Plants are dicks Intro+blood (DON'T NEED TO KNOW PICS. But for NAVLE you do, so...) (if tx left out, it's cause its just supportive)
how might toxic plants be a different story in ruminants?
in ruminants, microbes in rumen can detoxify the toxic material (or toxify it i guess. either way this extra metabolism to consider)
what are some different types of toxic constituents of plants?
(not sure if numbers are actually grouping them together or not, she just had separate bullet points) (1)Essential oils (myristicin, saffrole), alkaloids (2) Aminoacids (toxic- aminopropionic acid, L-β- cyanoalanine), coumarins and furanocoumarins (3) Cardioactive glycosides, cyanogenic glycosides (cyanhydrins), tannins (4) Plant acids (omega fluorinated fatty acids), phenols, saponins
sweet clover (Melilotus sp)- White and Yellow sweet clover: What is the MOA of this toxicity?
plant causes Dicoumarol--> inhibits vit K epoxide reductase (so can't make active Vit K1 for clotting)--> deplete prothrombin, factors 7,9,10.(So think of clover manga, and the bloodyness of it, think of klover bc vit K epoxidase... and then the K dependant clotting factors PROTHROMBIN IS FACTOR 2 )
CSs of sweet clover poisoning?
Signs associated with vit K inhibition: (remember need K for 2,7,9,10) Haemorrhage, Intractable bleeding (Blood from the nares, digestive tract, surgical sites), Haematoma. The Prothrombin time (remember prothrombin is factor 2) is prolonged from 15 secs. to 100-200 seconds
Bracken fern (Pteridium aquilinum)-- what is the toxin in this plant? When are concentrations of it high?
ptaquiloside (high concentrations in young plants) (mnemonic: ptaquiloside-- think of how a fern looks like quills on a stalk)
What is the MOA of the toxin (what is it again?) in bracken fern?
ptaquiloside forms pterosine B that alkylates purine bases in DNA (disrupts transcription) it also activates oncogenes (H-ras proto-oncogene) in GI/UT --> bovine enzootic hematuria (slow/chronic ingestion). Associated with BONE MARROW DEPRESSION (bracken fern Quils depress me down to my bone marrow too)
CS of bracken fern tox?
Remember its ptaquiloside, and it causes enzootic bovine hematura and BM depression via messing with the DNA (alkylates purines and activates oncogenes), can see: acute fever, Lethargy, anorexia, hges, Thrombocytopenia and neutropenia, followed by pancytopenia--> Increased bleeding time → epistaxis
what vitamins in the body does bracken fern mess with, and how? WHO is this a big problem in?
bracken fern, on top of the ptaquiloside, also has thiaminase 1 and 2 which break down thiamine. This can lead to a deficiency. This is generally more of a problem in monogastrics, bc rumen microbes can synth thiamine for them. REMEMBER THAT THIAMINE (B1) DEFICIENCY= PEM (polioencephalomalacia)
Onion (Allium cepa) is most toxic in which animals?
Most toxic for cats and dogs (less in horses, least in ruminants)
how do animals get intoxicated with onion? What is the MOA of how onion is toxic?
Eating large amounts, repeated doses. Basically causes free radical (Highly reactive oxidants, disulfides and thiosulfates) mediated oxidative damage on RBC membrane.--> hemolytic anemia. (denaturation of Hb, deformation of RBC’s, hemolysis, ↑ phagocytosis)
CSs of Onion tox?
(remember causes free radicals-->RBC membrane damage) Abrupt onset, Dark/coffee-coloured urine, depression, anorexia, weakness, Mucous membranes darker than with icterus, Strong onion odour (breath/body). Might see heinz bodies from denatured Hgb due to the free radicals (disulfides, thiosulfides), and might see LOW PCV (10-15%), but will also see regenerative response (makes sense if you know why anemia is happening)
Red Maple (Acer)--> which ss does this affect the most?
MOA for red maple?
Reactive oxidants (ROS) → target RBC glutathione reducing system --> abrupt lysis of RBCs (after 1-2 days of eating wilted leaves) (so like onions, oxidative damage leading to RBC lysis).
CSs of red maple tox?
Remember that it's ROS's causes RBC lysis, so you will see... Depression, anorexia, dark red/brown urine, ****SEE HEINZ BODIES ON SMEAR, anemia (PCV 8-10), see methemoglobin, oliguria, icterus, enlarged and congested spleen, enlarged kidneys, tubular nephrosis, Hb casts
How do you tx red maple tox?
Use ascorbic acid to treat the methemoglobinemia. (Red maple makes Brown pee. go fig.)
Field mustard (Brassica rapa) who is most susceptible to this?
MOA of toxicity of field mustard (brassica rapa)
eat plants for 2-3 weeks--> eats S-methyl-L-cysteine sulfoxide (SMCO), which is metabolised (glycosylated) to dimethyl sulphides (THIS ONLY HAPPENS IN RUMIS- the acidic environment of monogastrics does not allow it). dimethyl sulphides are ACTUAL HEMOLYSINS (brassica anemia factor). So these cause heinz bodies in the RBCs and eventually severe hemolytic anemia.
