F835
Toxic Substances and Plants

urea toxicity | salt toxicity | lead toxicity | molybdenum toxicity/copper deficiency | copper toxicity | mycotoxins | fescue toxicity | aflatoxins | plants that contain alkaloids | plants that contain glycosides | plants that contain cardiac glycosides | plants that accumulate nitrates | plants that contain lectins | plants that contain resinoids | plants that accumulate selenium | plants that cause photosensitization | plants that cause abortions | plants that contain organic acids or tannin | plants that cause bloody or dark urine | plants that cause mechanical injuries | miscellaneous plants | pictures of various plants

Introduction: Many of the most effective poisonous agents known to man are found in plants and represent various classes of chemical substances. There is little doubt that some illnesses still considered "idiopathic" (cause unknown) may be caused by ingestion of poisonous or noxious plants. All too often, the statement of "natural loss" is made by livestock owners when they find an animal that has died of an unknown cause. There is no such thing as "natural loss." Animals die from a cause. It may not be possible to determine the cause of death in each and every case, but by becoming acquainted with the information available on sheep and goat husbandry, an animal caretaker increases his/her chances of limiting such losses.

Noxious or poisonous plants have caused extensive animal losses in most parts of the United States since the early settlement years. Many of these plants continue to this day to impose major economic losses for sheep and goat producers, especially where natural or "native" vegetation has not been removed by cultivation, followed by reseeding of domesticated plants.

Some believe that acute (fast acting) illness and death are the only effects when noxious or poisonous plants are consumed by sheep or goats. However, some of the most toxic substances or compounds known to man can cause clinical signs resembling many infectious and nutritional diseases. In addition, these plants can also cause congenital deformities in sheep and goats.

Poisoning of sheep or goats by plants may occur when certain environmental conditions cause normally nonpoisonous plants to become poisonous by accumulating excess quantities of nitrate, hydrocyanic acid (HCN), selenium, alkaloids, and other toxic agents. At other times, environmental factors may cause normally poisonous plants to become less toxic. Thus, it has been apparent over the last number of decades, many cases of sheep and/or goat poisoning by plants have been improperly diagnosed, and significant amounts of economic expenditures have been made in treating diseases that were not present in these animals.

Diagnosis of plant poisoning in sheep or goats is not easily accomplished. Blood tests may provide information for some of the plant poisonings, though blood tests and chemical analysis of rumen contents are usually of little value. More importantly, increased knowledge and personal experience are required. This includes the ability to identify toxic plants, their stage of growth, and plant parts that are poisonous. It is also important to know what species of animals are susceptible, what signs of toxicity will appear in the animal, and the amount of plant that must be consumed for toxic and lethal doses. Training and expertise in conducting plant surveys to determine the types and names of plants and amount grazed will help aid in the diagnosis. Frequently much of this information is not available, resulting in an incorrect diagnosis.

To diagnose any plant poisoning, a detailed and exacting history of all events leading up to the time when the animals were found affected, and a careful description of the clinical signs are paramount. It is every producer’s responsibility to keep accurate records of his/her animals so that they can provide this information to other professionals (i.e. veterinarians, range managers, and other experts). An accurate history of sheep or goats suffering from poisoning will often provide a lead for the clinicians or help establish a correct diagnosis.

Many times, solving a case of intoxication includes taking samples of the feed from bunks and pasture. Samples may also need to be taken from an animal during a necropsy and evaluated for different toxic components. When a necropsy is performed, the liver, brain, kidney, rumen contents, and eye fluid (vitreous) are some of the most important tissues or areas to sample.

The key to solving any suspected case of intoxication is to take the proper samples and handle these samples correctly. Because collection and handling are so important, the following are a few suggestions:

1. All samples (both feed and tissue) must be labeled with information that will identify exactly where the sample came from. This can include writing the date, animal’s name and/or number, and location of where the sample was collected right on the sample. If multiple feed samples are collected, each one must be individually identified.
2. Feed samples should be placed in a brown paper sack, boxed, and delivered to the laboratory as soon as possible. If the sample must travel a long distance, freezing the sample is often recommended.
3. The entire plant should be collected and sent when a range sample is taken.
4. Tissue samples should be placed in individual plastic bags and shipped chilled or frozen.
5. Blood samples should be collected in red and lavender topped blood tubes. It is necessary to collect 5-10 mLs in each.
6. If water samples are needed, approximately 1 L (liter) should be collected.
7. If urine samples are needed, 50-100 mLs should be collected and chilled.

