INTRODUCTION
Selected poisonous plants most often seen as a cause of animal poisonings in our area.
Suggested 400-700 poisonous in U.S.
Most are eaten due to hunger.
Source of information:
1. PP of U.S. and Canada - Kingsbury
2. State bulletin
3. Land grant universities.
4. Effect of PP on livestock - Keeler et al
5. Clinical and diagnostic vet. toxicology - Buck et al
Methods of producing plant poisoning in animals:
1. Eating plant
2. Contact
3. Photosensitization
4. Imparts off flavors and odor to by products
5. Mechanical injury
Plant and animal factors contributing to plant poisoning in animals:
A. Plant factors
1. Soil
2. Climate
3. Stage of growth
4. Part of plant
5. Health of plant
B. Animal factors:
1. Natural resistance
2. Type of digestive system
3. Acquired resistance
4. Breed of animals
5. Age of animals
6. State of nutrition
7. Sex
8. Diet of animals
9. Addiction
Types of toxins present in plants - (See Kingsbury pp. 17-59)
1. Alkaloids - most frequent in plants
eg. Legumes - Croalaria, Senecio, Lupine, Lathyrus etc.
Nightshade family - physalis, nightshade, belladonna tobacco.
Ergot, Larkspur, Jimsonweed, poison hemlock
Most alkaloids end in "ine".
eg. Strychnine, atropine, monocrotaline
Alkaloids have tart taste - Animals deficient in minerals may eat them. Very active in animals but do not produce lesions. Act on CNS - Exception is pyrrolizidine alkaloids.
2. Glycosides: Yield one or more sugars and one or more other compounds (aglycones, toxins) when hydrolyzed (H2O).
Glycosides are bitter and colorless.
Glycosides more widely present in plants than alkaloids but many are non-toxic.
There are several groups of glycosidal poisons.
Included are:
1. Cyanogenic
2. Goitrogenic
3. Irritant oils
4. Coumarin
5. Steroidal
Main one of concern to us is cyanogenic. Toxicity is dependent on both plant and animal factors.
Plant -
Drought
Cold
Trampling
HCN potential of plant
Amount of free cyanide
Speed of release or rate of eating
Animal - Digestive system
Diet
Plants containing cyanide (Handout)
Hay and silage usually safe -
Toxic levels: 20mg HCN/100 gms green plant
(200 ppm)
2mg HCN/K BW/Hour can be detoxified
Test for Cyanide - Picric acid test
5gms Sod. bicarbonate
.5gm picric acid
100.cc H2O
Catalyst-few drops of chloroform
or dilute acetic acid -
Yellow solution to red = pos.
May use 1% sol. Mercuric chloride as preservative.
Method of action of HCN: HCN of plant released by action of B-glycosidase of plant with cyanogenic glycoside of plant to free HCN. Rumen microbes and pH may also break down cyanogenic molecule - HCN combines with cytochrome oxidase in the form of trivalent iron - This combination forms a HCN cytochrome oxidase complex which is quite stable. This trivalent iron does not allow O2 transport from blood to cellular respiration resulting in asphyxiation at the cellular level.
Clinical Signs:
Very acute - no chronic HCN poisoning in animals.
May first find dead animals.
Acute respiratory failure -
Rapid breathing -
Dyspnea - open mouth - salivation -
gasping for breath - Excitement - Hi venous pressure
Staggering - convulsions -
gradual loss of consciousness to state of coma (resembles milk fever)
Blood bright red until just before death -
Bloat -
Treatment -
Therapy is directed at splitting of the cytochrome-cyanide bond and subsequent rapid removal of a cyanide complex. The cyanide- cytochrome complex is broken by the addition of sodium nitrite with the formation of methemoglobin which competes with cytochrome oxidase for the cyanide ion and cyanmethemoglobin is formed. Thiosulfate then reacts with cyanide, under influence of the enzyme rhodanase, to form thiocyanate which is readily excreted in the urine. A recommended therapeutic regimen is the intravenous administration of a mixture of 1 ml of 20 percent sodium nitrite and 3 ml of 20 percent sodium thiosulfate, giving 4 ml of this mixture per 45 kilograms body weight. Commercial solutions for treatment of prussic acid poisoning are available.
