ruminant ruminants can generally adapt their rumen flora, and that will allow oxalates to be broken down into carbonates and formates. However, we can get absorption of free oxalates, and these will precipitate, as crystals in the submucosal arteries.
That will then cause a nephrosis in the kidneys. We can also see these collections, sort of in the bladder, forming, euroliths, which could lead to, a blocked bladder. Damage in the lung capillaries can lead to pulmonary edoema and generally you'll see hypercalcemia, so you might see signs of milk fever as well, because of the, the, the binding of the calcium and the oxalate.
So we can get a short term response by treating with calcium. But most animals will relapse and die, and that death is normally due to an acute renal failure. Urea and ammonia, as you're all aware, non protein nitrogen, is commonly used as a protein substitute in cattle feed.
And these supplements are either mixed directly into the feed or you can get them as liquid molasses or mineral blocks. You can find your rear in some fertilisers. And urea is a, a, is a common source of non-protein nitrogen, and this is to allow room bacteria to make proteins from it.
Your ear is quickly broken down to ammonia, and it's combined with products of carbohydrate metabolism to make the amino acids that the body needs. So we need to have a sufficient amount of carbohydrate for this system to work. The main issue is that we need the room and flora to adapt to use utilising higher quantities of ammonia.
So you can't just all of a sudden introduce it to the feed. So we need to slowly add that non-protein nitrogen or urea to the diet. If there's any break in that feed, to say you can't get your supplement for 1 to 3 days, then that acclimatisation of the room and flora is gonna be lost, and we need to restart again with a slow introduction.
Why do we get your ear toxicity, so. Again, like I said, if we haven't allowed the rumen to acclimatise, or if we're infrequently feeding, so they're acclimatising, then they're losing it, then they're re-acclimatizing. If we don't mix these supplements properly with the feed, there may be an increase, a slug of, product that, that some animals get.
Or if we've miscalculated and we're feeding too much. If they've got free access to these supplements, again, animals may, take in more than they should. If we use a palatable molass liquid supplement, again, animals may er take in more than than they require.
If there's access to fertilisers or fertiliser on the on the pasture that animals are grazing, or if the animals have access to a contaminated water source. So one of the ones that we would worry about would be if fertiliser is stored inappropriately and it rains, and then you get puddles that are rich in urea. Or if there's mineral licks with urea in that have been reined in or got standing water in, then the urea will sort of float to the surface and animals will will ingest it.
If there's rapid hydrolysis of urea, that will lead to the production of large amounts of ammonia, which the microbes cannot metabolise er which leads to excess ammonia absorption, and then we see the toxic effects. Excess ammonia will create an alkaline environment in the rumen, so the pH becomes greater than 7.5, leads to more further urea hydrolysis, so greater ammonia production and then increased absorption of ammonia again, so it's a, it's a never ending cycle.
The liver can normally will detoxify any ammonia, but that pathway becomes exhausted, so we see raised blood ammonia levels. And then that systemic ammonia is gonna inhibit the citric acid cycle, so we're gonna get decreased ATP leading to lactic acidosis, which will eventually lead to hyperkalemia, which will lead to heart failure. What are we gonna see with these poisonings?
So muscle and skin tremors, some ataxia, weakness, dullness. They may be restless, they may be excitable, we'll see hypersalivation, abdominal pain and vocalisation, might see bloat, ruminatiny, dysnea, tachypnea, dehydration, increased urination, defecation, recumbency, convulsions, death. So the, the whole range of sort of clinical signs, with this toxin.
But we may also see frothing at the mouth, regurgitation, marked jugular pulses, pyrexia, stiff front legs, staggering, hypersthesia, arrhythmias, nystagmus, cyanosis. So we really, these are very general clinical sciences we, we definitely need to put this in with the history of access to these substances. We can treat this, and the aim of treatment is to slow that hydrolysis of urea.
So we can use cold water. Cold water will lower the room and temperature, so decrease the urease activity, and dilute the ruin content, so we'll decrease the ammonia production and absorption. And then we can use vinegar, which will slow the rate of hydrolysis, but it also, again, will lower the ruin pH and, and prevent further ammonia absorption.