Summary: Controlling losses of sheep and goats from poisonous plants does not require that each producer become a plant specialist. Usually only about 4 to 10 different species of poisonous plants may be responsible for major losses in a general geographic area. The sheep or goat producer should learn to identify these plants at all stages of growth and recognize some of the general signs and/or symptoms animals can be expected to exhibit when affected by noxious or poisonous plants. Plants suspected of being poisonous can be taken for identification to the local extension agent or a representatives of the Bureau of Land Management or the U.S. Forest Service. If scientific names are a challenge, the common name of the plant or a self-devised name, can serve a producer’s needs. It is a challenge that can be not only interesting and educational, but will assist in reducing or eliminating sheep and goat losses.

There is no known treatment for many plant poisonings. Supporting treatment may be helpful if administered to affected animals in the early stages of the poisoning. However, affected animals are often not found until they are dead or in advanced stages of poisoning. It is always better, therefore, to try and prevent the problem than to rely on treatment. Many animal losses can be prevented by strict adherence to the following basic principles:

1. Learn to identify poisonous plants in the local area, pastures or native range.
2. Prior to grazing all ranges and pastures, inspect them for poisonous plants and be sure sufficient desirable forage is present. Generally, if enough desirable forage is available, most animals will not consume noxious or poisonous plants.
3. Do not allow hungry or thirsty animals to graze areas heavily infested with poisonous plants.
4. Supplement animals throughout the year with salt and phosphorous.
5. Plan each grazing program so areas where poisonous plants exist can be used when the plants are least toxic.
6. Water animals daily. If this is impossible, do not allow them to go more than 2 days without water. However, lactating ewes and does should always have daily access to adequate water supplies.
7. Do not put newly acquired animals on a range or pasture without first feeding them a salt and phosphorous supplement for the preceding 2 weeks.

Considerable data and information has been accumulated through research on the poisonous substances in plants, but the exact toxic properties have been identified in only a few cases. Some of the more commonly known types of poisons or toxins found in substances and plants are included in the following information:

Introduction: Alkaloids are complex compounds containing nitrogen. They are alkaline in reaction and form soluble salts with acids. In most cases, alkaloids affect the central nervous system and cause marked signs of toxicity and death.

Examples of plants that contain alkaloids:

Introduction: These plants release cyanide when they are damaged or exposed to drought and frost conditions. Following is a list which shows the plants that are most often associated with livestock poisoning. If careful attention is paid to the growth stage of the plant, and the growing conditions, some of these plants can safely be used. Cool, moist growing conditions and nitrate fertilizer are known to elevate levels of cyanogenic poison in the plants.

Ruminants (cud-chewing animals) are more frequently poisoned by cyanogenic plants because of the high water content and relatively alkaline pH of the rumen. Animals that are fed a grain ration tend to release the poison into their system slower because the grain increases the acidity of the rumen. Conversely, animals fed mainly an alfalfa or grass hay diet tend to release the poison faster, because the rumen is more alkaline. Therefore, animals with stomach contents that are more acidic are less likely to suffer fatal cyanide poisoning. Simple stomached animals (humans, horses, pigs, etc.), fit this criteria.

The lethal dose of cyanide is 2-2.5 mg/kg for most animal species. If the stomach is full of plant matter and carbohydrates, the animal may tolerate a higher dose of cyanide. Along with consuming one large dose of cyanogenic plants, consuming small amounts of cyanide consistently over a long period of time can also prove fatal.

Clinical Signs: In an acute case, sudden death is often the only sign. Animals rarely survive more than 1-2 hours after ingesting a fatal dose of these plants and are often dead within minutes of showing clinical signs. Early signs include rapid, labored breathing, frothing at the mouth, dilated pupils, muscle incoordination (ataxia), muscle tremors, and convulsions. Mucous membranes become a bright cherry-red in color once the animal has been poisoned and fade to a bluish color when the animal is close to death. An increased heart rate, vomiting, and recumbency, followed by bloating are other signs of poisoning.