Some beneficial effect has been shown for cobalt salts administered for cyanide poisoning. However, the nitrite and thiosulfate remains most effective.
3 parts 20% Sod. thiosulfate } 4cc per 100 lb BW IV
1 part 20% sol. of Sod. nitrite
660 mg/kg BW of Sod. thiosulfate alone IV or
.5 gm/kg of Sod. thiosulfate only at 10cc of a
20% sol./100 lb. BW IV.
First aid - sugars as drench - keep on sternum
Glycosides Cont'd
Goitrogenic substance -
Inhibit the thyroid gland from taking up iodide and thus inhibit
the formation of the thyroid hormone.
Plants contain thiocyanate and L-5-vinyl-2-thiooxozolidone which cause the above. Mainly in lambs.
From -
Brassica genus - Kale, brussel sprouts, broccoli, blindness-rape, collards, cabbage, rutabaga, turnip root.
Irritant Oils - mainly in cruciferae family - mustard oils
(isothiocyanate not goiterogenic) - LD50 of oil .001% of cattle BW.
from: mustard, radish, etc.
Cardiac glycosides: 400 from plants -
from Figwort, lilly, dogbane, foxglove, oleander.
Action - Act directly to increase force of contraction and via vagus to decrease rate - Overdose produce nausea, dizziness, blurred vision, diarrhea.
3. Oxalate: Found in many plants such as Rumex genus and chenopodiaceae family -
Occurs in plants in soluable (Na & K) and insoluable (Ca) forms -
Most injury due to soluable form - certain fungi may form oxalates in moldy hay.
Some plants that contain soluable oxalates:
1. Pigweed
2. Beet tops
3. Lamb quarter
4. Halogeton - 34% DW
5. Oxalis -
6. Rumex
7. Thistle, russian
8. greasewood
9. poke weed
Insoluable: Burn mouth etc. Ca oxalate
1. jack in the pulpit
2. Caladium
3. Elephants ear
4. Dumbcane - Diffenbachia
5. Philodendron
Toxin: Oxalate:
Cause Ca. deficiency or Kidney damage.
10% + DW to cause clinical kidney disease - may be 34% in Halogeton oxalates cause interference with CHO metabolism and is probably a factor in death of animal.
Causes:
1. Hypocalcemia
2. Kidney damage
3. CHO metabolism
Clinical signs: may be sudden onset (2-6 hrs)-over 1200 sheep overnight-
colic, depression, muscular weakness, ataxia, drooping head, get up and down, lag behind flock, prostration with milk fever attitude, Dyspnea, bloody froth from nose and mouth, polyuria and bloat. Some cases show tetney.
Increase: Phosphate, Sodium, potassium, SGOT, Lactic dehydrogenase
and BUN
Decrease: Calcium
Post Mortem: Fluids in peritoneal and thoracic cavities.
Hemorrhages of serous membranes and stomach - Blood in
esophagus and gut - edema of visera - Kidney pale and swollen -
Capsule loose - Cortex striated - due to oxalate crystals (Ca)
Treatment: none specific - Ca gluconate, fluids -
prevention: 5% dicalcium phosphate in pelleted feed -
Free choice 75lb. salt and 25lb. dicalcium phosphate.
4. Resins or Resinoids: not sure of chemical structure -
Based on physical characteristics -
Amorphous gummy, brittle, burn, soluable in organic solvents but not water -
Cause injury to nerve tissue and muscle tissue - very poisonous -
Plants containing resins:
1. milkweed
2. marihuana
3. water hemlock
4. Mt. laurel and Rhododendron
5. chinaberry
etc.
