Plant Related Toxicants -Nitrate, Cyanide, Oxalate Flashcards
How do plants accumulate nitrate?
Nitrate is absorbed from solid
Nitrate (NO3) —> Nitrite (NO2) —> ammonia (NH3) —> amino acids and protein
Rate of conversation of nitrate to nitrite is slower than uptake from soil resulting in accumulation
What factors favor plant nitrate accumulation?
Plant species - sweet clover, alfalfa, wheat, corn
Content and form in soil - nitrate or ammonia
Soil conditions - moisture, acid, low molybdenum/sulfur/phosphorus, low temp
Decreased light reduces activity of nitrate reductase
Phenoxy acetic acid herbicides increases accumulation
What are the nitrate accumulating plants?
Pigweed Oat Beet Johnson grass Corn Lambs quarters Sweet clover Alfalfa Wheat Sunflower
What are sources of nitrite toxicity?
Forages/hays containing high amounts of nitrate
Accidental ingestion of contaminated feed or water
Overdose with nitrite IV (vasodilator)
What is the LD50 of nitrate for ruminants?
0.5-1g/kg
Need huge amount for toxicity
What species are the most susceptible to nitrate poisoning ?
Ruminants
Is nitrite or nitrate more toxic?
Nitrate is 10x more toxic than nitrate
A forage nitrate greater than _____% can cause acute toxicosis
1
T/F: young ruminants are more susceptible than adults to nitrite toxicity
False
Young animals are more resistant because they have not developed the rumen microflora to convert nitrate to nitrite
Monogastrics are also more resistant because they do not have the microflora
What types of diseases will cause increased nitrate toxicity?
Anemia
Methemoglobinemia
How is nitrate normally used in the body? When do you see accumulation
Nitrate —> nitirite —> ammonia —> amino acids —> protein
Accumulation occurs when the rate of conversion of nitrite to ammonia is slower than the rate of conversion of nitrate to nitrite
What body system does nitrite ion affect?
Erythrocytes
Nitrite ion enters the erythrocytes in exchange for chloride ion (can also cross placental and enter fetal erythrocytes)
What is the MOA of nitrite?
One nitrite interacts with two hemoglobin —> oxidation of ferrous iron to ferric and conversion of hemoglobin to methemoglobinemia
Lack of oxygen carrying capacity —>Anoxia
In chronic nitrate toxicosis, abortion occurs due to decreased ___________ but in the acute toxicosis, abortion occurs due to _______
Progesterone; methemoglobinemia
What lesions do you see in nitrate poisoning?
Brown-chocolate colour of the blood
Congestion of organs
What clinical signs are observed in nitrate toxicosis?
Sudden death
Rapid breathing, restlessness, apprehension, dyspnea, weakness, ataxia, sternal recumbency, cyanosis, terminal convulsions
What would you do to diagnose nitrate toxicity?what is the specimen for choice?
Chemical analysis
- forage, hay, water
- ocular fluid for animals that have been dead for several hours
Methemoglobinemia concentration
What specific test can qualitatively determine presence of nitrate?
Ddiphenylamine test
-positive result (dark blue colour) indicate greater than 5000ppm nitrate
What is the DDX for methemoglobinemia and anoxia?
Agents causing methemoglobinemia
- nitrate and nitrite
- copper
- acetaminophen
Agents inhibit oxygen utilization of tissues
- cyanide (bright red blood)
- hydrogen sulfide (dark blood)
Hemolytic agents
-copper, since, naphthalene, bromate, iodate, arsine gas, onion, mustard red maple, gossypol, snake venom, other
Carbon monoxide (bright red blood)
Cardiac toxicants - digitalis, magnesium, calcium, potassium, flouroacetate
What is the treatment for nitrate toxicity?
Methylene blue IV for ruminant and monogastrics (except cat) as a reducing agent
Activated charcoal, ruminal lavage with cold water, oral antibiotics
Where the the cyanogenic plants?
Wild cherry
Sudan grass, Johnson grass and sorghums (fall grasses) -> these also accumulate selenium, nitrate and cyanide
What is usually the source of cyanide toxicity in small animals?
Hydrogen cyanide and cyanide salts
- rodenticide
- fertilizers
- sodium nitroprusside used as hypotensive
- combustion of plastic compounds
Cyanogenic plants contain ______________ that can liberate toxic amounts of HCN
Cyanogenic glycosides
What is the characteristic odor of cyanide?
Bitter almond or ammonical
Probably not a good way to diagnose if you want to continue living
Thiocyanate SCN, a metabolite of cyanide, has a ___________ effect
Antithyroid
Only see effects in chronic toxicosis
What species are most susceptible to cyanide poisoning?
Ruminants (cattle> sheep) > horse> swine
Hydrolysis by rumen microflora causes release of cyanide from cyanogenic plants
T/F: plant damage like wilting, frost, or drought decreases cyanide toxicity
False
INCREASE toxicity —> cause release of B-glucosidate that causes hydrolysis of cyanogenic glycosides and release of cyanide
What part of the plant has the highest concentration of cyanide? How does this compare to nitrate accumulation
Cyanide: Seed > leaves> bark > stems and fruit
Nitrate: stems> leaves > seeds
Will young or old plants accumulate more glycoside
Young
Same as nitrate accumulation in plants
HCN is absorbed from??
