Plants contain a large number of biologically active chemicals. Some of these have been found to be extremely useful for treating various human and animal diseases (e.g. digitoxin, colchicines and atropine). However, some plant constituents produce adverse health effects following exposure. The onset of these adverse effects can be quite sudden or take some time to develop. Fortunately, among the thousands of plants in the environment of animals, relatively few cause acute, life-threatening illnesses when ingested.
The magnitude of animal losses to ingestion of poisonous plants in the United States varies considerably between geographic regions. Losses include not only those due to mortality but also those due to poor productivity such as decreased weight gain or decreased milk or egg production. In addition, the economic cost of controlling poisonous plants needs to be considered. Economic loss in Pennsylvania due to poisonous plant ingestion by livestock is relatively small compared to that in other States, particularly those in the Western U.S. In 17 Western states, it has been estimated that yearly cattle and sheep death losses to poisonous plants are 1% and 3.5%, respectively (Nielsen et al., 1988). Although the value of livestock varies from year to year, the total annual economic loss in these states is estimated to be nearly a quarter billion dollars! Of course, with companion animals, the economic and emotional losses associated with the illness or death of a pet are much more difficult to quantify.
The diversity of chemical substances in plants is quite amazing. In many instances, the role that a particular chemical plays in the normal ecology of plants is unknown. The presence of certain chemicals in plants is believed to confer some degree of protection from plant predators such as insects and ruminants.
There are a number of broad categories of toxicologically significant plant constituents. These include alkaloids (basic substances with nitrogen bound in a ring structure), amino acids, peptides and proteins, glycosides (chemical groups such as cyanide linked to sugars), acids (oxalic acid), terpenes (substances that contain the branched 5-carbon skeleton of isoprene), phenolics and tannins, and essential oils (various steam-volatile, primarily lipophilic, organic plant metabolites stored in special plant organs and perceived by man through the stimulation of the sense of smell or taste) (Tisserand and Balacs, 1995). Within each broad category, there is tremendous chemical heterogeneity. See Figures 1 through 4 for examples of several plant toxins.
A number of factors can contribute to an animal being poisoned by plants. Fundamentally, there is the requirement that a sensitive species of animal ingest, or otherwise be exposed to, a toxic plant at an appropriate time of the year. There are many examples of species differences with regard to sensitivity to the toxic effects of plants. In addition, it is possible for animals to adapt to a potentially toxic plant if exposure is allowed to occur over a period of time. For example, ruminants adapted to oxalate-containing plants such as Halogeton glomeratus can tolerate concentrations that are lethal to non-adapted animals (Cheeke, 1998).
Ingestion of a potentially toxic plant is the number one route of poisoning in animals. It is important to emphasize that many, but certainly not all, toxic plants are not very palatable (see Figure 5). Therefore, if given the choice, animals will avoid ingesting them even though they may be prevalent in the environment of the animal. In these situations, animals will often eat such plants only when other suitable feedstuffs are unavailable or when the animal is not able to selectively avoid the plants. The latter situation may occur when toxic plants or plant parts such as seeds are inadvertently incorporated into hays, silages, or other feedstuffs.
Timing of ingestion may be critical. The concentrations of toxic constituents in plants can vary from year to year, throughout the growing season of the plant, or as a result of environmental factors such as drought. For example, the accumulation of potentially toxic concentrations of nitrate in forages most often occurs during periods of drought that prevent the normal growth of the plants (Pfister, 1988).
The diagnosis of plant poisonings can be difficult. Ingestion of many plants produces non-specific clinical signs that must be differentiated from other disease conditions. In addition, death due to toxic plant ingestion often does not result in characteristic post-mortem lesions. Unfortunately, relatively few laboratory tests are available to detect plant toxins in either ante-mortem or post-mortem samples. In most cases, the best way to support a diagnosis of plant poisoning is to confirm the presence of a toxic plant in the animal's environment (this will require positive identification of the suspect plant), confirm that the plant has been ingested (noting that the candidate plants have been chewed and/or finding plant fragments in vomitus or gastrointestinal tract samples), and correlate clinical findings, where possible, with those known to be associated with the suspect plant.