5. Phyto Toxins or Toxalbumins - Protein toxins -
May be most toxic of poisons: much more toxic if injected -
Absorbed from gut more easily than most protein toxins.
Plants containing phytotoxins:
1. Rosary pea
2. Castorbeans
3. Black locust
4. Tung tree
5. Barbadosnut
Toxin may be immunized against -
Cause severe gastroenteritis
Cause lysis and hemolysis of RBC in vitro
Causes ammonia accumulation due to protein breakdown -
One seed may kill adult man if chewed -
If given parenterally is toxic (LD50) at .000,000,01% BW.
May be detoxified with heat.
May be lag period between time consumed and onset of clinical signs.
6. Nitrates: One of the most important of toxic substances in plants -
Found in many crop plants and weeds -
1. Oats
2. Sorghums
3. Rye
4. Corn
5. Wheat
6. Sweet potato vines
and many others (see pp. 42-43 Kingsbury)
Weeds:
1. Pigweed
2. Thistle
3. Jimsonweed
4. Dock
5. nightshade
6. Johnson grass
(see pp 42-43 Kingsbury)
In plants nitrate as KN03 is toxic at 1.5% or in water at 1500+ ppm.
Lower levels may cause other signs as well as abortion - Clinical signs are seen when methemoglobin levels reach 30-40% and death at 80-90%. Nitrate in serum above 25 micrograms/ml and nitrite above .75 micrograms/ml -
Nitrate more toxic in ruminants than mono-gastric animals - 10X
Urea feeding does not affect nitrate poisoning.
Test for nitrate: See Dr. Buck's book
1. eye fluid
2. Urine dipstick
3. Brucine test
4. Diphenylamine
5. Boiling whole blood 2 samples - bilk in H20 bath 45 min.
Nor. blood - brown - pulls away from side of tube and convex
surface
NO2 - blood - Salmon pink - does not pull away form tube surface level or concave
Toxic action - Suffocation - nitrate to nitrite -
Nitrite ion oxidizes ferrous iron of hemoglobin to ferric state forming methhemoglobin.
Methhemoglobin cannot accpet molucular oxygen.
Veripuncture shows dark blood. Turns red on exposure to air.
Clinical Signs: Early onset
Irritant action of NO3 may cause salivation, diarrhea, colic, polyurea, abortion etc.
Mainly signs of respiratory distress due to anoxia. Same as cyanide and also marked cyanosis - Brown blood.
Nitroso compounds - Carcinogenic - occurs in meat curing from nitrite and heat - Reference - Newburne
Nitrogenous gases - Silo fillers disease - Atypical Int. Pneumonia and pulmonary adenomatosis of man - silo fed animals may see idiopathic interstitial pneumonia
Nitrogen dioxide NO2 and nitrogen tetroxide N2O4 -
EPA safe at 10 ppm for NO2 - Have seen 58,500 ppm
Post Mortem: Very Few -
1. Dark blood
2. Cyanosis of MM
3. Reddened mucosa of stomach and gut.
4. Peticial hemorrhage of serous membranes.
Treatment: methylene Blue - give slowly IV
125-250 ml 1% sol IV
20 mg/k - Ruminants
Serves as a reducing agent to convert methemoglobin (Fe+++)
to hemoglobin (Fe++)
Mineral oil orally -
Purge with saline cathartics -
Rumen antibiotics -
Cold water orally -
7. Selenium: Is a component of the soil and is taken up by plants growing there. Soils containing 2+ ppm may produce toxic levels
in plants growing there.
5 ppm plant is toxic.
Some plants require Selenium in the soil in order to grow -
These are obligate species and are referred to as "indicator plants" -
1. Astragalus spp. "Locoweeds" - miserotoxin
2. Xylorrhiza spp - Asters
3. Stanleya - Princes plume
4. Onopsis - golden weed
Facultative or secondary absorbers: Accumulate Se if grown in Se soils but will grow elsewhere. Usual cause of animal poisoning.
