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LIVER DISEASE INDUCING PLANTS
Surprisingly, few plant toxins cause liver disease, probably because the liver has tremendous capabilities for detoxifying many compounds that are absorbed from the gastrointestinal tract. Furthermore, the liver has a great reserve capacity and will continue to function at near optimal levels until approximately 80% of it is destroyed. Only then will clinical signs of liver failure such as weight loss, depression and abnormal behavior, icterus, bloody urine, anemia, and photosensitization be observed. Photosensitization occurs because of the damaged liver’s inability to eliminate the body’s normal breakdown products of plant chlorophyll, which then accumulate in the blood. When these photosensitive substances are exposed to sunlight, they fluoresce, causing the skin damage responsible for secondary or hepatogenous photosensitization. As described in the previous section, photosensitization may also be caused by the ingestion of plants, such as buckwheat (Fagopyrum esculentum) or St. John’s wort (Hypericum perforatum), that contain photosensitive pigments but do not cause liver damage. Because signs of secondary or hepatogenous photosensitization, or other clinical signs of liver disease, appear only when a majority of the liver’s functions are destroyed, horses showing clinical signs as a result of any plant-induced liver disease have a guarded to poor prognosis.
The most important plant toxins responsible for causing secondary photosensitization, as well as other manifestations of liver damage, are pyrrolizidine alkaloids.
PLANTS CAUSING PYRROLIZIDINE ALKALOID POISONING
Senecio
Hound's Tongue
Fiddleneck or Tarweed
Rattlebox or Rattlepod
Effects of Pyrrolizidine Alkaloids
Variations in the PA content of plants, the quantity eaten, and susceptibility of individual animal species result in wide variations in the severity of PA poisoning in animals. Flowers tend to contain the greatest amount of the alkaloid, although seeds of rattlebox or rattlepod, fiddleneck, and tarweed contain high levels of PA.
Pigs are the most susceptible to the effects of PA, followed by poultry, cattle, horses, goats, and sheep. Sheep can eat approximately 20 times the amount of Senecio it would take to poison a cow on an equivalent bodyweight basis. Horses show about the same susceptibility to pyrrolizidine toxicosis as do cattle. The chronic lethal dose of dried tansy ragwort (S. jacobaea) in cattle is only 0.02 to 0.05 mg/kg body weight fed over several months. This would equate to a 1000 lb (450-kg) horse eating about 5% of its body weight of green tansy ragwort over a period of 1 to 3 months.
Fortunately, herbivores will not readily eat plants containing PA unless they are forced to do so through lack of other feed. However, the dried plants, which have only a minimal reduction in their alkaloid content, are more palatable, making them a particular risk when present in hay. Although acute poisoning and death can occur from a few days’ consumption of plants high in PA, chronic poisoning is more common. The effects of PA are cumulative, so symptoms of liver disease and photosensitization may not appear for many months after animals have eaten toxic quantities of PA-containing plants. This makes identification of the suspected poisonous plants difficult, since the plants will often not be present in the pasture or hay when clinical signs become evident in the horse.
Pyrrolidizine alkaloids are readily absorbed from the digestive tract of horses and are converted in the liver to toxic substances that bind to cellular proteins, causing rapid liver cell death. Similar cellular damage may also occur in the kidneys, intestinal tract, and lungs. Pyrrolizidine alkaloids may also induce cancer, birth defects and abortion. Although secretion of PA in mare’s milk has not been established, there is potential risk to the suckling foal, as PA has been shown to be present in small quantities in the milk of cows and goats fed tansy ragwort (Senecio jacobaea).
Acute PA poisoning occurs occasionally in horses that ingest large amounts of alkaloid-containing plants over a few days. Affected animals may show only depression, coma, and death as a result of severe liver damage.
Chronic PA poisoning, which is more common, is characterized by irreversible liver disease clinically manifested by one or more of the following clinical signs: weight loss, nervous signs, icterus, anemia, bloody urine, and photosensitization. Nervous signs due to liver damage are often the first clinical indication of PA poisoning, and may include drowsiness, head pressing, blindness, aimless wandering or ‘‘walking disease,’’ frequent yawning, and incessant licking of objects. The first sign of PA poisoning in a small percentage of horses is difficulty in breathing in, destruction of red blood cells and a bloody urine. Photosensitization may occur in some horses that have areas of nonpigmented skin. In these horses, severe dermatitis that develops when the horses are exposed to sunlight results from the liver’s failure to excrete phyloerythrin, a photoreactive by-product of chlorophyll breakdown. Photosensitization is described earlier in this chapter in the section on primary photodermatitis.
Pyrrolizidine alkaloid poisoning is usually not suspected and, therefore, not detected until severe liver damage has occurred and clinical signs of liver failure are evident. At the present time, the only widely available and reliable means of confirming PA-induced liver failure is detecting specific microscopic alterations in a liver biopsy. The only other disease to mimic these alterations is aflatoxin poisoning, which occurs when horses eat moldy grains containing aflatoxins, but which, as described in Chapter 19, is uncommon in horses.
Horses showing signs of liver disease should be fed as described in that section of Chapter 17. However, the prognosis is poor for confirmed cases of PA poisoning.
Animals showing signs of photosensitization should be provided shelter from the sun and preferably kept stalled completely out of sunlight. Sunlight through glass will not induce photosensitization as it blocks ultraviolet rays. Gentle daily cleaning of the affected skin with a mild organic iodine antiseptic solution will aid in the healing process. Antibiotics may be indicated in cases where there is severe secondary bacterial infection of the skin.
NONPYRROLIZIDINE ALKALOID LIVER POISONING PLANTS
Indigo
Alsike Clover and Klein Grass
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