Unfortunately, there are few antidotal therapies for treating plant poisonings. The best approach for treating intoxicated animals often involves routine decontamination procedures such as induction of emesis (in appropriate species) and the administration of activated charcoal and a cathartic to hasten elimination of the plant from the gastrointestinal tract. In addition, symptomatic and supportive care needs to be provided. Obviously, continued exposure to the suspect plant should be stopped. For a few plant poisonings, specific antidotes may be indicated; the treatment of cyanide or nitrate intoxicated animals are examples (see Prunus and Nitrate-Containing Plants for specific treatment protocols).
When submitting plants for identification it is important to collect specimens of the entire plant, including the roots. Wet newspaper should be wrapped around the roots of the specimen and the specimen placed in a plastic bag (it is acceptable to bend the plant along its stem so that it will fit in the plastic bag). The specimen should then be kept chilled until it arrives at the laboratory. Alternatively, plants can be dried and pressed, although this will take more time for processing.
Information on poisonous plants can be found in a number of veterinary texts (see list below). In addition, veterinary toxicologists at veterinary schools and/or veterinary diagnostic laboratories can provide information and identification services. There is a wealth of information available on the internet.
Cheeke, PR (1998): Natural Toxicants in Feeds, Forages, and Poisonous Plants, Interstate Publishers, Danville, IL, pp. 330-331.
Nielson, DB, Rimbey, NR, and James, LF (1988): Economic Considerations of Poisonous Plants on Livestock. In: (James, LF, Ralphs MH, and Nielson, eds.), The Ecology and Economic Impact of Poisonous Plants on Livestock Production, Westview Press, Boulder, CO, pp. 5-16.
Pfister, JA (1988): Nitrate intoxication of ruminant livestock. In: (James, LF, Ralphs MH, and Nielson, eds.), The Ecology and Economic Impact of Poisonous Plants on Livestock Production, Westview Press, Boulder, CO, pp. 233-260.
Tisserand, R and Balacs, T (1995): Essential Oil Safety: A Guide for Health Care Professionals, Churchill and Livingstone, Edinburgh, UK, pp. 159-160.
Figure 1: Examples of plant alkaloids. The structure on the left is solanidine a steroidal alkaloid found in Solanum spp. such as Solanum nigrum (black nightshade). The structure on the right is a piperidine alkaloid called coniine, which is found in Conium maculatum (poison hemlock).
Figure 2: Example of a plant glycoside. The illustrated compound is called melilotoside, found in white and yellow sweet clovers (Melilotus spp.). This compound is converted in the plant by b-glucosidase to coumarin. If the plant becomes moldy, coumarin is converted by the mold to dicoumarol, which is a vitamin K antagonist.
Figure 3: Isoprene is the basic unit for the synthesis of plant terpenes. Monoterpenes are composed of two isoprene units (10 carbon atoms), sesquiterpenes are composed of three isoprene units (15 carbon atoms) and diterpenes are composed of four isoprene units (20 carbon atoms). Terpinoids are compounds with varying numbers of carbon atoms that are derived from isoprene units. Helenium spp. (sneezeweeds) and Hymenoxys spp. (bitterweeds) contain sesquiterpene lactones.
Figure 4: Pennyroyal oil, an essential oil derived from either Mentha pulegium (European pennyroyal) or Hedeoma pulegioides (American pennyroyal), contains d-pulegone, which is extremely toxic. Pulegone is metabolized in the liver to reactive epoxides, which damage hepatocytes.
Figure 5: Brassica kaber or wild mustard. This plant is a common weed of nursery, horticultural and agricultural crops, especially small grains and fall-seeded forage crops. Note the horses grazing in the pasture containing the plant. This is an example of an unpalatable plant that is avoided if other forage is available.
Natural Toxicants in Feeds, Forages, and Poisonous Plants by Peter R. Cheeke, 1998, Interstate Publishers, Inc., Danville, IL (ISBN 0-8134-3128-X).
Toxicity of Houseplants by David Spoerke, Jr. and Susan Smolinske, 1990, CRC Press, Boca Raton, FL (ISBN 0-8493-6655-0).
Toxic Plants Dangerous to Humans and Animals by Jean Bruneton, 1999, Lavoisier Publishing, Inc., Secaucus, NJ (ISBN 1-898298-62-9).