Locoweeds also contains toxin that causes teratogenic defects -
Selenium? - Also contains nitro compounds that cause poisoning -
Deficiency also causes disease.
Single dose - toxic at 1-5 mg/k BW
Diet of 25ppm or greater will cause acute poisoning.
Seen as both acute and chronic forms.
Acute: Vary much like any heavy metal poison eg. As.
Signs include changes in gait and posture - ataxic and depressed -
Diarrhea
Dyspnea - Blood in nasal discharge
Polyuria -
May show colic and bloat
MM cyanotic
Dialated pupils
May have myocardial failure
Post mortem: Congestion, severe enteritis, widespread hemorrhage,
and degeneration of liver and kidneys.
1st Chronic Syndrome: Blind staggers organic sel.- aimless wondering - walk over obsturctions - slow intake of Se.
Permanent weakness , dyspnea, cyanosis, respiratory failure
and death.
2nd Chronic Syndrome: Alkali disease -
chronic intake of forage or grain crops of 5-40 ppm over weeks to months Signs are Dullness, emaciation and lameness due to hoof deformities
There are also erosions of articulation of joints of the legs.
Snow shoe hooves. Animals may graze from kneeling position -
Loss of hair from mane and tail.
Swine - failure to gain - alopecia - >SPPM - 40 PPM
Death, hoof deformity
Diagnosis: Requires lab help -
Differentiate from frostbite, Fescue, chronic ergotism and chronic laminitis.
Treatment: not much to do -
Diet high in protein seems protective -
Arsenic may be preventative - 40 PPM in salt
Iodine has a catalytic effect -
8. Molybdenum:
Found in certain soils and may be taken up in plants in toxic concentrations. Found in US in Calif, Nevada, Florida and few other places. First recognized in England called "Teart".
Molybdenum and copper are antagonistic in diets - both are strongly influenced by inorganic sulfate -
Normal molybdenum and low copper may see molybdenum toxicosis -
Normal copper and low molybdenum may see copper poisoning.
Toxicity: Most likely seen in alkaline soils. Soils with more than 5 ppm toxic - Hi organic matter in soils may be toxic at 3 ppm. Sulfates enhance secretion of molybdenum in urine.
Legumes take up more than grass. +/- 20 ppm in forage may be toxic -
Clinical signs: Usually seen in ruminants (cattle)
Main classical sign is greying of dark hair coat -
No melanin in absence of copper - Takes about 1 month for signs to develop.
1. Diarrhea - more severe in calves
2. Anemia
3. Stiffness
4. Reproduction difficulties
Postmorten lesions: Copper and molybdenum
Microcytic hypochronic anemia rarefecation of bone
No diagnostic lesions of Molybdenum
Prevention & Treatment:
Add copper to diet - CU:MO level > 2:1 Need >7PPM in ration
Injectible copper glycernate - good for 3-9 months -
CuSO4 in salt or water -
Acid soil reduce plant uptake
Legumes take up more than grasses
9. Compounds causing photosensitization:
May occur by 2 methods.
1. Photodynamic substances in plants -
e.g. Buckwheat - Hypericin (Hypericum perforatum)
St.John's Wort - Fagopyrin (Fagopyrum sagittatum)
Blue Green Algae - Phyocyan
Probably others also.
2. Hepatogenic phtosentization - many plants
e.g. clover, vetch, lantana, crotolaria, ceral grain,
grasses and many others.
3. Contact dermatitis - unknown
Plants causing mechanical injury - self explanatory
Examples:
1. grain owns
2. spear grass
3. cockle burs
4. squirrel tail grass
MAJOR TOXIC PLANTS AND THEIR TOXIC EFFECTS
1. Algae: Blue Green Algae, Several different genera and specie - cyanobacteria new genus? most common ones refered to as "Annie, Fanny and Mike". This refers to genera eg. Anabaena flos aquae, Anphanizomenon flos aquae and Microcystis aeruginosa (Anacytis Cynea).
