Identifying poisoning signs, sequelae

Identifying poisoning signs, sequelae

Oct 01, 2007

This is the third in a series of articles on toxic plants that are likely to poison horses in North America. This installment covers myotoxic plants, those that damage muscle and the cardiovascular system.

Horses find many of these plants unpalatable, but, when feed selection is restricted or when toxic plants are included in prepared feeds, many horses eat them and become poisoned. Some are very palatable ornamentals; animals are poisoned whenever they are allowed access to the plants or to plant clippings.

Following are some common myotoxic plants, for which we outline the clinical signs, lesions and sequelae of poisoning and present current recommendations for treatment and prognosis for poisoned animals.

Trematol-containing plants

Photo 1a: Eupatorium rugosum (white snakeroot, richweed, white sanicle, snakeroot) is a perennial that grows from 100 cm to 140 cm tall. The leaves are ovate and opposite with long petioles. The leaf margins have marked serration with three distinct veins and pointed tips. The flowers are tubular and white. White snakeroot grows in low, moist areas along waterways and in dense woodlands. Photo 1b: Haplopappus heterophyllus or Isocoma pluraflora (rayless goldenrod, jimmy weed, burrow weed) is an erect, branched perennial that grows up to 1 m tall. The leaves are linear and alternative with a sticky surface. The flowers are yellow with small clusters of seven to 15 terminal flowers. Rayless goldenrod is commonly found in alkaline soils in arid rangelands of Texas, Arizona and New Mexico.
Eupatorium rugosum (white snakeroot, richweed, white sanicle, snakeroot — Photo 1a)

Haplopappus spp. (rayless goldenrod, jimmy weed, burrow weed — Photo 1b)

White snakeroot poisoning, or "milk sickness," is an important historical disease that in the 1800s probably caused half of the deaths in early settlers in Illinois, Indiana, Kentucky, North Carolina, Ohio and Tennessee. Entire settlements were abandoned due to the unexplained epidemic deaths of stock and people. Although various causes, including infectious bacteria, were proposed, it took nearly a century to positively identify Eupatorium rugosum as the cause.

Though animal-husbandry improvements, feeding practices and quality-assurance programs for dairy products have eliminated human exposure, poisoning in livestock continues to be a problem throughout the Midwest and East.

Though less widely distributed, rayless goldenrod contains similar toxins and consistently causes problems in the Southwest.

Both white snakeroot and rayless goldenrod are toxic year round and probably are toxic in stored feeds. Most poisoning occurs in summer and late fall when other forages are exhausted.

The toxin, trematol, has a long excretion time, allowing it to accumulate until a toxic dose is obtained. Trematol is highly lipid-soluble and is transferred in the milk. Poisoning in nursing neonates and people that drink the contaminated milk is commonly reported even with no signs of toxicity in lactating cows. Doses of 1 percent or higher body weight of the plant are toxic if ingested over one to three weeks.

Clinical signs of poisoning include incoordination, muscle tremors, elevated heart rate, muscle weakness, congestive heart failure, jugular pulse, tachycardia, cardiac arrhythmias, profuse sweating, pitting edema and quidding.

As these plants directly damage muscle, especially heart muscle, poisoned animals often are cardiac cripples with decreased work capacity. More information is needed to determine long-term effects and costs of sublethal poisoning.

Clinical blood changes are those indicative of muscle damage (increased activities of many serum enzymes that leak into the blood from damaged muscle — CK, AST and LDH).

Most animals have increased myoglobin in the blood and urine. Post-mortem findings include patchy necrosis of heart and skeletal muscle, liver necrosis and myoglobin-induced kidney disease.