Mary C. Smith DVM
Poisonous Plants 647 - Fall 1999


Kingsbury, pp 33-36
Radostits, Blood and Gay 8th, pp 1539-1543
Kimberling's 3rd edition of Jensen's Diseases of Sheep, pp 245-248
Keeler et al., pp 139-145

A. Oxalic acid

COOH is corrosive because acid, but usually the problem is

Soluble oxalates:

1) potassium acid oxalate

2) sodium oxalate

3) ammonium oxalate

Insoluble oxalates include calcium and magnesium salts

B. Sources:
1. Ethylene glycol (antifreeze) is metabolized to oxalates - kittens and puppies at risk
2. Plants - usually 10% or higher oxalic acid on a dry weight basis - most are palatable.
a. oxalate ion, sap pH of 6
Halogeton - can be 34% soluble oxalates on DM basis
Sarcobatus (greasewood) - 10 to 20% oxalates
Amaranthus - usually nitrates
b. acid oxalates, sap pH 2
Rumex (dock)
c. both or unspecified
Rheum (rhubarb) - petiole contains malonic acid
Beta (sugar beets) at green and leafy stage, also may have toxic level of nitrates
Aspergillus - oxalate producing fungi may elevate oxalate content to toxic level in some moldy feeds.
d. calcium oxalate crystals - insoluble, but once theorized that sharp, cause intense burning if bite plants. Now suspect proteolytic enzyme.
Arisaema (Jack-in-the-pulpit)
Dieffenbachia (dumbcane - house plant)
Symplocarpus (skunk cabbage)
Philodendron - house plant
Caladium - house plant
C. A large amount of oxalates must be eaten to cause poisoning because most either
1. made insoluble as calcium oxalate, if sufficient calcium in diet or
2. digested to bicarbonate; rumen can handle this metabolism better than simple stomach, also increases in ability to metabolize oxalates with continued ingestion - adapts. Oxalate metabolized to formate and then to CO2.
D. Results of oxalate poisoning vary according to the ion.
1. GI irritation if eat large amount. Ex. experimental diets with more than 6% oxalates cause diarrhea in sheep - secondary fungal invasion of rumenitis and hepatitis lesions may follow.
2. Removal of calcium from blood - precipitated as calcium oxalate, leads to a hypocalcemic muscle weakness syndrome with hemorrhages (Na oxalate is an anticoagulant because it binds calcium). Hypocalcemia contributes to great decrease in GI motility. Oxalates also have effect of immobilizing calcium in the gut if already on calcium deficient diet.
3. Acute nephrosis and uremia if calcium oxalate crystals precipitate in and block many tubules of the kidney - cumulative damage is possible; more tubules blocked with further exposure.
4. Oxalate calculi in kidney, bladder, urethra if smaller amounts over longer time.
5. Osteodystrophia fibrosa - metabolic bone disease; horses in Australia grazing an introduced grass (Setaria sphacelata) which contains ammonium oxalate and is also low in calcium - interference with calcium metabolism. No such chronic syndrome reported in sheep.
E. Signs for
1. diarrhea. Colic in Halogeton poisoning.
2. dullness, sheep lags behind others, head drooped at 45 degrees. Signs occur 2-6 hours after ingesting toxic amount - get weakness, muscle tremors, staggering, go down; rapid weak pulse, rapid labored respiration; rumen atony, dilated pupils; hemorrhages; may see excess salivation, froth at mouth. Coma and death about 10 hours after ingestion. Must differentiate in sheep from
a. hypocalcemia at parturition or with starvation or forced exercise, also lactation tetany.
b. toxic indigestion - history of overload of grain - splashy, atonic rumen; cold, comatose, hypocalcemic.
Pregnant and lactating animals are most susceptible to oxalates because greater demand for calcium
3. and 4. depression, anuria, may strain to urinate if calculi in urethra. Foul smell from mouth when uremic. Urine may be red-brown.