Factors associated with algae poison.
Toxic factors: "Fast death factor" - Microcystin cyclic decapeptide.
"Slow death factor" - Once thought to be due to bacterial toxins, now thought to be due to smaller quantities of microcystin. Chronic form with photosensitization - Photodynamic substance in algae called phyocyan and liver damage due to microcystin. All animals and man may be poisoned. City water systems.
Symptoms: May be very rapid - +/- 30 min.
Mainly respiratory due to action of toxin causing a post sympatic neuromuscular blockade and death by respiratory arrest.
Resembles cyanide and/or nitrate.
Resp. distress
Muscle twitching
Staggering - coma and death
Later if live - Abdominal pain, diarrhea
Later still - Liver damage and icterus and photosensitization
Post Mortem:
Blood dark and not clotted
Petechial hemorrhages of Heart and Lungs
Liver discolored and swollen - mottled and yellowish
+/- Severe gastroenteritis with +/- Hemo.
Control: CuSO or other algaecides - Remove animals from source -
Watch for accumulation along shore line and ponds.
Treatment: Sod. Thiosulfate and Sod. nitrite -
20% sol. - 3 parts Sod. thiosulfate/1 part Sod. nitrite -
4cc/100 lb - IV.
Treat diarrhea and photosensitization
2. Bracken Fern: Pteridium Aquilinum -
Perennial herb - leaves (fronds) are triangular in shape with bifurcations along mid rib (differs from most ferns). May have reproductive spores along undersurface of fronds.
Toxic factors: At least two or more. In monogastric animals there is thiaminase which causes marked signs of B1 deficiency. This does not occur in ruminants. In ruminants there is a depression of bone marrow activity. May be carcinogenic -
Bladder and GI tract - may cause blindness in sheep.
In monogastric animals:
eg. horses:
Pathogensis: After prolonged ingestion there develops clinical signs of a thiamine deficiency. See clinical signs.
In Ruminant: Large amounts causes bone marrow depression -
Hemorrhage due to depressed platelet count and heparin from mast cell destruction - infection due to low WBC. In sheep may see retinal degeneration. May see tumors in both ruminants and monogastric animals.
Clinical signs - Monogastric eg. horses
Fern staggers - Loss of condition - Brace themselves to remain
upright - Muscle tremors - Cardiac arrythmia - Low B1 blood
levels - High pyruvate - Course 2-10 days.
Ruminants: Requires prolonged ingestion -
Toxic principle not known - causes blood dyscrasias resulting in hemorrhages and ulcers. May cause tumors of bladder.
temperature - Nasal hemorrhage - Anorexia - petechial hemorrhage of visible mucus membranes - Hematuria - Fly bite hemorrhage - Edema -
Blood changes:
Low granulocytes including platelets
Low RBC
Relative hi lymphocytes
Sheep are also affected plus retinal damage
Diagnosis: CBC - PM lesions - clinical signs - clot retraction test - pyruvate levels - B1 levels. Cruise pasture and examine hay -
Differential:
Blackleg
Oak and acron poison
Anthrax
Sweet clover and Warfarin
Anaplasmosis - Radiation - Prolonged sulfur therapy -
Trichlorethylene extract soybean meal - Benzene -
Therapy:
Thiaminase - Give high doses of B1 - 100-400/day/1,000 lb Eq - IV or
IM - Supportive therapy - Be sure to remove source
Ruminants: D.L. Batyl Alc. 1 gm/day/cow
Protamine sulfate - 10 ml of 1% sol. IV and Blood - A B
in all cases - Whole blood transfusion -
Prognosis in ruminants: If platelet count is less than 50,000-poor
J. So. AFVMA 39(3):91-199, 1968.
Other plants containing thiaminase:
1. male ferns - Dryopteris felix-mas
2. Horsetail fern - Equisetum arvense and E palustre
Equine: usually E arvense in hay - Toxicity not lost by aging
Signs of B1 deficiency -
Cattle & Sheep: Usually E palustre - From grazing or hay.