Diagnosis: Cyanide poisoning is usually diagnosed at necropsy. In order for the necropsy results to be accurate, tissue samples must be collected within a few hours of death and frozen immediately. Liver, muscle, and rumen contents must be frozen in air-tight containers and sent to the appropriate laboratory for analysis and diagnosis.

Treatment: Treatment involves accelerating the rate the body metabolizes the poison, thereby inactivating it. This is accomplished in animals by administering an intravenous (IV) dose of a mixture of 1 mL of 20% sodium nitrite, plus 3 mL of 20% sodium thiosulfate (for total of 4 mL). For every 100 lbs. of body weight, administer 4 mL of this solution. The dose may be repeated in a few minutes if the animal does not respond. Use caution when administering additional doses of this solution, because additional nitrite can also cause poisoning. An additional method of administering 660 mg/kg of sodium thiosulfate and 22 mg/kg of sodium nitrite has also been recommended in sheep. After administering the above mixtures, additional thiosulfate can be given orally (PO) to detoxify any cyanide still left in the rumen. Any animals suspected of ingesting cyanogenic plants should receive the oral dose of sodium thiosulfate regardless of whether they show symptoms or not. After the IV and PO treatments with sodium thiosulfate, an oral dose of vinegar mixed with water can be administered by stomach tube to help acidify the rumen and reduce cyanide absorption.

Prevention: Pasture management to limit livestock’s access to toxic areas prevents losses. Sorghums are toxic during early regrowth after cutting, drought, or frost. Sorghum that is at least 2 feet high is safe to use as forage. Proper curing of silage and hay greatly reduces the risk of cyanogenic poisoning of livestock. There are also varieties of sorghum and white clover available that have been selected for low cyanide content. Herbicides can be used to control areas dense in poisonous plants, but usually it is not cost effective to control large areas of plants this way. If there is any uncertainty about the cyanide content of forage crops, they should be tested before being fed.

Examples of plants that contain glycosides:

Clinical Signs: These plants cause problems with the heart and the intestinal tract. Signs such as a rapid heart rate, rapid breathing, heart arrhythmia, bloody diarrhea, abdominal pain, and weakness are common. Death usually occurs within 24 hours after the toxic plant is consumed.

Diagnosis: Because the toxin acts so rapidly, diagnosis of this problem is difficult.

Treatment: If it is determined that an animal has consumed this type of toxic plant, activated charcoal can be administered (2-5 gm/kg body weight). If it is determined early on that these plants have been consumed, a rumenotomy can be performed and the toxic plants removed. There is no specific treatment to reverse the effects of the cardiac glycosides. Supportive care (fluids, anti-arrhythmic drugs) is all that can be done. These animals should also be kept as quiet as possible to avoid additional stress on the heart.

Plants containing cardiac glycosides: Dogbane (Apocynum spp.), Lily of the Valley ( Convallaria spp.), Foxglove (Digitalis spp.), Oleander (Nerium oleander), Yellow Oleander (Thevetia spp.), and Milkweeds (Asclepias spp.).

Introduction: Nitrate poisoning is a common problem in livestock worldwide. Nitrates are compounds found in the soil which are necessary for a plant’s growth. Under normal circumstances, the concentration of nitrate in plants is not substantial enough to poison livestock. However, modern farming practices which use large quantities of nitrogenous fertilizers have the potential to raise nitrate levels in plants high enough to reach toxic levels. These fertilizers also have the potential to contaminate water the livestock drink, and if not stored properly, livestock may gain access to fertilizer and ingest it.

While many weeds and crops have the potential to poison animals, nitrate poisoning is most commonly associated with ruminants that are fed sorghums. Some other crops that have been associated with nitrate poisoning of livestock are sugar beet tops, turnips, oats, silage, kale, red root pigweed, variegated thistle, Italian ryegrass, and white clover. There are many factors that can affect the nitrate levels in plants. Drought, acidic soils, and soils that are deficient in sulfur, phosphorus, and molybdenum are common conditions that may cause high levels of nitrates to accumulate in plants. Cool, cloudy days, and early mornings are times when nitrate levels are the highest in plants. This is because the enzyme present in plants which helps convert nitrates into other compounds is less active when there is not adequate sunlight and warmth.