Brassica rapa (Field mustard): After copious feeding of rape seed meal/cabbage, aside from the hemolysis (which is mainly a rumi prob bc their rumen allows conversion of SMCO to dimethyl sulphides) what other body systems are affected (and commonly effected sp?)
Can cause GIT damage and liver hge, as well as CHANGES IN THYROID METABOLISM--> ENLARGEMENT OF THYROID GLAND. Can be a big prob in chickens apparently (rape seeds)
how does field mustard (brassica rapa) cause goiter?
Thiocyanate ions/goitrogens → inhibitory effect on biogenesis of thyroid hormones (compensatory enlargement of thyroid gland)
How can you help treat the goitrogenic effects of ___ (name that plant)?
(remember in chickens this is a prob) Problem with field mustard/brassica rapa-- SUPPLEMENT IODINE!!!
Nitrate poisoning (pearl millet, sorghum, sudan)--> who is most susceptible to this? why?
Ruminants, because their rumen converts nitrates to nitrite (which is worse) .....this also happen in horses, in their cecum.
what are some factors which can inc the nitrate levels in plants, which plants are particularly prone to this?
(PLANTS: pearl millet, sorghum, sudan) Accumulation of nitrate in plant (growth conditions) – following a prolonged dry period/ frost damage, high nitrate soil content, immature plants (also consider amount eaten, nitrate release/reduction)
MOA of how nitrate does toxic damage? What are some related problems?
Rumen microbes convert nitrate--> nitrite. Nitrite absorbed and OXIDIZES the Fe in Hgb--> makes methhemoglobin (we learned about this with pigs and werners). Mhgb can cause abortion if it crosses the placenta
CSs of nitrate tox?
(remember the main prob is Nitrate-->nitrite-->oxidize hgb to methemoglobin) Abrupt onset; hours after eating hay, fatal in minutes. Weak, labored respiration, trembling of certain muscles, weakness, staggering gait & sometimes apparent blindness, The animal may sink to the ground, fall on its side, and lie with its mouth open. The tongue and whites of the eyes turn blue. Death usually takes place with little or no struggling, possibly dark mucous membrane, Pregnant animals that are affected may abort later (ALL CSs RELATED TO REDUCED ABILITY TO CARRY O2)
if you want to send in food (forage/silage) samples to test for nitrate tox, what should you do?
be taken from many points within the stack, sent in air-tight container to prevent loss of moisture--> keep delivery time as short as possible
2 big treatments for nitrate tox?
(1) Methylene blue to treat the methemoglobin (idk why in red maple tox it is ascorbic acid, but w/e) (2) Adapt animal using oral Propionobacterium paste-- these are probiotics (help reduce bugs converting nitrate to nitrite- good management tool for producers when they need to feed drought-stressed-high-nitrate forage to cattle)
what are plants in the Lectins group?
Peanuts, soyabean, lentils, peas, beans, Abrin <--only one we care about
Lectins: What is lectin, what is the MOA that makes them toxic?
its composed of amino acids, bind to sugar in glycoproteins on outside of RBC. Lectin blood poisoning--> ANAPHYLAXIS (small proteins so taken up easily)
Abrin (rosary pea, Jequirity beans): what kinda toxic group is this plant in? What is the basic structure of this compound? Explain how the structure plays a role in toxicity
It is a type of lectin and is 2 peptide chains linked by disulphide bridge. B-CHAIN attaches toxin to cell surface. And then the A-CHAIN is the TOXIC AGENT (a for agent)
What is the toxic portion of the abrin (rosary pea, jequirity bean) and what is it's MOA?
THE A-CHAIN (remember it is a dipeptile chain) is the TOXIC PART (B-chain attaches to endothelial cell surface) it is a N-glycosidase that inactivates ribosomes by cutting out elongation factors – affects protein synthesis. Without good protein synth--> Endothelial cell damage → vascular leakage and edema
milkweed (Asclepias sp): What is the toxic MOA, and what are the CS?
**CARDIAC GLYCOSIDE=INHIBIT Na-K ATPase in the cardiac sarcolemmal membrane. So CS: Dec, irregular HR, weakness and trembling. (also see Depressed, weak, abdominal pain, odontoprisis (grinding of teeth), diarrhea, Irregular labored respiration with a groaning grunt)
how do you treat milkweed tox?
(CARDIAC GLYCOSIDE)= Atropine ( to tx AV block), Anti-arrhythmic drugs
toxic MOA for digitalis (foxglove)
ANOTHER CARDIAC GLYCOSIDE: inhibit sarcolemmal Na-K ATPase (inc intracellular Ca++)
CSs of digitalis tox?