Toxicity in cattle and sheep not due to Thiaminase -
Equisetum also contains
1. Silica
2. Aconitic acid
3. Palmitic acid
4. Nicotine
2 alkaloids - equisitine and palustrine
6. DMSO
Clinical signs ruminants:
Nervousness and excitability
loss of condition
weakness
diarrhea
decreased milk production
Treatment: Remove from diet
3. Ergotism - In S.E.U.S. is refered to as Dallis grass poisoning
(Paspalium dialatatum) - Produce acute form - In western U.S. have
chronic form from growth on wheat, rye, barley etc.
Acute form due to ergotfungus Claviceps paspali
Chronic from due to Claviceps purpura
C paspali also grows on Argentina bahia grass (not pensacola)
Toxins: Ergotalkloids: Ergotamine, ergotoxine, and ergometrine. From these alkaloids come various amines including LSD. In my opinion the cause of the acute form. Vasoconstrictive alkaloids cause dry gangrene of the extremities and abortion in C purpura - Toxins causing the acute form refered to as Tremogens - from various molds ie penicillium.
Found in crab grass (Digitaria) - chronic poisoning in cattle on rye grass - Bermuda grass staggers
Ergotism in man:
Chronic or acute - Salem, Mass. witch trials -
Clinical signs: Chronic -
gangrene in cattle and maybe acute signs and abortion -
Sheep and goats - ulceration of GI tract, diarrhea. One instant of
gangrene in goat kids -
Pigs - Agalactia, abortions, small liters and neonatal deaths.
Clinical signs: Acute (Dallis grass poisoning)
1. Darrangement of consciousness
2. Hyperirritability, aggressiveness
3. Convulsions
4. Unflexed forelegs - Goose stepping
5. Discoloration of hair of face and forelimbs
Differential: Fescue foot, Selenium poisoning and Frost bite -
Control - Over graze - Cut heads off grass - Remove cattle -
Treatment: Remove source - If chronic can't do much - AB and
supportive. If acute may tranquilize or sedate - Ca gluconate -
Need not do anything. Explain to owner - Care during convalescence.
4. Bitterweed: Helenium Amarum
Local plant representing the plants of the western U.S.
The western plants referred to as Sneezeweeds
H Autumnale
H Hoopesii
H Nudiflorum
And others of different genera also called bitterweed ie. Hymenoxys -
Hymenoxys odorata causes a factor X deficit in sheep and subsequent hemorrhage.
Description and pictures of plants -
1-11/2 feet tall - fine leaves - odor - taste - winged stems -
disc flowers - ray flowers.
colors of each -
Aut - yellow and yellow
H A. - yellow and yellow
H H - yellow and yellow
Hymenoxys - yellow and yellow
H Nud - yellow and purple disc
Toxic principle - Sesquiterpene lactone
H Autumnale - Helenalin
H Amarum - Tenulin
H Hoopsii - Hymenovin
Hymenoxys odorata - Hymenovin - causes factor X deficiency
Older literature and some recent may refer to all toxins of this group as a glycosid called Dugaldin.
Animals may be poisoned on one dose of +/- 5% B.W. but are usually
poisoned due to prolonged ingestion -
Other quantities
Clinical signs: Mainly in sheep -
Called Spewing Disease
Obviously sick - Lag behind herd
Must rest frequently - Incoordinated - muscle tremors -
Vomiting (projectile) - stained wool form vomitus
PRT - usually normal - up if pneumonic
Bloat - Diarrhea
May have gangrenous pneumonia
PM Lesions:
Gastroenteritis -
Gangrenous pneumonia
Congestion and necrosis of Liver and Kidney
High liver enzyme - SGOT
Presence of plant in stomach
Therapy: Not much - Remove from source - prevent by feeding mineral
supplement of 75 lb salt and 25 lb Dicalcium phosphate - High protein
is protective - also Sodium sulfate
5. Chinaberry: Melia Azedarach
Asiatic import -
Introduction into South after Civil War. Seems more toxic in other parts of world.
Toxicity is unpredictable - Why?
Description of tree:
Umbrella shaped - 20-40 feet tall
Leaves bipinnately compound - Leaflets serrated deeply - Small lavender flower petals about 1" across. Fruit is a drupe - green early and yellow when ripe - about 1/2" across -
Animals usually poisoned when fruit is ripe.
Suggested MLD for pigs - 150 gm berries to kill 50 lb pig -
.5% of BW
Toxin - In all parts of plant but mainly the seeds - Suggested to be a resin and an alkaloid.
Good Vermafuge
Clinical signs: 2 syndromes
1. Enteric
2. CNS
May be due to quantity ingested.
CNS - Running fits, paddling, circling, weak heart and dyspnea -
Enteric: Nausea and Vomiting
+/- Diarrhea - may be some blood (fresh)
Chinaberries in vomitus
Incoordinated
Course of disease short - 1 hour - 3 days - Usually die or recover in 24 hours.
Usually effects pigs but may see in people, birds - Robins - cattle - horses. Epidemiology of poisoning.
PM lesions: Enteritis - Hemorrhage - berries in gut - Fatty changes in liver and kidney.
Therapy: GI protectives - AB - Resp. stimulants ie. Caffeine -
Purge, Lentin - 1-2 cc 150 lb Hog.
6. Oleander: Nerium oleander
Description: Fresh Specimen and color picture -
Introduced from Mediterranean - Is grown as an ornamental here
and in southern and southwestern U.S. Is not cold hardy - shrub
up to 20 ft tall.
Leaves are characteristic - prominent midrib with parallel venations - Look and feel leathery - whorled - 4-12" long - Laneeolate - Flowers are white to red - May have small seed pods.
Toxicity: Usually results from pruning - people from sucking flowers - Does not loose toxicity upon drying - Smoke from burning is toxic (eyes) - used as meat skewer may cause poisoning - Plant is very poisonous - 15-20 leaves to kill a horse or cow - One to kill human - Fowler gives 45.5 mg/lb of leaves. Toxin is a glycoside - 2 of them - Oleandroside and nerioside - closely related to digitalis - Has been used therapeutically - Is used in some countries to commit suicide. Action of Toxin - Heart failure due to paralysis of muscle - Causes heart block - Causes severe gastroenteritis -
Signs in Animals:
1. Abdominal pain, colic
2. Vomiting
3. Diarrhea - +/- hemorrhage
4. Rapid pulse
5. Temperature normal
6. Sweating
7. Cold extremities
8. Dialation of eyes
9. Goat - continued urination
In man additional signs are - Dizzyness, Drowsiness, weak and irregular heart; dyspnea and coma.
Respiratory signs seem to predominate in cattle - pulmonary edema and froth from nose.
Relative short course, 1-2 days
PM lesions: Gastroenteritis - Free hemorrhage on occassion -
Petechia of organs and membranes.
Microscopic changes in kidney and liver.
Brain hemo.
Pulmonary edema - Free fluids in air passages
Leaves in stomach.
Diagnosis: Heavy metals - other plants - mainly inquiry
and detective work.
Therapy: none specific
Antidiarrheal - supportive - AB - May use Digitalis antidote -
Potassium chloride and procainamide -
Atropine - Dogs .035-.070 mg/K IV or IM until heart rate is up then propranolol (Inderal) at .9-1.1 mg/K IV or IM to effect maybe several days -
Ref. Archives Internationales de Pharmacodynamie et de Therapie -
Vol 189 - No. 1 - Jan. 1971.