The highest concentration of nitrates is in the plant stem, and the next highest concentration is in the leaves. Flowers, seeds, and fruit contain no nitrate, so grains should not be suspected in cases of nitrate poisoning. Silage that is properly cured can significantly reduce the incidence of nitrate poisoning, while the level of nitrates present in dried hay can rarely be reduced. The use of herbicides on crops meant for livestock can be a problem, not only because it increases the nitrate level in plants, but it also increases the palatability as well.

Fertilizer runoff frequently causes nitrates to reach toxic levels in water. Water should be tested if it is suspected as a source of extra nitrates. Nitrate levels in water should not exceed 45 ppm, although in some situations levels of up to 400 ppm can be tolerated. When measuring the nitrate levels in water, it is important to keep in mind that these numbers are based on the animals receiving a normal diet which does not contain excessive nitrates. An above average nitrate level in water, while it may be in the acceptable range, could combine with high levels of nitrate in the diet and have fatally toxic effects.

Nitrate poisoning causes the formation of methemoglobin in the bloodstream (methemoglobinemia). Methemoglobin does not carry and exchange oxygen properly; therefore the animal basically dies from a lack of usable oxygen in the bloodstream.

Clinical Signs: The first signs of nitrate poisoning include drowsiness and weakness. These are followed by muscle tremors, increased heart and respiratory rates, staggering gait, and collapse. The mucous membranes, especially vaginal membranes, usually show a brownish discoloration. The vaginal membrane discoloration usually occurs well before any of the other clinical signs. This discoloration of the vaginal membranes can be a good indicator of nitrate poisoning, before severe toxicity develops.

Depending on the amount of nitrates ingested and the amount of stress
the animal has been subjected to, death usually occurs within 2-10 hours. Nitrate poisoning may induce abortions due to the effects of methemoglobinemia on the fetus. Fetal death and abortion may occur at any stage in the pregnancy. Normally, there is little, if any secretion of nitrites in milk.

Diagnosis: Sudden death in animals grazing post-harvest crops, Sudan grass, or weeds is a good indicator of nitrate poisoning. This should be confirmed by testing the forage and/or water source for toxic levels of nitrate. The animal should also be tested for toxic levels of methemoglobin in the bloodstream.

Since methemoglobin levels decrease rapidly following death, blood samples should be taken as soon as possible after the animal’s death. A veterinarian can take samples of blood, eye (vitreous) fluid, and possibly a sample of the rumen contents for testing and analysis.

Treatment: Animals with nitrate poisoning should not be over-stressed or excited. An intravenous (IV) dose of methylene blue is the most effective treatment for nitrate poisoning. The dose range is from 4-15 mg/kg body weight administered as a 2-4% solution. Care should be exercised when administering methylene blue to animals other than ruminants. Horses, and more often, dogs and cats are especially susceptible to the potential toxic effects of methylene blue. Veterinary assistance should be sought in cases of nitrate poisoning, whether sheep/goats or other animals are involved.

To counteract the effects of nitrates on the gastrointestinal system of ruminants, mineral oil administered orally (PO) via stomach tube will help speed up nitrate passage. Some other treatments to counteract the effect of nitrates in the rumen include 0.5 gallon of cold water administered orally with broad spectrum antibiotics added, or cold vinegar also administered orally.

Introduction: Resins or resinoids are complex compounds which differ widely in their chemical makeups but are similar in certain physical characteristics. They affect both nervous and muscular systems. Specific toxic signs depend on the species of animal affected. Toxic resins are commonly found in the milkweed species.

Examples of plants that contain resins or resinoids:

Introduction: Certain plants are able to accumulate high levels of selenium. The amount of selenium that a plant accumulates is dependant on the climate, stage of growth, and plant species. Animals rarely eat selenium toxic plants unless other forages are unavailable. Many times consumption of natural grasses that are on soils with high selenium levels and consumption of contaminated water sources compound the problem. Sheep are considered more susceptible than cattle to selenium toxicity.

