Toxicants Flashcards
cyanogenic plants
- sudden death
- bright red MMs, bright red venous blood
- cyanosis, dyspnea, muscle twitching, staggering, convulsions, coma
- contain hydrogen cyanide
- Tx= sodium thiosulfate, sodium nitrate
nitrate accumulating plants
- sudden death
- weak, drowsy, chocolate MMs, tremors, tachycardia/tachypnea, staggers
- Tx= methylene blue
copperweed
- sudden death
- oxytentia acerosa
death camas
- zigadenus
- sudden death
- salivation, bloody froth, vomiting, muscle weakness, staggers, tachycardia
- Tx= atropine
dogbane
- apocynum
- contains cymarin
- sudden death, blue MMs
easter lily
- zephyranthes atamasca
- sudden death, staggering, D+
false hellbore, skunk cabbage
- veratrum
- contain cyclopamine, cyclopasine, jervine
- sudden death, salivation and frothing, weak, V+, tachyarrhythmias
teratogen - cyclops lambs
fitweed
- corydais
- containe isoquinolone alkaloid
- sudden death, neuro signs
foxglove
- digitalis purpurea
- contains digitoxin, digitalin, digoxin, saponins, alkaloids
- sudden death
- colic, melena, anorexia, PU, arrhythmias
jimsonweed, thornapple
- datura stramonium
- contain tropane alkaloids
- sudden death, colic, ileus, D+, mydriasis, tachycardia, anorexia, spasms, seizures, PU
larkspur
- delphinium
- contains alkaloids
- sudden death, weakness, staggers, twitches, bloat, tachyarrhythmias
- die within 3 hrs
- range cattle
-Tx= IV phyostigmine, neostigmine
milkvetches
- astragalus
- contain miserotoxin
- SUDDEN DEATH, NEURO
- acute resp distress, emphysema, wheezing, drooling
- goose stepping, knuckling, collapse
milkweed
- asclepias
- contain cardenolides
- sudden death, depression, weakness, resp paralysis
mistletoe
- containe amines, toxic proteins
- sudden death, colic, D+, bradycardia, hypotension
nightshade
- solanum
- contains solanine and other glycoalkaloids
- sudden death, dyspnea w/ exp grunt, salivation, weak and trembling
perilla mint
- perilla frutescens
- contains perilla ketone, egomaketone, isoegomaketone
- sudden death, acute resp distress
poison hemlock
- conium maculatum
- contains coniine, gamma coniceine, cyanapine
- sudden death, trembling, ataxia, resp paralysis, abortion or birth defects
- Tx= ATROPINE
rayless goldenrod
- isocoma
- contain tremetol
- sudden death, trembling legs and nose, stiff gait, constipation, urine dribbling, acetone breath
sweet clover
- melilotus
- contains coumarin, converted to dicoumarol by molds
- sudden death, hemorrhage
white snakeroot
- eupatorium rugosum
- contains tremetol
- sluggish behaviour, acetone breath, melena, constipation, dysphagia, tachyarrhythmias, CHF, myoglobinuria
plant poisoning of range cattle
1) locoweed
2) tall larkspur
blocks molecular oxygen transfer in cytochrome oxidase systems in mitochondria, causing tissue anoxia
cyanide
causes of nitrate accumulation in plants
- fertiizer
- photosynthesis is impaired by shade or prolonged cloudiness
- drought, frost, hail
bracken fern
- pteridium aquilinum
- contains ptaquiloside
- neuro signs, thrombocytopenia, bladder and GI cancer
-Tx= thiamine
castor bean
- ricinus communis
- contains ricin
- neuro signs, bloody D+, tenesmus, colic
horse nettle
- solanum carolinense
- contains solanine
- neuro signs
-Tx = physostigmine
horse tail or scouring rush
- equisetum
- contains aconitic acid, palustrine, thiaminase
- neuro, paresis
-Tx = thiamine
Jamaican nettle tree
- contains trema toxin and ammonia
- blindness, signs of hyperammonemia
johnson grass
- sorghum halepense
- contains hydrocyanide
- neuro, posterior ataxia, urinary incontinence and cystitis
locoweed
- astragalus and oxytropis
- containe swainsonine
- neuro, abnormal behaviour, abortion, reduced fertility, skeletal malformations
lupine
- contain piperidine, quinolizidine
- neuro, frothing, dyspnea, birth defects
oak
- quercus
- contains gallotannins
- neuro, ileus, mouth ulcers, mucosal discoloration, patchy sweating, dark urine
yellow star thistle
- centaurea solstitalis
- contains sesquiterpene lactones
- neuro signs, twitching lips, tongue flicking, chewing, poor prehension, facial paralysis
4 syndromes of milkvetch
1) sudden death from methemoglobinemia, cattle and sheep
2) respiratory dz and emphysema, sheep
3) neuro
4) selenium toxicosis