By converting ammonia, increasing the conversion of ammonia into ammonium. We do need to treat these rapidly, and so as soon as possible as we see the effects and we suspect that it is urea or ammonium. Ammonia, toxicity.
So we're gonna pass a stomach tube, which will relieve any bloat. And then we're gonna give 30 to 40 litres of cold water, so at 0 to 4 degrees, in adult cattle, obviously, different, less for, for small ruminants. And then acetic acid, we can use a 5%, acetic acid vinegar solution and give 2 to 6 litres.
If the signs recur, we can repeat that by using half those volumes again. Alternatively, we could do a rheinotomy or ruminal fistulation, and evacuate the contents and release the ammonia gas, . Then our further treatment is gonna be symptom symptomatic and supportive, making sure there's adequate hydration, so IV fluids.
We could use a rumen probiotic or transformation to help recover cattle, particularly if we've emptied out the rumen. And then furosemide has been used in some cases to reduce the pulmonary edoema that you might see. We can prevent it by ensuring there's adequate nutrition and that it's er introduced appropriately.
But also if we are concerned about a buildup of excess urea anywhere on the farm, make sure animals do not have access to it. Photosensitizing agents, so we talked a bit about these and the effect that they have on the skin. Well, photosensitization occurs when we get an accumulation of these metabolites under the skin.
They then react with the sunlight and lead to necrotic damage. Sizes are usually restricted to wool-free or unpigmented areas. So we get the face, the ears, and the limbs being most commonly affected.
And we'll see skin necrosis, sloughing, regeneration will occur, but it can take several months. And these animals is quite a painful condition, so they're often inappotent, so rapidly lose condition. We get different types of sensitization, so primary photosensitization could be due to chlorophyll, so excess chlorophyll on lush pasture, or hypericin if if animals ingest Saint John's Wort or phagoyucin if they ingest buckwheat.
But we can also get a hepatogenous photosensitization, so this is due to the ingestion of things like ragwort or bog asphodel which contained phylo erythrin. And that leads to obstruction of the bili excretion of the toxins, which can then build up and lead to photosensitization as the metabolites accumulate under the skin. These are some of the signs that we might see.
So, hair loss or fleece loss, reddening. Sometimes you'll see these demarcated lines, on the fleece, or you can get the loss of the pinna, loss of eyelids, . What are we gonna do?
I mean, immediately get them out of the sunshine, until the lesions heal. You know, this could be 3 weeks, but it actually could be longer. I've, I've had animals, in shaded areas for, for 2 months for them to recover.
We can give them supportive care, so as we said, this is, this is a painful condition related to inflammation, so steroids may help, or NSAIDs might make them feel more comfortable as well. We can get aminotoxins in mushrooms, so these can cause severe abdominal pain, diarrhoea and coma. And as we mentioned, hepatotoxic peptides, which are found in blue-green algae.
So we get these blooms on still water. They are quite stable toxins, so they're not inactivated by any water treatments. Smethylcysteine sulfoxide in brassica crops, .
The reason it causes the problem is that this is converted to dimethyl disulfide in the rumen, and the clinical signs you'll see will be poor growth rates and a hemolytic anaemia. Thiaminese in horsetail and Bracken, we'll see poliocephalomalacia, in, in pigs and other monogastrics. Tannins from oak trees, er, as we mentioned, unripe acorns, particularly toxic.
Animals can develop sort of cravings for these, because of the bitter taste. They bind to protein, . And they're broken down to toxic metabolites in the GI system, which leads to necrosis of renal tubules, so we'll see renal effects.
But we'll also see dullness, anorexia, constipation. Cessation of urination, we might see dark urine, serious discharges, persistent diarrhoea and dysentery. And then postmortem we get sort of a uremic smelling carcass.
We will find acorns, oak leaves in the room and in the intestines. We might see a hemorrhagic abomaitis, and a subcutaneous haemorrhage and edoema. How do we treat this?
If we suspect tannins, then we can administer liquid paraffin with milk, er or mucilage, which is a plant product. And then we can also give appetite stimulants. Saline purgatives, are contraindicated because of the, the kidney damage that tannins can cause.