Clinical Signs: In an acute selenium poisoning situation, where high levels of selenium are consumed over a short period of time, the animal may experience damage to the liver, kidneys, and lungs. Toxic levels of selenium can also be administered through improper injections and supplementation. Signs can include weakness, diarrhea, difficulty breathing, bloating, and abdominal pain. Death results because of respiratory failure due to fluid buildup. In cases where the selenium toxicity has taken place over a long period of time (chronic poisoning or alkali disease), the animal may experience changes to the hair and hoof wall. Longer hair will be broken off short and the hoof wall on all four feet can have uneven growth with circular lines and cracks in a horizontal fashion.

Diagnosis: Selenium poisoning can be detected in a blood sample taken from a suspect animal. Selenium levels can also be measured in hay or forage samples submitted for analysis. If the poisoning has been going on for long periods of time, hair and hoof samples can also be sent in for analysis.

Treatment: Access to the toxic plant must be denied as soon as it has been determined what plant(s) is causing the selenium toxicity. Once the plant has been removed from the diet, high levels of protein and adequate copper levels can be fed. Recovery from selenium poisoning does occur if the proper diet is fed and attention is given to correct (trim) any hoof abnormalities.

Examples of plants that accumulate selenium:

1. Primary photosensitization - The skin reactions with primary photosensitization are caused by compounds found in plants that are ingested and travel to the skin in the blood stream.
2. Secondary photosensitization - The skin reactions with secondary photosensitization are the result of liver damage. The liver can be damaged by consuming many different toxic plants. Once the liver is damaged, it is unable to excrete phylloerythrin which is a breakdown product of chlorophyll.
3. Defective pigment metabolism - These are birth (congenital) defects that alter the way the body handles certain pigments.

Clinical Signs: No matter the initial cause, all animals experience the same external clinical signs. These animals are very sensitive to sunlight (photophobic) and may scratch areas of light or non-pigmented skin most commonly on the ears, around the eyes, and the muzzle. These areas can become swollen, red, irritated, infected, and ooze serum.

If sunlight exposure continues, the skin in the problem areas can die (necrose) and slough, leaving an extremely painful lesion. If the tongue is exposed, it can become ulcerated and necrose. If the liver is involved, icterus (yellow coloration to the gums and white of the eye), weight loss, and elevated liver enzymes can be seen. If ammonia levels are high, these animals develop hepatic encephalopathy and act lethargic, disoriented, and eventually die.

Diagnosis: A diagnosis can be made based on clinical signs, blood work, and liver biopsy.

Treatment:

1. Remove the plant source causing the photosensitization.
2. Protect the animal from sunlight.
3. If liver disease is the cause, provide energy sources (glucose) that require less liver metabolism. Vitamin B12 is also recommended.
4. If the problem is recognized early, corticosteroids can be given.
5. If infections are a problem, topical and injectable antibiotics should be administered.
6. Prevent additional irritation by flies and other insects.

Examples of plants that cause photosensitization:

Prevention: Restricting pregnant animals from having access to pasture where there are known teratogenic plants will greatly reduce the incidence of having newborns with defects due to plant toxins. Usually, it is sufficient to restrict the animals’ access to these pastures during the first trimester of pregnancy; however, where plants such as milk vetch and locoweed are prevalent, animals should not be allowed to graze these pastures at all during pregnancy. These plants, along with others that are from the Astragalus spp., cause deformities and abortions throughout gestation, so it is best to let non-pregnant animals graze on pastures known to have these plants.

Examples of plants that cause abortions and/or defects:

Introduction: Plants that are toxic to the kidneys are termed nephrotoxic. The plants that will be discussed below are ones that accumulate oxalate or tannic acid. Both of these toxic compounds can cause severe kidney damage and death if they are consumed in sufficient quantities.