F. Clinical pathology
1. serum calcium - total may be normal; just unavailable because tied up as calcium oxalate. Ionic, available calcium may drop to 20% of normal at time of death
2. better to assay suspected plant for oxalate level.
3. albuminuria, hematuria from kidney damage. Elevated BUN, creatinine.
G. Postmortem - no characteristic signs.
1. cystitis, urethritis, ureteritis
2. calculi in urethral process of ram, sigmoid flexure of bull and ram.
3. swollen kidney, dark red cortex and medulla of kidney separated by line of gray where oxalates accumulated. Histologically, see birefringent crystals in renal tubules - small, rhomboid, nearly transparent crystals or rosette of crystals occluding lumen of tubule. Crystals in rumen wall also.
4. splashy hemorrhages due to anticoagulant action.
H. Treatment
1. calcium borogluconate: 50-100 ml in sheep, 500 ml in cows, IV or SC. Usually not enough to save animals because imbalance of other ions has occurred. Na+ and K+ liberated when Ca++ precipitated, may get alkalosis. Also oxalates have interfered with enzymes activated by calcium and magnesium, thus interfering with energy metabolism. Halogeton sheep don't respond to calcium, but still try.
2. fluids to flush kidneys - dextrose solution IV, forcefeed water (does save experimental Halogeton sheep).
I. Prevention
Ruminants safer than monogastrics physiologically (detoxify, making carbonates and bicarbonates in the rumen) but management endangers. Sheep are kept on that kind of range, readily eat the oxalate plants.
Sarcobatus eaten in the spring when sheep unaccustomed to it.
Halogeton most toxic with rapid growth in autumn after dry summer.
Sheep vulnerable, according to Jensen, when eat indiscriminately:
a. trailing thought dense growth of oxalate plants
b. unloaded into dense growth of oxalate plants
c. autumn and winter when snow covers other forage
d. watering thirsty animals where plant abounds
1. Salt hunger may predispose, so supply ample salt in diet.
2. Ample water for kidney function
3. Safer if full rumen, so don't trail hungry sheep
4. Keep off these pastures in the West, don't feed rhubarb leaves and sugar beet tops in the East.
5. Can become adapted: switch slowly to high oxalate diet if nothing else to feed; thin stand of Halogeton. Low dose for 4 days allow for adaptation, fatal dose is increased by 30%. Slow grazing safer than rapid consumption.
6. Prophylactic dicalcium phosphate during times of exposure;
a. 1/4 - 1/2 pound alfalfa pellets with 5% dicalP/day (protects 2-4 hours)
b. salt free choice that is 25% dicalP
c. alfalfa hay
J. The plants and kodachromes thereof
1. Sarcobatus - perennial shrub
2. Halogeton - introduced from Russia, first found in early 1930's. Grows on barren soil, is adapted to deserts, accumulates water in sausage-like leaves by being hypertonic with sodium oxalate. Grows fast, seeds heavily - 1 plant produces 50,000 seeds. Annual, but seeds may survive 5 or more years. Bulldozing great for the plant! Don't spray either. Must control by competition with perennials. Seedlings prostrate with 4 main branches (cruciform) and taproot. As many as 1200 sheep have been poisoned at one time.
3. Rumex - curly broad leaf, 3-winged seeds dark brown color in fall. Rarely high enough level of oxalates to kill.
[4. Oxalis pes-caprae (Soursob) in Australia - acid oxalates, serious problems; acute hypocalcemia and tetany, subacute stiff gait or recumbent, chronic kidney damage.]
5. Rheum - rhubarb, oxalates in blade. Livestock or people killed. Few leaves won't hurt a horse, wheelbarrow full can kill pigs.
6. Arisaema - jack-in-the-pulpit. Calcium oxalate crystals. Hooded flower, red berries, 3-part leaf outlined by marginal vein. Protects plant. Poisonings from children's dare.
7. Dieffenbachia (dumbcane) ornamental in hotel lobbies, restaurants. Actually a proteolytic enzyme in the sap causing irritation, edema. Swelling in pharynx may hinder respiration and thus kill. Tongue can't move, hence the name. Cats chewing on house plants at risk.
8. Symplocarpus - skunk cabbage to easterners - in wet woods, learn only to distinguish it from Veratrum (called skunk cabbage by westerners). In the spring its hooded purple flower generates enough heat to melt snow around it.
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