GI tract
Inhalation
Intact skin
Where is HCN metabolized and then excreted?
Liver and serum met: CN-in presence of thiosulfate —> thiocynate (excreted in urine)
Excreted in urine or expired air
What is the MOA of cyanide?
Excess CN- binds with ferric iron and cupric copper to mitochondrial cytochrome oxidase. —> block electron transport chain —> unable to use oxygen resulting in histotoxic anoxia (brain and neuronal damage)
Metabolic acidosis due to anaerobic glycolysis
Vasoconstrictor effect
Irritant to mucus membranes
What are the clinical signs of acute cyanide poisoning?
Rapid onset
Tachypnea, apparent anxiety, severe panting, gasping, and behavioural alarm
Salivation, muscle tremor,s lacrimation, urination, deviation, colic, vomiting, bright red mucous membranes, clonic convulsions,
What are the clinical signs of chronic cyanide poisoning?
Posterior paralysis, urinary incontinence, and cystitis/constipation due to lower spinal cord degeneration
Goiterogenic effect (due to thiocyanide )
What are the specimens of choice for determining cyanide poisoning??
Forage, rumen content, liver, muscle, brain and heart
All should be frozen immediately and kept frozen
Elevated levels of thiocyanate can be found in ____________
Urine
What commercial test can help detect toxic levels of cyanide in rumen contents of plant?
Sodium picrate paper test
Yellow colour changes to brick red for positive test
What lesions do you see due to cyanide poisoning?
Mucus membranes are bright red and blood is cherry red and may not clot
GI tract and lung may be congested with petechial hemorrhage
Smell of cyanide may be present but leaves the rumen contents quickly
What is the DDX for cyanide poisoning?
Carbon monoxide (bright red blood) Hydrogen sulfide (rapid tissue death due to anoxia but tissues are dark green-purple) Nitrate (blood is brown-chocolate colour) Urea - causes few lesions but causes colic and nervous behaviour and odor of ammonia
How do you treat cyanide toxicity?
Sodium nitirite IV -> causes methemoglobinemia which can bind the CN- and reactivate cytochrome oxidase
Sodium thiosulfate -> convert CN- to thiocyanate which is less toxic
Oxygen therapy
Vinegar and cold water to slow microbial hydrolysis
Mineral oil as laxative
What plants contain large amounts of soluble oxalates?
Pigweed Beat Lamb quarter Halogenton Sorrel Rhubarb Sorrel Greasewood
What are the sources of soluble oxalates poisoning?
Plants
Potassium and sodium oxalate in household cleaners
Fungi
Ethylene glycol
What species are most susceptible to soluble oxalate toxcity?
Sheep and cattle
What is accommodation of the rumen microflora for oxalates?
Ruminants allowed to graze on small quantities of oxalate contains plants gradually results in detoxification of up to 70% more soluble oxalates than normal
What part of the plant contains highest amounts of soluble oxalates?
Leaves > seeds > stems
A diet rich in __________ decreases oxalate toxicity by making insoluble oxalates which cannot be absorbed
Calcium
Binds to make calcium oxalate
How are soluble oxalates metabolized in the rumen??
To carbonates and bicarbonate
What is not metabolized is absorbed to the blood and may affect serum tissue calcium
What is the MOA of soluble oxalates?
Soluble oxalates combine with Ca to form insoluble Ca oxalate
—> hypocalcemia and tentative in acute cases
—> affect bone and milk production in lower levels
—> precipitation of crystals in kidney —> kidney damage and necrosis
What are the clinical signs associated with soluble oxalate ??
Colic, dullness, depression, muscle twitching//weakness
Head and neck pulled to one side in sheep (seen in milk fever in cattle)
Prostration, coma, death
Rapid breathing and blood tinged froth at mouth
Convulsions
Animals that do not die from acute form of soluble oxalate poisoning develop what signs??
Fatal renal tubular toxicosis and signs of oligura, depression, hyperkalemia, and cardiac failure
Chronic tubular necrosis and polyuria
What lesions are present due to soluble oxalate poisoning>?
Plant in rumen
Excess fluid in abdominal and thoracic cavities, petechial hemorrhage in GI mucosa
Emphysema of lungs with aspirated ingesta
Esophagus and mouth with blood tinged froth
Kidney with dark cortex and medulla separated by gray line from accumulation of oxalate crystals in tubules
How can you make a laboratory diagnosis of soluble oxalate poisoning?
Presence of Ca oxalate crystals in kidney tubules
Hypocalcemia
High BUN
What is the DDX for soluble oxalate toxicosis?
Rumen acidosis -but pH of rumen with oxalate is alkaline
Milk fever - lacks oxalate lesions
Hypocalcemia
What is the treatment for soluble oxalate toxicosis ?
Activated charcoal or limewater
Calcium gluconate IV slowly may cause transient improvement
Saline glucose to treat alkalosis and cause diuretics
Supplement of calcium salts or Ca rich diet
Supportive therapy for nephrosis