tremetol
- cumulative effects on skeletal and cardiac muscle
- white snakeroot, rayless goldenrod, and burrow weed
atypical myopathy
- box elder seeds - Hypoglycin A
- damages mitochondria, impairs lipid metabolism in muscle cells, –> cell death
- weakness, recumbency, myoglobinuria
- dysphagia, choke, colic
plants containing cardiac glycosides
milkweed, dogbane, indian hemp, blue-eyed grasses, foxglove, hellbores, hyacinth, oleander, periwinkle
important plants that damage myocardium in large animals
yew, avocado, death camas, and summer pheasant eye
PA
- loss of appetite, lethargy, D+, constipation, icterus, photosensitization
- liver failure
- HE
oleander
- tachycardia
- severe gastroenteritis, diarrhea, abdominal pain
- sweating, weakness
red clover
- mold slaframine
- slobbers, bloat, D+, blindness, abortion, laminitis
enzootic hematuria
bracken fern (ptaquiloside) -carcinogenic to bladder epithelium
alsike clover
-hepatic encephalopathy or photosensitization
plants containing PAs
groundsel (senecio) heliotrope houndstongue (cynoglossum) kochia patersons curse (echiu plantagineum) rattlebox, rattlepod (crotalaria) tansy ragwort (senecio) tarweed, fiddleneck (amsinckia) vipers bugloss (echium vulgare)
ergot alkaloids + fescue
claviceps purpurea
-failure to develop udder, agalactia, prolonged gestation, placental abnormalities, dystocia
ergot alkaloids + livestock
- vasoconstriction
- gangrene and lameness in cold weather
- heat stroke
- summer slump
perilla mint in ruminants
- compounds are bioactivated in the lung
- cause atypical interstitial pneumonia and acute resp distress
common photosensitization plants
st johns wort (hypericum perforatum)
buckwheat (fagopyrum)
dutchmans breeches, bishops weed, rain lily, spring parsley, giant hog weed, cow parsnip (heracleum)
syndromes of excess selenium
1) acute toxicosis
2) blind staggers
3) chronic alkali disease
oxalate poisoning is most common in
sheep
- sequestration of ca and mg
- tetany or flaccid paralysis
most common cyanobacterial dz (algae)
acute hepatotoxicosis from microcystin exposure
-hypovolaemia, shock, blood loss into disentegrated liver lobules and hepatocyte emboli traveling to lungs
aflatoxins
- aspergillus flavus and parasiticus, corn, nuts, cottonseed
- hepatic insult/failure
- cancer
zearalenone
- corn, wheat, barley
- hyperestrogenism
fumonisins
- corn
- equine leukoencephalomalacia = moldy corn poisoning
- swine = pulmonary edema
- hepatic dz
bovine bonkers
- ammoniated feed
- hyperexcitability
action of organophosphates and carbamates
- acetylcholinesterase inhibitor
- AcH accumulates at junctions and causes excessive synaptic action
- nervous and skeletal muscle signs
-Tx= pralidoxime chloride (2-PAM)
Monensin
Ionophore Antibiotic
Biologically active compound (produced by a fungus in nature)
Uses: coccidiostat (poultry) and for feed efficiency (cattle)
Mechanism: selective transport Na+ and K+ ions b/w intra and extracellular spaces
Horses most sensitive to toxicosis
Monensin Toxicity
- LD50 in horses 1-2mg/kg
- Primary target organ = heart, severe mitochondrial damage
- Dx samples: the feed itself, serum, liver, GI content, feces
- Tx: laxatives / charcoal, vit E / Se, IVFT and electrolytes / acid-base correction
(there is no antidote)
Clinical Presentations of Monensin Tox
Peracute toxicity (death within hours):
Severe hemoconcentration, hypovolemic shock
Acute toxicity:
feed aversion, colic, watery feces, intermittent sweating, stiffness, progressive muscle weakness (especially hindquarters), ataxia, recumbency, tachycardia, hypotension, dyspnea, polyuria
Survive sublethal dose:
Reduced athletic performance, ill-thriftiness, cardiac failure (tachycardia, AF)
myocardial sarcolemma damaged and replaced by fibrous tissue
Lasalocid
Accepts monovalent AND divalent cations
CS, Dx and Tx similar to monensin toxicosis
Ataxia + paresis and paralysis
Least toxic ionophore, LD50 21.5mg/kg
Salinomycin
Accepts just monovalent cations (like monensin)
CS, Dx and Tx similar to monensin toxicosis
Lethal dose not provided in text
Ionophore Toxicity
Critical evaluation of cardiac function of any previously intoxicated horse that is destined to return to some form of athletic endeavor is judicious.
