Millions of people worldwide have a fondness for the avian species. In the US alone, over 10 million birds are kept as pets. Birds are beautiful to watch in the wild, and a great loving companion animal to own, but are extremely complex because of their specific nutritional needs, husbandry, behavioral concerns, and anatomy. Veterinary professionals and bird enthusiasts often are unaware of the dangers of toxicosis from certain plants, and may have difficulty determining healthy, non-toxic plants that can be given to a bird to ingest and to play with. This article will highlight some of the plants that are commonly kept in the home or in the garden that can be harmful or fatal to companion parrots or other birds, and that should be avoided.
In the realm of veterinary medicine, actual cases of plant toxicoses in birds are not well documented. From 2004 to 2010, Pet Poison Helpline, an animal poison control based in Minneapolis, Minnesota, USA, and Toxcall, an animal poison control based in London, UK, received over 1200 calls relating to toxic exposures in birds alone, with approximately 2% of these calls comprising plant-related calls. Actual numbers affected by toxins from plants may, however, be higher because some bird owners may not be financially vested in calling for toxicity advice, while others may not correlate their bird's illness with symptoms that develop secondary to plant toxicosis. Most companion birds are kept caged for the majority of the time and ingestion of great quantities is generally not possible; in these situations, exposure is often caught quickly. In addition, the curious, playful nature of birds means that most plants that birds come in contact with are shredded and played with, rather than ingested. Because of this, and in combination with the rapid gastrointestinal (GI) motility rate of birds, many of the frequent plant toxicities that are often seen typically only involve local oral irritation (Gfeller and Messonnier, 2004). However, because of the small size of birds, their stoic nature, and their often delicate and unpredictable health, a few plants warrant careful consideration. Appropriate client education is imperative as it will aid in poisoning prevention by even the most well-intentioned bird owner.
Avocado (Persea americana)
The avocado, often known as the alligator pear, is a large fruit-bearing tree native to Central America, South America, Mexico, some regions with the Caribbean, and warm locations within the US (e.g. California). In the UK, this imported fruit is found in most supermarkets throughout the year. Even dried, packaged ‘ready to make’ guacamole is considered toxic, as the toxin is likely still present when reconstituted.
While the avocado fruit is rumoured to be toxic to dogs, this is rarely the case. With dogs, the ‘toxicosis’ primarily lies with the risk of foreign body obstruction from seed ingestion. However, in the bird, the avocado is highly toxic. Well-intentioned bird owners may offer this as part of a fresh-fruit variety to their birds, not knowing the severity of the toxicosis associated with it. Toxicosis from the leaves, bark and fruit/seeds has been reported in both companion and wild birds. It is thought that persin, a compound found in the plant, is responsible for its toxic effects (Plumlee, 2002; Peterson and Talcott, 2006). Birds such as canaries, parakeets, cockatiels, large parrots, geese and turkeys have been shown to suffer a variety of symptoms ranging from subcutaneous (SC) oedema of the neck, chest and pulmonary system, pericardial effusion, myocardial necrosis and liver and kidney damage when avocado is ingested in even small quantities (Plumlee, 2002; Peterson and Talcott, 2006). In a clinical study, parakeets fed a 1.0 ml solution of equal water and avocado died within 24–48 hours, most likely from sudden death resulting from cardiopulmonary collapse (Hargis et al, 1989). It is speculated that larger parrots may initially show less severe symptoms, including fluffed feathers, general malaise, or an inability to perch; however, there are no strong data to support this. Because of the variance of symptoms, species differences, and variation in both experimental and anecdotal amounts that birds have been poisoned by, a true median lethal dose (LD50) has been difficult to determine.
Treatment for avocado poisoning
Treatment for birds that have been exposed to avocado includes basic decontamination: stabilization with oxygen; intravenous (IV), intraosseous (IO), or SC fluids; and supportive care as each symptom arises. Decontamination (Figure 1) includes removal of any remaining avocado by crop lavage, followed by immediate administration of activated charcoal (Lightfoot and Yeager, 2008). Most birds exposed to avocado that have already developed clinical signs have a poorer survival, based on clinical experience from Pet Poison Helpline and Toxcall Veterinary Helpline. As a result, prevention is key. Bird owners should be made aware during routine examination visits about pet-proofing their environment, appropriate diet, and which toxins could endanger their bird. Owners should be strongly advised to keep avocado well away from companion birds.
Dieffenbachia (Araceae)
This common plant, also known as ‘dumb cane’ and ‘mother-in-law's-tongue’ (Figure 2), has about 30 different species. It is often found in the work environment and households because of its ability to tolerate low light and low moisture, making it ideal for people without a ‘green thumb.’ Dieffenbachia is noted for its broad uniquely patterned leaves, its ability to grow almost anywhere, and its expansiveness (it can grow up to 2 metres tall, given the right conditions and care). Some varieties grow from a single stem-like flower from the centre. These plants contain a heavy content of calcium oxalate crystals within the leaves and stem of the plant. When ingested orally this can result in local irritation because of the grooved needle-like crystals. It is historically said to have been given to slaves as a form of torture, as it is painful to the mouth when ingested.
Because this is such a popular houseplant, exposure to companion birds may occur when birds are allowed to climb and play in its large expansive leaves. When ingested, dieffenbachia can cause a painful burning of the tongue, as well as localized oedematous swelling of the tongue and crop, resulting in difficulty eating and breathing (Burrows and Tyrl, 2006). While there is no ‘antidote’ for this specific plant ingestion, it often responds well to supportive care.
Treatment for dieffenbachia poisoning
Treatment includes rinsing the mouth with lukewarm water to help dilute the crystals in the mouth and tissues; addressing inflammation with nonsteroidal anti-inflammatories or steroids; supportive fluids (SC, IV, or IO); changing the diet to a soft, slurried, bird-specific diet (e.g. Emeraid's Omnivore-Avian critical care diet; Roudybush formula AA Acute Care); and providing nutritional support in the form of tube feeding, if needed, until clinical signs resolve. The crystals found in dieffenbachia are insoluble, and are not typically associated with acute renal failure (as seen with star fruit, rhubarb (Table 1), and lilies, which contain soluble calcium oxalate crystals). Nevertheless, deaths in small animals have been reported from secondary respiratory distress.
| Other toxic plants to birds and active toxin (if known) | Clinical signs |
|---|---|
| Yew (Taxus medial) Specific toxin: unknown | Ataxia, regurgitation, CNS agitation, respiratory depression/dyspnea, death |
| Rhododendron (Rhododenrdon spp) Toxic agent: andromedotoxin | Lethargy, weakness, GI distress (regurgitation, diarrhoea), cardiac effects (including hypotension and cardiovascular collapse), CNS depression and death |
| Black locust (Robina pseudoacacia) Toxic agent: robitin | Depression, respiratory signs (dyspnea, sneezing, coughing), GI distress (vomiting) |
| Clematis (Montana rubens) Specific toxin: unknown | GI distress (regurgitation) |
| Castor bean (Ricinus communis) Toxic agent: ricin | GI irritation (vomiting, diarrhoea), polydypsia, seizures, organ damage (acute renal failure, necrosis of liver, spleen, lymph nodes, etc) |
| Virginia creeper (Parthenocissus quinquefolia) Specific toxin: unknown | Depression, GI distress (regurgitation) |
| Poinsettia (Euphorbia pulcherima) Toxic agent: resin | GI distress (red-stained faeces, diarrhoea, gastroenteritis), hepatic necrosis |
| Lily of the Valley (Convallaria majalis) Toxic agent: cardiac glycoside | GI distress (vomiting, diarrhoea), cardiac arrhythmias (bradycardia, heart block), electrolyte disturbances (hyperkalemia), hypotension, CNS agitation, possible death |
| Rhubarb (Rheum spp) Toxic agent: oxalate crystals | Acute renal failure |
CNS, central nervous system; GI, gasrointestinal
Milkweed (Asclepias)
Milkweed is native to several countries, particularly South America, but is widely spread throughout the world. It is considered a weed to some, and grown in gardens intentionally by others as part of a butterfly plant collection (Figure 3). Milkweed grows well in dry areas, blooming in the hot dry summer months. Its strong stem makes it a popular long-lasting cut flower. Milkweed's genus name (Asclepias) comes from the Greek god of healing (Asklepios), as it has been known for its curative anecdotal herbal remedies in people. In birds and other animals, this plant can be highly toxic due to the primary toxicant, which is a cardenolides and uncharacterized neurotoxin, affecting the heart and central nervous system (CNS) (Poppenga, 2007). There are two types of milkweed: one that is opposite-leaved (leaf attachments are paired at each node); and the other that is whorled-leaved (three or more leaves attach at each point or node on the stem). Both varieties grow to be 1–2 metres tall, and have a large, thick stem. Milkweed typically has either wide, long thick leaves or thin narrow leaves. The purple, pink or white flowers produce large seed pods containing silk-like fluff within the pod. When any part of the plant is damaged, a sticky, white sap oozes out. Luckily, milkweed's poor taste usually limits the amount ingested. Small acute oral exposure can cause salivation, regurgitation, and loose stool. With small chronic ingestions, weight loss can be noted. More severe exposure may result in generalized weakness, inability to perch, heart irregularity, bradycardia or tachycardia (Knight, 2006). Ingestion of the whorled-leaved varieties can cause CNS-related symptoms, including seizures, tremors, and weakness.
Treatment for milkweed poisoning
Birds exposed to either variety of milkweed require aggressive decontamination and symptomatic and supportive care. Unfortunately, both types of milkweed result in severe toxicosis and carry a poor prognosis. With ingestion of the opposite-leaved milkweed, the use of anti-arrhythmias may be necessary. With bradycardia and/or atrio-ventricular block, atropine may be necessary, while lidocaine may be necessary with severe tachycardia. With ingestion of the whorled-leaved variety, the use of muscle relaxants or anticonvulsants may be necessary. Once the bird is stabilized, crop lavage followed by activated charcoal administration is imperative to prevent further absorption. Additional supportive care includes fluid therapy, GI protectants (e.g. famotidine), or antidiarrhoeals (e.g. metronidazole, carnidazole) (Burrows and Tyrl, 2006).
Oleander (Nerium spp.)
Oleander is an evergreen-like, flowering plant that is found throughout the world, including parts of Europe (e.g. Portugal, Morroco), Africa, Asia, the middle-east, the Mediterranean, and warm-locations of America (e.g. California). Marketed for its ‘mediterranean feel,’ oleander is commonly found in the garden, patio or balconies as it is quick growing, drought and cold resistant, easy to maintain, and has beautiful, long-lasting pink, white, or red flowers. It is thought to be potentially the most toxic commonly kept home and garden plant, and one of the most toxic plants in the world. Humans, farm animals, horses, domestic pets, and birds are poisoned each year by oleander (International Programme on Chemical Safety, 2005).
Oleander's primary toxicosis is a cardiac glycoside effect from the toxin oleandrin (Alfonson et al, 1994; Micromedex Healthcare systems, 2007; Poppenga, 2007). All parts of the plant are considered toxic including the sap, flowers, leaves and stems. Even when the flowers and leaves are dried, the toxic principle still remains. It is estimated that as little as 0.18 mg/kg of body weight is lethal to livestock and companion animals (Alfonson et al, 1994). It is expected that any ingestion in an animal will result in significant clinical symptoms at the very least, if not death (Alfonson et al, 1994). Generally, horses and farm animals are most susceptible to oleander toxicity because of the potential for chronic grazing of large amounts. However, because of the small size of birds, only a small amount of oleander would need to be ingested to result in severe toxicosis.
Clinical signs seen from oleander's cardiac glycoside effects range from mild symptoms such as dermal irritation (when exposed to the leaves and sap) to more significant symptoms such as GI signs (including hypersalivation, anorexia, regurgitation); cardiovascular signs (arrhythmias, hypotension, shock, death); CNS-related signs (ataxia, seizures); and clinicopathologic findings (hyperkalaemia) (Micromedex, 2007). Clinical signs can be seen within a few hours, although larger ingestions can result in death shortly after exposure.