Clinical Signs: If sufficient oxalate levels are consumed, the animal may experience low calcium and magnesium levels, weakness, tremors, lethargy, coma, and death within 12 hours. If toxic levels of tannic acid are consumed, the animal may go off feed, have dark, hard manure, and act like it is in pain. Once the liver and kidneys are damaged, the animal becomes dehydrated and can have red colored urine.

Diagnosis: A diagnosis of oxalate poisoning can be made based on identifying the plants that are consumed, low calcium levels in the blood, and oxalate crystals in the urine. Diagnosis of tannic acid poisoning is made on the clinical signs and a history of eating oak. Both problems can also be identified at necropsy.

Treatment: Treatment for both toxicities is difficult and rarely successful.

Examples of plants that contain organic acids or tannin:

1. Onion toxicity
   Clinical Signs: Most animals become weak, experience anemia (low red blood cells), have pale mucous membranes, and eventually collapse. These animals can also have dark urine and may have an onion smell to the breath, urine, and milk. Sheep and goats are the most resistant livestock species to onion toxicity.
   
   Treatment: The feeding of onions to these animals should be discontinued immediately and all efforts should be made to not over stress the animal.
   
   Prevention: Onions can be fed as much as 25% of the dry matter in a ration. The onions should be chopped, well mixed, and fed in increasing amounts until the desired level is achieved.
    
2. Brassica poisoning (turnips, kale, rape, cabbage)
   Clinical Signs: These signs are similar to onion toxicity. In addition, Brassica poisoning has been associated with poor growth, polioencephalomalacia, bloat, and reproductive problems. Sheep are less susceptible than are cattle to this type of poisoning.
   
   Treatment: The treatment for Brassica poisoning is similar to onion toxicity.
    
3. Moldy sweet clover (Melilotus officinalis)
   Clinical Signs: The signs noted here are related to bleeding disorders caused by fungi found on moldy sweet clover. Dicumarol is the toxic substance that causes the animal to not be able to coagulate the blood. Dicumarol is considered a mycotoxin (see above). These animals experience weakness, swelling of the joints, bleeding from the nose (epistaxis), bloody urine (hematuria) and bloody manure (melena). Any area that is injured will bleed or swell significantly. Sheep seem to be fairly resistant to the effects of this problem.
   
   Treatment: Administering vitamin K (1 mg/lb) is essential and may need to be repeated for 4-5 days. If many animals are affected, oral doses of vitamin K can be given.

Treatment: When possible, the plant/foreign body should be removed from the mouth or body part. Antibiotics may also be required in severe cases where infection is a problem. With buttercup toxicity, once the animal does not have access to the buttercup, the problems often resolve.

Examples of plants that cause mechanical injuries:

1. Locoism caused by swainsonine
2. Respiratory and nerve problems
3. Selenium toxicity

Depending on the type of plant that is consumed, an animal can experience one or all of the above syndromes. Animals generally consume small amounts of these toxic plants over a period of days to weeks. Toxicity results when a "toxic threshold" has been reached in the body.

Plant Description: Locoweeds come in many different colors and sizes. The most common plants are white, purple, or rose colored and have small leaves and seed pods.

Clinical Signs: As stated in the introduction, the clinical signs produced vary from plant to plant. Some of the most common signs include lethargy (depression), abortions, birth defects, a staggering gait ("blind staggers" ), "crazy" behavior, respiratory distress, and weight loss. Some animals can develop a compromised immune system. Goats tend to be more alert until just a few days before death and do not tend to develop the respiratory signs that sheep often experience.

Diagnosis: Many cases can be identified by clinical signs and history of exposure to locoweeds. Blood samples can also be evaluated for swainsonine levels and lymphocytes can be observed with a microscope looking for the characteristic "cytoplasmic vacuoles." However, blood levels of swainsonine drop dramatically in 20 hours and can return to normal within 6 days after the animal stops eating the toxic plant.

Treatment/Prevention: There are no effective treatments for locoweed poisoning. Attention should be placed on stocking rates and pasture rotation. When stocking rates are too high for the available forage, animals turn to locoweed as part of their diet. On the other hand, in some situations where locoweeds are very abundant, it might be feasible to keep stocking rates high, therefore reducing the total amount of toxic plant one animal will consume.

Examples of miscellaneous toxic plants: