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SUDDEN DEATH INDUCING PLANTS
Sudden death of horses due to plant poisoning with few or no previously occurring clinical signs is relatively uncommon. When it occurs, it is important to determine the cause as quickly as possible so further losses can be avoided. Sudden death due to plants most often occurs when horses have been placed in situations where they have been compelled to eat unusual plants in hay or overgrazed pastures. Unintentional poisoning may occur when garden clippings or prunings are fed to horses, or when horses are tied or placed in pens adjacent to plants to which they are unaccustomed and which they would otherwise leave alone. There are three major types of plant toxins that may cause sudden death: cyanogenic glycosides, cardiac glycosides, and alkaloids.
Cyanide-Induced Sudden Death:Plant Causes of Cyanide Poisoning
There are approximately 1000 different plants known to contain cyanogenic glycosides with the potential of producing cyanide poisoning in animals. However, relatively few of these plants are common causes of cyanide poisoning in animals. Some plants with a potential for cyanide poisoning, such as sorghums, clovers (Trifolium spp.), and corn (Zea mays), are commonly grown as feed for animals. These can be safely used provided they are not grown under the circumstances in which they become toxic.
Serviceberry or Saskatoon Berry
Wild Blue Flax
Western Chokecherry
Elderberry
Sorghum Grasses
Arrow, Pod, or Goose Grass
Effects of Cyanogenic Glycosides
Plants rarely contain free hydrogen cyanide (hydrocyanic or prussic acid) but rather have one or more complex cyanogenic glycosides in their leaves and stems. When acted upon by plant enzymes, these glycosides form hydrogen cyanide. This enzymatic conversion occurs when plant cells are damaged or stressed as they are chewed, crushed, droughted, wilted, or frozen. Application of herbicides and nitrate fertilizers may increase the cyanogenic glycoside content of plants. Generally all parts of the plant are toxic, with the young rapidly growing portion of the plant and the seeds being most toxic. Drying of the plant reduces its cyanogenic content.
Ruminants are more likely to be poisoned by plant cyanogenic glycosides than are horses and other simple-stomached animals, because the less acidic rumen (pH 6–7), with its high water and bacterial enzyme content, optimizes the rapid hydrolysis of the glycosides to cyanide. Animals that drink water immediately after eating cyanogenic plants enhance the hydrolysis of the glycosides to cyanide. Acute cyanide poisoning depends on detoxification of the cyanide radicle to thiocyanate. Traditionally this has been accomplished by intravenously injecting sodium nitrite and sodium thiosulfate.
Cardiac Glycoside-Induced Sudden Death: Plant Causes of Cardiac Glycoside Poisoning
At least 34 plant genera contain cardiac glycosides that are potentially toxic to man and animals, but relatively few have attained notoriety as causes of animal poisoning. These include foxglove (Digitalis spp.), oleander (Nerium oleander), and lily of the valley (Convallaria majalis), which are widely grown as ornamental plants and have escaped to become established in the wild. Dogbane, or Indian hemp, (Apocynum cannabinum) is an indigenous plant containing cardiac glycosides but is rarely a problem to livestock. Milkweeds are common cardiac glycoside-containing plants that are widely distributed throughout much of North America and are toxic green or dried.
Milkweed
Foxglove
Oleander
Yellow Oleander
Effects of Cardiac Glycosides
Cardiac glycosides are found in all plant parts with their concentrations highest during rapid plant growth. Toxicity varies with the plant and growing conditions; however, all oleanders, foxglove, and milkweed should be considered potentially poisonous, especially the oleanders, foxglove, and narrow-leafed species of milkweeds. Very little of these plants needs to be eaten to invoke the potent effect of these toxins. In cattle and horses, as little as 0.005% body weight, or less than 1 oz for the 1100-lb horse (25 g/500-kg horse) of green oleander leaves, is lethal. About 1˛ 2 lb of green labriform milkweed is lethal to the 1100-lb (250 g/500 kg) horse. The relative toxicities of the various species of milkweed are given in Table 18–13. Horses, however, rarely eat green oleander or milkweed plants, apparently because of their taste, but do seem to find the dried leaves more palatable. Because the cardiac glycosides are retained in dried plants, although in reduced quantities, oleander and milkweed pose the greatest threat if present in the horse’s hay.
The most important of the cardiac glycosides are digoxin and digotoxin, present in Digitalis spp., oleandroside and nerioside in Nerium oleander, thevetin in yellow oleander (T. peruviana), and cardenolides in milkweed. Acute death from these plants results from their cardiac glycoside ouabain- like toxic effect on the heart. This effect inhibits the cell membrane’s sodium-potassium pump, resulting in frequent and irregular depolarization of the cell. This results in disorganized cardiac electrical activity that is manifested as a variety of abnormal heart rhythms and eventually cardiac arrest. The glycosides also act directly on the gastrointestinal tract, causing hemorrhagic enteritis that results in vomiting, colic, and diarrhea. The cardiac glycosides, at least those in milkweed, also act on the respiratory and nervous systems, which may cause difficulty breathing, tremors, seizures, and head pressing.
Animals consuming sufficient cardiac glycoside-containing plants are often found dead 8 to 10 hours later due to the profound effects of the toxins on the heart. Colic, vomiting, and diarrhea are also signs commonly encountered in animals poisoned with cardiac glycosides. If observed early in the course of poisoning, animals will exhibit labored breathing which may be rapid, although it is slow in sheep poisoned by milkweed. They also exhibit muscular tremors, incoordination, inability to stand, bloating, and colic prior to death. Horses, once unable to stand, have periods of tetany and chewing movements. The extremities are cold and there is a rapid, irregular and weak pulse due to the decreased heart output. All types of abnormal heart rhythms and heart blocks may occur at various stages of cardiac glycoside poisoning. The duration of symptoms rarely exceeds 24 hours before death occurs. Convulsions prior to death are not common.
There is no specific treatment for counteracting the effects of cardiac glycosides. Affected horses are usually given adsorbents such as activated charcoal by stomach tube with a saline laxative to prevent further toxin absorption. The heart irregularities also may be treated. Poisoned animals should be removed from the source of the plants; given fresh water, good-quality hay, and shade; and kept as quiet as possible to avoid further stress on the heart. Animals that have not consumed a lethal dose of the plants recover over several days.
Larkspur or Poison Weed
Monkshood
Poison Hemlock
Water Hemlock
Yew
Death Camas
Avocado
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