NITRATES AND NITRITES
Nitrate poisoning is common in ruminants but rare in horses
Nitrates naturally undergo microbial decomposition to nitrites
Risk is when horses are exposed to preformed nitrite — ingesting feed / water where nitrates have decomposed to yield large amounts of nitrites (both are water soluble)
Moist haystacks, water troughs, farm ponds, silages, pig swills
Clinical signs related to severe oxygen deficiency
Clinical signs of nitrate toxicity become evident when ___% of hemoglobin is oxidized to methemoglobin?
30-40%
Nitrate Toxicity
Vasodilation leads to hypotension and decreased CO
Dx: Test forage/feed/water for nitrate or nitrite
Blood test for methemoglobin (quickly, not stable)
Ocular fluid on post mortem
Tx: Methylene blue 4.4mg/kg as 1% solution with isotonic saline
Repeat in 30min if needed
Vitamin C - less effective alternative
Supportive – oxygen, laxatives / charcoal
Cyanide CS
Affected animals commonly are found dead — anoxia in the brain
*Tachypnea, panting/gasping, excitement, salivation, lacrimation, muscle tremors, defecation, urination, mydriasis. Followed by convulsions, death
Horses surviving > 90 - 120 minutes after exposure usually survive
Don’t need further treatment
what toxic syndrome does ingestion of black walnut shavings cause in horses?
laminitis
Horses have a favourable prognosis for recovery if they are removed quickly from the offending bedding.
horses with chronic wild jasmine ingestion develop lameness and weight loss despite a good appetite. what else can affected horses develop?
Hypercalcemia and renal failure
Solanaceae family plants contain a potent steroid glycoside
- Vitamin D– like activity
- Normal vitamin D negative feedback mechanism bypassed
- Excessive Ca and P absorption at level of the GIT exceeds renal capacity to excrete
- Soft tissue mineralization (dystrophic calcification) of flexor tendons, suspensory ligament, other elastic tissues
- Renal azotemia and hypercalcemia (phosphorus may be WNL)
the toxic mechanism of tall fescue is
fungal endophyte that grows within the stem, leaf sheaths, and seeds
ergopeptine alkaloids: Ergovaline and ergosine
AT WHAT POINT IN GESTATION ARE PREGNANT MARES SUSCEPTIBLE TO TOXICITY BY INFECTED FESCUE?
late >300 days
summer slump or summer syndrome
also caused by tall fescue
characterized by anorexia, weight loss, poor hair quality, pyrexia, and hypersalivation.
SIGNS OF IODINE TOXICOSIS
A: nasal discharge due to increased respiratory tract secretions
B: excessive lacrimation
C: intermittent non-productive cough
D: nonpruritic generalized alopecia and scaling
Carbamate Pesticides
CS of toxicity in horses reflect muscarinic and nicotinic cholinergic overstimulation:
profuse salivation, severe GI, hypermotility, severe pain, abdominal cramps and diarrhea, excessive lacrimation, miosis, sweating, dyspnea, cyanosis, and urinary and fecal incontinence. Affected animals also may cough frequently as a sign of excessive accumulation of respiratory tract secretions.
The signs reflected by nicotinic overstimulation include excessive stimulation of the skeletal muscles. The muscles of the face, eyelids, and tongue, in addition to the general musculature, may twitch. Some animals exhibit signs of generalized tetany that causes them to walk in a stiff-legged fashion. This hyperactivity may be followed by weakness and paralysis of the skeletal muscles
Diagnosis can be made based on history to exposure, clinical signs, and response to atropine.
organophosphates cause death by ?
asphyxia
the combined effects of nicotinic, muscarinic, and central cholinergic overstimulation or receptor paralysis. These effects include hypotension, bradycardia, bronchoconstriction and excessive bronchial secretion, inability of the respiratory muscles to work properly, cyanosis, and central respiratory depression. The animal actually dies of asphyxia.