Moving on to some mycotoxins, so, these are probably becoming something that we think about a bit more in in problems, and there are now labs doing microtoxin tests on feed. So aflatoxin is produced by toxic strains of aspergillus, and it's commonly found on peanuts or soybeans and cereals, either in the field or in storage. And it grows well when there's a high moisture content and a high temperature.
Toxic responses will vary depending on species, sex, age, and the amount that they've they've taken in. And adult ruminants are relatively resistant to acute toxicosis. So they can tolerate up to 300 parts per billion, whereas calves will tolerate up to 100 parts per billion.
But we generally see clinical disease at twice these levels. Aflatoxins have also been detected in, in milk, so it may have implications for, for, human health. Aflatoxin is metabolised in the liver, to produce epoxide, which binds macromolecules.
And it can cause, it can have mutagenic effects, carcinogenic effects, teratogenic effects. It will lead to reduced protein synthesis, immunosuppression, liver necrosis, and reduced growth rates. So, again, quite a range of problems.
Clinically, we might see inapetence or vomiting, but we might also see respiratory disease, depression, decreased rheum contractions, haemorrhage, icterus, generalised weakness, reduced growth rates, and then potentially death. If we take bloods, we might see raised liver enzymes. We could see a hypo thrombinemia, hyperbilirubinemia, hypocholesterolemia, or a hypoalpinemia.
And on PM we're gonna see widespread haemorrhage, sinus virus, an enlarged liver, perhaps hepatic necrosis and hepatic megalocytosis. Xeralanone. So this is a microtoxin produced by Fusarium species, and it generally contaminates growing plants and stored feed.
Most commonly maize, wheat, barley, and soy. And it does prefer moderate climates, humid conditions. How's, what's the toxic effects, it's a potent non-steroidal oestrogen, so it primarily has estrogenic effects.
So it will bind to estradiol receptors, and it will bind to estradiolcytes on, estradiocytes on DNA, and then RNA synthesis leads to signs of estrogenism. So we're gonna see repeated signs of stress, we might see vulvovaginitis, hypertrophy of mammary glands, and also reproductive dysfunction. So reduced ovulation rates, prevention of implantation, early embryonic death.
And in males, it can have this effect of causing atrophy of the testicles. Postmortem signs, you might see ovarian atrophy, follicularotresia, uterine edoema or cystic endometria. Dumonicin, another microtoxin produced by Cusarium, found in cereal crops, commonly associated with warm conditions and crops that have suffered insect damage.
And this is a main, a cause of pulmonary edoema in swine, but it's also been shown to be toxic to the liver of ruminants. It's structurally similar to the sphingocene, which is found in myelin, and the toxin blocks the synthesis of sphingolipid. Poor sign pulmonary edoema due to fumonicin is usually acute and fatal.
The toxin will lead to immunosuppression. Pulmonary hypertension, leading to transulating the thorax, which leads to interstitial pneumonia and hydrathorax. So the morbidity might be greater than 50%, but the mortality would generally be 50 to 100%.
Clinical signs related to respiratory system would be acute dyspnea, cyanotic mucous membranes, weakness, recumbency, abortion, and death. Ruminants are generally less susceptible, so they'll tolerate 100 parts per million, but 150 to 200 parts per million may see an appetence, weight loss, and mild liver damage. Ergots, which we again, we've, we've talked about briefly, it's a toxin produced from Claviceps, and it's found on rye and other forage plants, fescues, rye grasses.
So it sporadically will affect farm animals. Poisoning comes from the infected seed heads or infected grain in the ration. And we see these signs, when animals ingest 200, 600 parts per billion.
It causes vasoconstriction, so it has a direct action on the muscles of the arterios, and repeat doses will injure the vascular endothelium. So we get this initial reduced blood flow and then complete stasis and terminal necrosis, so a dry gangrene. Can cause stimulation of the central nervous system, which is often followed by depression, and it will also inhibit the pituitary release of prolactin.
Clinical signs, so lameness, so due to the pain related to the sloughing of the extremities, hypothermia, hyper salivation, galactia and abortion. Er, pigs can show reduced feed intake and reduced growth rates as well. So we've talked about the actual toxins involved in some of these processes, so where are we gonna find these toxins?