Treatment for oleander poisoning
Treatment for oleander toxicosis includes rapid decontamination, including crop lavage, followed by administration of activated charcoal. Supportive care with fluid therapy (ideally IV or IO) should be given to maintain perfusion and blood pressure. Treatment with anti-arrhythmics (e.g. lidocaine for ventricular arrhythmias; atropine or glycopyrrolate for bradycardia) may be necessary as arrhythmias develop (based on electrocardiogram evaluation or physical examination findings). The use of an antidote, digoxin specific antibody fragments (Digibind®, GlaxoSmithKline, Middlesex, UK), may be necessary if the bird is severely affected; however, because of its high price, lack of a true therapeutic avian dose range, its potential for adverse effects, and lack of veterinary literature or information on its use in birds, it is often not used (Peterson and Talcott, 2006). If the ingestion is addressed quickly with appropriate decontamination, the overall prognosis is fair. If, however, the ingestion was significant and decontamination was not immediate or effective, or symptoms have already begun, most birds poisoned by oleander carry a poor to grave prognosis.
Oak (Quercus)
There are two native species of oak in the UK, the sessile oak (Quercus petraea) and the pedunculate oak (Quercus robur). Oaks belong to the beech family, Fagaceae. They are long-lived trees that grow quite slowly, at least in their initial years. Both the sessile and pedunculate oak can grow to be very large trees — old trees can have a circumference of some 10 to 12 metres (Kingsbury, 1964). It is not always easy to distinguish between the sessile and pedunculate oak as the two species hybridize quite readily, and it may be difficult to find a ‘pure’ representative of each species (Potter, 1994). Because of the tannin found within the bark, oak trees are resistant to insect and fungal infestation; however, this helpful property is also what results in the toxicity for companion birds exposed to oak. Toxicosis can arise from well-intentioned owners giving the bird oak branches or twigs to use as perches, or acorns to pick apart for environmental enrichment.
Oak toxicosis is thought to be caused by the high concentrations of tannins and their metabolites (including digallic acid, gallic acid, and pyrogallol). These metabolites may result in acute renal failure and GI upset (Gupta, 2007). Clinical signs from toxicosis include anorexia, diarrhoea, regurgitation, generalized malaise, polydypsia. Wild birds are known to have been poisoned by ingesting large quantities of the leaves (particularly the early buds) and acorns (particularly green acorns). With oak toxicosis in wild birds reported findings include GI upset, followed by diffuse hepatocellular swelling and signs of acute renal failure. A case of oak poisoning was reported in a double wattled cassoway that died following ingestion of oak leaves (Kindle, 1988). The bird developed anorexia, diarrhea and polydypsia. Necropsy findings revealed that the bird had severe enteritis, sloughing of the intestinal villi, swelling of the kidneys with nephrosis, and generalized interstitial oedema of the muscle. High content of tannins were found in the bird's liver and intestinal tract (Kindle, 1988).
Treatment for oak poisoning
Treatment for oak toxicosis includes appropriate decontamination (with crop lavage and activated charcoal), fluid supplementation, antidiarrhoeals, nutritional support, and clinicopathologic monitoring for acute renal failure or hepatic injury.
Other toxic plants
The plants discussed are some of the most common causes of plant toxicosis in birds. There are, however, numerous other plants that birds should avoid (Table 1).
Conclusions
Bird owners should be aware of the common plant toxicities that can be seen in both caged indoor and outdoor birds. Ideally bird owners should be educated on the common plants and flowers that are poisonous, and be taught how to pet-proof the environment appropriately. Client communication and education are imperative to prevent avian toxicosis. Birds do not show their clinical illness until signs are severe, and the outcome is often poor when clinical signs have already developed. Aggressive decontamination with crop lavage and activated charcoal is the mainstay therapy for any poisoned patient, including birds.