7. Tung Tree: Aleurites fordii
Oil used as base for paints - Best paints - not widely used now - Isolated trees or abandoned orchard -
Description - Plants and slides
Leaves - simple - ovate - amy have 2 deep indentations near apex - oil glands at base of leaf - Palmate venation - nuts, 2-3 inches in diameter with 3-7 white seeds - Tree 15-20 feet tall. Introduced from China - High in portein - Tried to use as animal feed.
Toxic Principle - All parts of plant - most in fruit but foliage eaten more often.
Two toxic components -
Saponin and toxalbumin (protein toxin). Main clinical signs are due to the saponin - Usually caused after pruning or after wind storms and from fallen fruits - 1 3/4 lb. foliage will kill 500 lb. steer - U. of FL.
Clinical Sign: Severe hemorrhagic gastroenteritis - onset may be sudden or there may be a 3-7 days lag period - important in history - man the onset is sudden - Both man and animals show nausea, cramps, weakness (extreme), burning diarrhea and if prolonged dehydration and shock. In chronic or prolonged poisoning of cattle may show additional symptoms - Anorexia - Rumen atony - depression and listless - excess salivation - nasal discharge - cracked muzzle.
Post Mortem lesions: Mainly hemorrhagic gastroenteritis especially of abomasum and first 6 feet of duodenum and large intestine - may be some ulcers and rectal protrustion - congestion of various abdominal organs - fluid in abdominal cavity.
Therapy: No antidote - Correct dehydration - IV fluids and electrolytes - AB and protective for GI tract - May do rumenatomy or flush. For chronic or convalescent period - Stimulate rumen movement - Try to improve appetite - IV fluids for energy.
8. Caley Pea or Wild winter pea: Lathyrus Hirsutus
One of several of this genera that cause lathyrism in man and animals. There is extensive literature relating to man. Requires a diet consisting mostly of the pea for weeks to months. Is closely related to early European history but is now seen mainly in 3rd world countries and in asiatic countries during famine. Interesting write up in Kingsbury.
Caley Pea: Lathyrus hirsutus -movie -
Legume vine - Looks like vetch - 1-3 foot long vines - winged stems - compound leaves. Tendrils - flowers are pea like - fruit a pod - stems hariy -Grows well on poor soil and in very nutritious when not seeding.
Toxic Principle of Lathyrus - but not sure of caley pea - The following are Lathyrogenic Amino acids - may be refered to as lathyrogenic nitriles:
1. B - Aminoproprionitrile - Osteogenic
2. A - Amino - B - Oxalylaminoproprionic acid neurogenic
3. L - a, gamma - Diaminobutyric causes ammonia poison like urea.
Clinical signs of Caley Pea poison: See signs only during seeding stage - May develop signs in 5 days - Looks soimething akin to laminitis and/or tying up syndrome - at some period like acute ergotism - very reluctant to move - May be excitable - muscle soreness with lameness - no local pain - Horses - like stringhalt - pharyngeal paralysis - "Roaring" -
Lesions: no gross - boney change in man and rats - Histopathology
Degeneration of motor tract of spinal cord.
Therapy: None needed - Remove and recovery - In man paralysis is permanent.
Cyanide plants:
See Glycoside for action of toxin etc.
Large group of plants with cyanogenic potential. See list
Ones in this area -
9. Wild Black Cherry: Prunus serotina
Tree - may be up to 90' feet - Bark rough on main trunk - rather smooth with horizontal striations - small
The ear should be examined with a scope and a swab taken if an infection is suspected. Many dogs have vestibular syndrome with no typical signs of ear inflammation such as head shaking, scratching of the ear, inflamed ear canal or inflamed eardrum. Other investigations such as X-rays, CT scans, or best of all MRI scans [see specific fact sheet - neuro investigation] can help to detect disease located behind the eardrum such as a deep ear infection or a tumour. CT and MRI scans of the brain are also useful for detection of brain disease. Your vet may also want to collect a sample of the fluid that bathes the brain and spinal cord (CSF) [see specific fact sheet - neuro investigation] for further tests.