Where, where are these toxins gonna be? What are the common poisons or poisonous plants or poisonous substances? So we have talked about a lot of these, bracken is a key one, where the whole plant is toxic and younger plants are more toxic, but also more appealing to animals to eat.
But animals won't preferentially eat bracken, er, unless that's all that is available. Generally, the toxin does require large amounts to be consumed over a long time. And there are multiple toxins in bracken, thhiaminase, piqueicide, aplastic anaemia factor and prunocin.
So the clinical signs are quite variable. We'll see a pyrexia, a dullness, diarrhoea. We might see bleeding from the, the nose, vagina, conjunctiva.
The heart rate and respiratory rate could be increased. We'll see blood in the urine related to the acralla side. So that's enzootic hematuria, and death on PM, lots of internal haemorrhage, necrosis and sloughing in the elementary tract, and we'll see pale bone marrow due to the aplastic anaemia factor.
On haematology, we'll see a thrombocytopenia, leukopenia, and anaemia. Treatment is generally just treating secondary infections. There's no direct treatment.
And sheep poisoning is uncommon, but if we do see it, it'll thrift and anaemia, they'll also show signs of progressive retinal degeneration. So they'll separate themselves from the flock. They'll have a high stepping gait, and their eyes will shine brightly in semi-darkness.
It's also associated with tumours in the jaw, again, related to that, to qualaide toxin. So the main thing that we think about with bracken poisoning is enzootic hematuria, . And the ingestion of bracken and, the taquelay toxin will lead to the development of hemangiomas in the bladder wall.
And this is, due to exposure for a long time and can be associated with papillomas as well. This bleeding can lead to anaemia, intermittent hematuria. They're obviously more susceptible to secondary infections, so we'll get cystitis and pyelonephritis.
Rhododendron is a common ornamental shrub found worldwide. Poison's common following heavy snowfall, because again, if there's heavy snowfall, animals are restricted in what they have available to eat, so may choose to eat the leaves of this. The key toxin is a dromedotoxin, will cause hypertension, respiratory depression, CNS excitation, and then depression.
So we'll see er attempts to vomit, excess salivation, signs of colic, and those will develop into more severe neurological signs, and death. Ragwort, again, we've talked about in various instances so far today, but as you all know, it's commonly found on pasture. More commonly thought as a problem for horses, but it can also cause problems in farm species.
It generally is unpalatable. And the flowering plants are the most toxic of our, farm species, cattle are the most susceptible, and again, it is a cumulative effect. The toxin involved is pyrolizidine, which is metabolised into reactive pyros and will affect the liver.
So we're gonna see signs of liver damage. So chronic wasting, ill thrift, jaundice. As we said, we can get hepatogenous photosensitization.
Sometimes we'll see short periods of mania, and death. On PM we'll see diffuse subendocardial haemorrhage, inflammation of the gastrointestinal tract, scarring of the liver, but we might also see spongy degeneration of the brain and spinal cord. Yew trees, so we talked about taxing in ewes, common in churchyards, and gardens, and all plants, parts of the plant are poisonous.
Why do we see exposure, fallen branches, so it's easier for animals to, to eat, but also if people dispose of the cuttings of the tree, indiscriminately, maybe, you know, fly tipping them over into a into a farm field. The taxiner has a strong depressive effect on the heart, so we see sudden death. If we see a more acute, we'll see dyspnea, muscle tremors, weakness and collapse, and then death.
There's no specific signs on PM but we'll look for huge twigs and leaves in the rumen. And if you do suspect a poison, there's probably a good diagnostic tool will be to euthanize an affected animal, er, and send it for postmortem so that plants can be looked for within the within the rumen. Or even on farm if you don't have the option to send it to a a postmortem centre.
Laburnum, again commonly found ornamentally, all parts toxic, all parts are toxic. The specific toxin is cyst cytosine, which stimulates respiratory and excitation of skeletal muscle, but it also leads to paralysis of peripheral sympathetic nerve ganglion. We're gonna see abdominal pain, muscle spasms, salivation, diarrhoea, and again, PM findings, non-specific, and we'll be looking for the leaves, in the rumen.