Strychnine
Clinical signs appear within 10mins - 2hrs
—Initial signs include apprehension, nervousness, and muscle stiffness
—Later signs are tetanic spasms – extreme extensor muscle rigidity
—Death occurs when the spasm become more frequent until exhaustion or anoxia
—The entire clinical episode typically lasts 2 hours
Levamisole Toxicity
Is effective in eliminating lungworms, ascarids, and adult pinworms from horses. The drug also has been used in human beings and other animal species in an attempt to enhance immune system function.
Clinical signs occur within 1 hour of administration and include hyperexcitability, muscle tremors, hyperactivity, excessive sweating, and lacrimation. Recumbency may follow these signs, but animals that recover generally appear normal within 12 hours after exposure.
Nicotine Toxicity
Large doses result in a descending paralysis of the CNS
Death results from respiratory failure caused by paralysis of the diaphragm and chest muscles
The effects of a sublethal dose should diminish in a few hours
why are urea and non protein nitrogens (added to ruminant feed in addition to other uses) toxic in horses?
Hydrolyzed to AMMONIA
Bracken Fern
- The toxic agent is Thiaminase
- Horses can exhibit signs even If they have not ingested the plant for 2-3 weeks
- Signs begin after ingesting the plant continuously for 30-60 days
- Toxicity results in the systemic accumulation of a variety of metabolites, including pyruvate and lactate. –> thiamine deficiency
which plants are implicated in nigropallidal encephalomalacia?
A) yellow star thistle (Centaurea solstitialis)
B) russian knapweed (Acroptilon repens)
C) Centaurea melitensis
Jimson weed contains
Tropane alkaloids (atropine, scopalomine)–mydriasis, tachycardia, decreased gut sounds
Castor bean (Ricinus communis) contains
Ricinnoleic aci–60S ribosome disruption, RBC agglutination
Nightshade (Solanum spp) contains
Solanine–salivation, colic, increased borborygmi, diarrhea, mydriasis, depression, weakness
Pokeweed (Phylotacca americana) contains
Phytolaccine, mitogens–GI irritation, hemorrhagic gastritis, hemagglutionation, mitotic activity
Phosphorous Toxicity
Toxic signs start within hours of ingestion, undergo a latent period of 48 -96 hours, then recur
initially shows as severe colic, GI irritation, occasional diarrhea, arrhythmias, cyanosis, shock, coma, death
late signs = liver dysfunction, including icterus and bleeding from the gingiva, GI, or kidney
Locoweed
Horses may have progressive clinical signs over several years due to addiction to the plant
Clinical signs include lethargy, weight loss, incoordination, and nervousness under stress
Indolizidine alkaloids, swainsonine, and swainsonine N-oxide are the suspected toxic agents
The alkaloids, which may be due to an endophyte in the plant, cause vacuolization of the kidneys first (as early as 4 days), followed by the CNS by 8 days. If removed vacuoles go away, but exposure for >30 days results in permanent vacuolization in all tissues EXCEPT cardiac and skeletal muscle. Swainsonine is an alpha-mannosidase inhibitor, which causes oligosaccharide build-up in lysosomes
Mild cases may resolve 1-2 weeks after plant removal, but chronic cases generally do not recover
Zinc Toxicosis
A) gradual onset lameness and stiffness
C) joint swellings
C) osteochondrosis
three clinical syndromes attributed to selenium toxicity
B) Acute (within 6 hrs): sweating, diarrhea, tachycardia, tachypnea, mild pyrexia, lethargy, and mild to severe colic, death in 24 hours; may be “dumb” before death
C) Chronic (weeks – months): blind staggers, aimless wandering or circling, muscle weakness, incoordination, respiratory difficulty, and decreased vision, paralysis and death
D) Alkali disease (weeks – months): initially lameness and swelling of the coronary bands; anorexia and mild depression –> transverse cracking of the hoof wall, loss of hair from mane and tail
Several horses in a herd become lame and have dark and discolored skin on the fetlocks with a line of demarcation. These areas are cool. Skin in some horses is sloughing. Other horses are showing signs of colic. What is the most likely causative agent?