(remember: cardiac glycoside) Weakness, diarrhea (with blood), Dogs & cats – excess salivation, vomiting, Most animal species – colic, labored respiration with a peculiar forced respiratory sound, Arrhythymias → bradycardia, AV block, ventricular fibrillation
how do you treat foxglove (digitalis) tox?
supportive care, atropine (treats AV block), propranolol (Beta-blocker, slow HR, tx hypertension, help with CHF)
Nerium oleander- what is the toxic component, when is it most toxic?
ANOTHER cardiac glycoside (she said Steroidal; consists of cardenolides glycosides, still blocks Na-K-ATPase) dried leaves are at greatest risk
CSs of oleander ingestion?
(remember- cardiac glycoside) Depression, anorexia, excess salivation, diarrhea (with blood), Vomiting (dogs and cats), Bradycardia, Paroxysmal tachycardia, ST-segment depression, arrhythmias with AV block, Flaring, soreness around mouth, colic type signs in horses
how might you describe oleander leaves?
Tough, leathery leaves distinctive in stomach, secondary veins almost perpendicular to midvein, leaves fragments ribbed as trout skeleton
tx for oleander?
same as other Cardiac glycosides: Supportive care, Atropine and propranolol
what did she say was the most hazardous plant in north america?
The yew o_o
Yew (Taxus sp): who is most at risk? what parts of the plant are toxic?
Dogs, cats, other indoor/outdoor pets at risk.. All parts are toxic except the fleshy aril of fruit
what are the toxins in Yew? what is their MOA?
Consists of cardiotoxic taxines A, B → inhibit cardiac conduction! (heart block, slowing of heart, widening of QRS)
which plant has cardiac taxines A and B?
most common CSs of yew ingestion
sudden death (most hazardous plant in N. america)
what can you use to tx yew?
supportive, atropine (to help with heart block)
Locoweed (Astragalus) causes what problems? main toxic component?
Toxic component swainsonine. Cardiomyopathy, edema with heart failure--> arrhythmias
White snakeroot (Eupatorium sp) causes what problems?
Cardiomyopathy, edema with heart failure → arrhythmias
Gossypium (Cottonseed): what is the toxic substance? what problems does it cause?
Gossypium is toxic substance. the seeds and esp seed cotyledons are toxic. (sometimes seeds used as protein suppliment BUT SHOULDNT EXCEED 100 PPM) cumulative effects – results in congestive heart failure. Can also dec sperm production.
CSs/path of gossypium (cottonseed)- who is most affected?
swine, pre-ruminant calves and lambs. chronic ingestion of cottonseed meal –> cardiac failure, abrupt onset of muscular weakness, frothy salivation, generalized edema. respiratory distress, death in days/week. Highly risk in mature ruminants IT CAUSES CONGESTIVE HF ((so see: Widespread congestion and edema, Large amounts of free fluid in chest and abdominal cavities & pulmonary edema, Liver mottled (nutmeg in appearance), Heart dilated, flabby and edematous)
what is the toxic component of avocado? What main problem does it cause?
Toxic: persin, causes sterile mastitis as well as myocardial degeneration
CSs of avocado toxicity?
(remember persin, causes sterile mastitis and myocardial degeneration) Swollen, reddened mammary gland (75% decrease in milk production), Watery/curdled milk; clots in milk, Fluid accumulation in heart sac, thorax and abdomen, Heart is pale & flappy, Myocardial degeneration of heart, necrosis of ventricular walls and septum → cardiac arrhythmias. Edema in gall bladder & peri-renal tissues. Pulmonary edema (cough/respiratory distress) and subcutaneous tissue in neck and brisket, weakness/depression, reluctance to move, Serum LDH, CPK, AST are elevated
Hoary alyssum (Berteroa sp): how are animals intoxicated by this? WHO does it affect most?
CONSUMPTION of plant by HORSES
Hoary alyssum (Berteroa sp): CSs/problems it causes?
VASOSPASM AND LIMB EDEMA so see: Laminitis/limb edema in horses, ↑ hoof temperature of horses, Edema in distal portions of limbs, Colic, bloody diarrhea, slow capillary refill time, fever, increased heart and respiration rate, dehydration, red urine.
Tx for hoary alyssum intox?
Basically NSAIDs to help with inflammation, and support
how are hoary alyssum and black walnut similar?
both cause vasospasm and limb edema in horses. But one is eaten (hoary) and one is laid on (BW bedding)
Black walnut (Juglans sp)- WHO is affected by this, how are they intoxicated by this?
HORSES, from having the wood shavings as their BEDDING
What problem does black walnut shavings cause?
TOXin UKnOWN!! however, causes vasospasm resulting in ischemia within capillaries of laminae with subsequent reperfusion. --> limb edema (look out for laminitis). Can cause fever too.
Tx for black walnut tox?
similar to hoary alyssum- NSAIDs to dec inflammation. Also Adrenergic blockers (prazosin) or calcium channel blockers (nifedipine) (both are vasodilators, since this causes VASOSPASM)