Rapeseeds, so commonly seen across the UK as a member of the Brassica family and it's most toxic when it's in flower, so it's very yellow flower. And we can see er various syndromes affecting various systems. Multiple toxins involved.
So it contains a goitergenic glucoside. So we'll see goitre reduced growth rate. It can contain high levels of nitrates, which can be converted to nitrates, where we see that dysnea, tachardia, muscle tremors and weakness and brown mucous membranes.
It also contains Smethyl cysy foxide, which can lead to poor growth rates and hemolytic anaemia. So PM signs are gonna be quite varied depending on which toxin has caused a problem, but anaemia, an icic cut carcass, we might see liver necrosis, renal congestion, looking for the plants in the rumen, and we may see a goitre. Unbelifery, so, the carrot family.
So it does include carrots, parsnips, parsley, hemlock. So most of these are commonly grown as food, but we do get some very poisonous species within this within this plant species. So poison hemlock is very poisonous.
And in the wild, so be aware if you are, a wild forager, the leaves can look very similar to parsley. The roots can look very similar to parsnip, and the seeds can look very similar to an ice. So just be aware of that, if people are, are, are foraging or feeding their animals from things that they're finding out and about.
It's an alkaloid toxin, so as we've mentioned, it mimics or blocks neurotransmitters, so we see a range of clinical signs. It also contains furocuerins, which is a contact photosensitized agent. So if animals rub up against these wet foliage, or if they ingest it, it will alter the skin so it can be damaged more readily, by sunlight.
Moving on to some, two metal poisons, so we're gonna talk about copper poisoning and lead poisoning, . Copper poisoning commonly occurs due to the use of fungicides or algaecides, anthomintics, excessive dietary supplementation, poultry litter scattered on pasture, or molybdenum deficiency. What do we see?
Well, with chronic copper poisoning, we're gonna get weakness, pale mucous membranes, anorexia, haemoglobin urea, icterus. But in the acute situation we're gonna get all of those, but we're gonna get signs of GI pain, diarrhoea, and also animals going into shock. It's very common in sheep, but there is a variation in breed susceptibility.
So blueface Lesters, North Ronaldsy, Texels and Suffolk have a high susceptibility to copper point is the thing, whereas Cheviots and Scottish blackface are, are, are more, are less susceptible. We occasionally see it in cattle, and we do see both chronic and acute poisonings. So chronic copper toxicity, when we have sub-clinical liver damage, about 8000 micromoles per kilogramme, dry matter, .
Then the capacity for copper storage is exceeded. At over 15,000. Which can be influenced by stress.
This leads to lysosomal rupture, release of copper into the circulation. So serum concentration might be 38 to 200. We get intravascular hemolysis, due to the reactions between the copper and red blood cells.
We'll see jaundice, renal and generalised tissue failure. Excuse me. In the acute form, we generally see this when animals ingest 20 to 100 milligrammes per kilogramme, or 200 to 800 in adult cattle.
And this will cause severe gastroenteritis, ulceration and erosions in the Abermason and will develop into a hemolytic crisis. In sheep, the signs that we see would be sudden onset, progressive ataxia. They'll wander aimlessly, they'll head press.
They'll be, it'll show signs of jaundice, haemoglobin urea. They'll have rapid shallow breathing. They'll be anaemic, and they'll start to produce methemoglobin, and that will progress to recumbency and death.
So here we see, you know, very obvious signs of jaundice, in the sclera, in the mucous membranes, in the, in the, in the gums. So we're gonna diagnose it based on feed and farm management, potentially if it's a more susceptible breed, then we're gonna link it into those clinical signs. If we take bloods, we can find raised copper.
We could see non-specific inflammation, and we would see raised AST, but again, this is non-specific. On postmortem, we might find enlarged gum metal kidneys, discoloured red urine, jaundiced carcass, and signs of a pattern necrosis. And on histopath, we're gonna find yoplasmic cytoplasmic faculation of hepatocytes and renal tubular necrosis.
We can also submit kidney and liver samples for copper concentrations. So here we have our dark kidneys, sort of swollen jaundiced liver, jaundice carcass, and this dark red brown urine. It is generally a low morbidity, but a high mortality.