Ergotism (Claviceps purpurea)
Ergotamine is a vasoactive substance that causes arterial and venous constriction and may damage capillary endothelium
Iron tox mechanism
Toxicity occurs when serum iron levels exceed the iron-binding capacity of transferrin. Free circulating iron then damages blood vessels, may cause erosion and ulceration of the stomach and intestine, causes hepatocellular necrosis and fatty degeneration of the myocardium, and can produce cerebral edema
What are the main clinical signs seen with sorghum toxicity?
hindend ataxia and urinary incontinence
CS of VitD toxicity
A) depression, anorexia, weakness
B) PU/PD
C) murmurs and tachycardia
D) stiffness and reduced mobility
What body system is affected by vit K3 toxicity?
acute renal failure
Mercury Intoxication
acute – ARF, oliguria and depression, GI irritation
chronic – oral ulceration, progressive respiratory difficulty, terminal azotemia
treatment is with activated charcoal, dimercaprol, and supportive
Nigropallidal Encephalomalacia - onset of signs is
always sudden
beginning w variable degrees of impairment of eating and drinking
Nigropallidal Encephalomalacia - Characteristic necropsy findings
bilaterally symmetric, and sharply defined softening and necrosis in areas of the globus pallidus and substantia nigra
LEUKOENCEPHALOMALACIA
Most cases occur from late autumn through early spring, and most outbreaks have been associated with a dry growing period followed by a wet period
ingestion of mycotoxin fumonsin B1 produced by molds on corn –> neurologic and hepatoxic syndromes
The onset of clinical signs is abrupt after 3-4 weeks of daily ingestion
Older animals are more likely to be affected than younger animals
Neuro syndrome: incoordination, aimless walking, intermittent anorexia, lethargy, depression, blindness , head pressing –> may be followed by hyperexcitability, belligerence, extreme agitation, profuse sweating, delirium. Recumbency and clonic-tetanic convulsions possible before death.
Hepatotoxic syndrome - swelling of lips and nose, somnolence, severe icterus, petechiae of mucous membranes, abdominal breathing, cyanosis. Affected horses acute onset csx w death within hours to days.
Typical gross lesions: liquefactive necrosis, degeneration of cerebral hemispheres – degenerative changes also possible in brainstem, cerebellum, spinal cord. Bilateral or unilateral lesions.
Lead sensitivity
Horses are much more sensitive than cattle to prolonged, low-dose exposure to lead,
but
much less sensitive than cattle to short-term exposure of large doses
Lead Poisoning
primarily peripheral nerve dysfunction - motor nerves at greater risk
—Depression and wt loss worsen over time
—Laryngeal and pharyngeal paralysis, dysphagia, dysphonia, and proprioceptive deficits
—Progressively may exhibit flaccidity of rectal sphincter; paresis of lower lip; and difficulty in prehension, mastication and deglutition. Aspiration pneumonia common, also intermittent fine muscle tremors
—Terminally: severe incoordination, anorexia, emaciation, and almost complete pharyngeal, and oesophageal paralysis w the inability to swallow food and water.
Intoxication primarily through ingestion
Peripheral neuropathy associated with Pb toxicosis in horses thought to be caused by peripheral nerve segmental demyelination, which impedes nerve impulse conduction and contributes to clinically observed signs.
Oleander
sudden death
do not give calcium
cyclops lamb
veratrum californicum
false hellebore
cyclopamine teratogen
alkali disease
—Chronic excessive selenium ingestion
—skin and hoof abnormalities
—livestock in areas with seleniferous soils, such as the Great Plains
—Common seleniferous plant species with this potential include primary selenium accumulator plants, such as milkvetch (Astragalus spp.)
enzootic hematuria in cattle
Bracken fern’s toxin, ptaquiloside, is carcinogenic to bladder epithelium
TOXIN:
nephritis with necrosis and renal tubular casts is observed, possibly leading to acute renal failure
oak poisoning
microcystins
produced by multiple cyanobacteria and detected in fresh and coastal waters worldwide
most commonly reported cyanotoxin poisoning in large animals is
acute hepatotoxicosis subsequent to microcystin exposure
the ____ is the target organ of aflatoxin metabolites in all species
liver
two species most suceptible to fumonisin
horses and swine
who is susceptible to zeralenone
perpubertal gilts
possibly first calf heifers
the pathogenesis of clinical signs associated with dietary exposures to EAs can generally be explained in terms of:
vasoconstriction (ruminants) and/or hypoprolactinemia (mares)
mechanism behind summer slump, dry gangrene, fescue foot, gangrenous ergotism
vasoconstriction!
Copper causes ____ hemolysis
Intravascular
___ are most sensitive to copper
Sheep, often chronic by getting the wrong species feed
How does copper kill sheep?
Methemoglobin
Anemic from hemolysis
Pigment trashes the kidneys
Nitrate vs cyanide
Nitrate = brown blood
Cyanide = cherry red blood
Calves not thriving, can’t thermo regulate
Summer slump
Fescue
Onion, brassica
Hemolysis
Heinz body anemia
Pine needles
Late term abortion in cattle