So how are we gonna treat them? Supportive therapy with fluids. Chelation therapy might work, but again, using this, not only cost wise but in food producing species, the licencing may not, allow it.
How do we control it? Well we remove sources of copper, er we can if we think that we have a copper issue, we can administer molybdate in the feed to bind some of that copper. But it's really making sure that animals are fed appropriate supplements and appropriate food.
Lead, thankfully is quite an uncommon poisoning. However, we do still see it, and this can be due to lead paint that's been discarded or on in old buildings where it's flaking on the walls, car batteries being discarded, gunshot or fishing weights, old ones which were were lead, or industrial waste, contaminating pasture or watercourses. We see neuros signs of blindness, circling and head pressing, and then we also get signs of Bruxism and excessive salivation.
We do see it more commonly in cattle because they tend to be a bit more indiscriminate, you know, they'll they'll just take mouthfuls of er pasture, er and might take in other things as they eat. And young animals are more susceptible. Clinical signs anorexia and depression, but the neuros signs which are more common, are blindness, circling, head pressing, slow twitching of the ears, bobbing of the head.
But we also will see GI signs of decreased rumour motility, ruxy and excessive salivation. The lead's ingested and absorbed in the small intestine by a calcium transport system and it will interfere with various enzymes. It will replace zinc as a co-factor in some pathways and it can also inhibit haemoglobin and erythrocyte synthesis.
We're gonna diagnose it based on the history of exposure to lead, clinical signs, serum concentration is greater than 0.6 parts per million, or greater than 0.35 parts per million with clinical signs.
We would take the blood into EDTA or heparin tubes. All this is gonna do is indicate exposure, but not the dose, the duration of the severity. We can take, from a postmortem, we can take renal tissue samples and concentrations above 10 parts per million would be indicative.
Treatment is gonna be remove that source of lead or remove the herd from the contaminated feed source. We could increase defecation by giving oral magnesium sulphate. Again, chelation therapy, but there may be residual lead in the rumen.
Chelation by calcium, disodiumedotate. So 70 to 100 mg per kg in 2 to 3 doses, and give that daily for 3 days. Treatment with thiamine may reduce the CNS signs as well.
Control, don't let athlete lead, you know, this can be actually quite hard if people have discarded car batteries into fields that are then turned into silage, . But we do need to be aware that if we do successfully treat these exposed animals, then er the Food Standards Agency may place significant withdraw withdrawal dates on meat and also milk. So finally to finish, a little bit about prevention, .
As we've sort of discussed, there are lots of toxins that will have similar clinical signs, and we have to put into place the history, the clinical signs to come up with what is the most likely. And if we have diagnostics, particularly a postmortem, then that can really help us to identify what the, the toxin might be and where that source of contamination might come from. Once we know that, then we should be thinking, right, how do we avoid sources of these known contaminants?
. Make sure cattle don't have access to storage areas. If we know that fields are particularly bad for poisonous plants, we should not use them. But farmers should be encouraged to investigate any suspicious signs or if they're seeing clinical signs that they are not used to.
If they are providing adequate quality feed, then that should not encourage animals to feed off poisonous plants. If we do have, contaminated feed stuff with mycotoxins, we can dilute it with non-contaminated feed. Personally, I think that that is a bit of a risk, but obviously if, if a whole shed of feed is contaminated, that's a lot of money, to throw away for farms.
Ideally we want to remove the contaminated feed or change the pasture. So good pasture management is really important. And we want to control livestock access to any of these areas, and regularly check fields for dumped materials.
So when farmers are out checking their stock every day, just doing, you know, a, a drive around the, the perimeter, particularly areas that back roads or, or, footpaths. So there are lots of resources out there to help you sort of with toxins. What I would hope is that this has been a bit of a whistle stop tour of the clinical signs that can be asso associated with toxins, but also some of the common ones that you might see.
Hopefully the handout will give you a way, to complete an investigation, but also we'll give you an easy way reference guide to what toxins might cause and what we can do about them. But I'd be happy to take any questions or er take any email questions er after this er session is is released. Thank you very much.