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Crown vetch (Coronilla varia) poisoning in a budgerigar (Melopsittacus undulatus).

Abstract: A 9-month-old, male budgerigar (Melopsittacus undulatus) was presented with an acute onset of weakness and vomiting. The bird had recently ingested leaves of freshly harvested crown vetch (Coronilla varia) from a fresh cutting of the plant placed next to the bird's cage. During the following 10 hours, the bird exhibited tachypnea and showed progressive neurologic signs of weakness, incoordination, tremors, and depression. The bird was treated with supportive care and activated charcoal. Its condition stabilized in the following 8 hours, with improvement within 48 hours and complete recovery in 2 weeks. Crown vetch grows in disturbed soils, tolerates dry conditions, and is often planted to prevent soil erosion. The toxic constituent of crown vetch is the nitrotoxin, [beta]-nitropropionic acid, a potent neurotoxin.

Key words: crown vetch poisoning, Coronilla varia, nitrotoxin, [beta]-nitropropionic acid, neurotoxicity, avian, budgerigar, Melopsittacus undulatus

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A 9-month-old, male budgerigar (Melopsittacus undulatus), weighing 32 g, was presented to the emergency clinic at the Veterinary Teaching Hospital at Colorado State University because of an acute onset of weakness and vomiting. The bird had repeatedly vomited seeds during the hour before presentation.

The client had purchased this bird along with a female budgerigar 3 months earlier from a local pet store. Both birds shared the same cage. Both birds appeared healthy before the onset of illness in the male bird, and the female bird never showed signs of illness. The birds were the only pets in the household and were not allowed outside their cage. They were fed a commercial seed mixture free choice, supplemented with occasional fruits and vegetables. Supplements had not been given in the 3 days before presentation. The birds were fed from plastic food and water containers. The cage was a standard birdcage that was also purchased from the pet store.

Before the onset of signs, the client had placed freshly picked wildflowers in a vase adjacent to the birds' cage. Two hours later, the male bird appeared weak and had vomited seeds multiple times. The owner noticed that 2 leaves from the wildflower plant adjacent to the cage were hanging in the cage and had been partially chewed by 1 or both birds. It appeared to the client that one half of each of the 2 leaves had been ingested.

On initial examination, the bird appeared bright, alert, and responsive and was no longer vomiting. Because the bird appeared stable and had likely vomited the plant leaves, treatment with an oral activated charcoal was not done. The client was offered the choice of hospitalizing the bird for overnight observation or taking the bird home for observation, and the client elected to take the bird home.

During the next 10 hours, the bird's neurologic signs became progressively more severe. The client returned with the bird the next morning, 11 hours after the initial presentation. At that time, the bird was weak, markedly incoordinated, and moderately depressed, and it had difficulty perching in a normal manner. Instead, the bird would drape itself over the perch for balance (Fig 1). The bird exhibited mild, rapid tremors and had frequent contractions similar to those seen in a bird during egg-laying. Its respirations were rapid and shallow, and its heart rate was too rapid to count. The bird appeared to be aware of its surroundings and had a normal pupillary light reflex.

[FIGURE 1 OMITTED]

The client was asked to bring in the plant that was adjacent to the birdcage for identification. The plant was identified as crown vetch (Coronilla varia) (Fig 2). Crown vetch contains the toxin [beta]-nitropropionic acid, a neurotoxin. (1) Therefore, the presumed diagnosis was crown vetch poisoning. The bird was hospitalized and treated with 0.5 ml of liquid activated charcoal. Because the bird could not eat or drink, it was treated with subcutaneous fluids (lactated Ringer's solution; 1 ml q8h SC) and a commercial enteral solution (0.8 ml q8h PO; Emeraid-II, Lafeber Co, Cornell, IL, USA) by gavage for the next 24 hours. It was maintained in a padded box within a heated oxygen cage that provided an environmental temperature of 29[degrees]C (84[degrees]F) and 40%-60% oxygen.

[FIGURE 2 OMITTED]

After 8 hours, the bird's condition began to improve. Although it remained weak, exhibited difficulty in grasping a perch, and was unable to stand in a normal upright posture, the tremors gradually disappeared. After 24 hours, the bird's condition was stable and it appeared normal, although it was not eating on its own nor vocalizing.

The client elected to take the bird home and continue the nursing care by syringe feeding a commercial diet for nestling psittacine birds (Exact, Kaytee, Chilton, WI, USA). According to the client, the bird was eating normally in 2 days. However, the client felt that the bird was having difficulty in seeing because it would stay on its perch most of the time, only leaving to move to the food or water bowl. It also did not vocalize as much as it normally would. The female parakeet remained normal. After 2 weeks, the male appeared normal. Ten months later, the birds remained normal.

Discussion

In this case report, a diagnosis of crown vetch toxicity was made based on a history of an acute onset of signs after ingestion of the plant. Differential diagnoses for vomiting followed by the onset of neurologic signs include infectious agents, household toxins, and human foods that might be toxic to birds. However, given that this bird had essentially been in isolation for the past 3 months and was confined to a cage at all times, and the history ruled out exposure to human foods, these are extremely unlikely. Additional diagnostic tests that would be appropriate for birds exhibiting these signs include radiographs, a complete blood cell (CBC) count, examination of feces, and a plasma biochemical panel.

Few biotoxicoses have been reported in companion birds. Biotoxins are poisonous substances that are produced by living organisms. The most frequent biotoxins affecting wild birds are botulinum, mycotoxins, and blue-green algae toxins. (2-4) Phytotoxins are biotoxins produced by plants. Phytotoxicosis is rarely reported in poultry, wild birds, or companion birds. (5) A list of plants reported to be toxic specifically to budgerigars includes avocado (Persea americana), black locust (Robina pseudoacacia), clematis (Montana rubens), lily-of-the-valley (Convallaria majalis), oleander (Nerium oleander), philodendron (Philodendron scandens), poinsettia (Euphorbia pulcherrima), Virginia creeper (Parthenocissus quinquefolia), and yew (Taxus media). (6-8) Plant poisonings produce a variety of clinical signs based on the toxic chemicals in the phytotoxin. Plant neurotoxicants cause weakness, incoordination, depression, agitation, tremors, convulsions, and bizarre behavior that can result in death.

Crown vetch grows in disturbed soils, tolerates dry conditions, and is often planted to prevent soil erosion. It is a perennial herb that grows from a taproot with branching and trailing stems. Crown vetch is identified by alternate, odd-pinnate, hairless leaves, with up to 25 lanceolate leaflets. The pink-to-white flowers are found on the leaf stalks that are 7.5-12.5 cm long, with 5-20 pea-like flowers on each stalk. Typical of legumes, they produce seedpods. The pods are 2.5-5 cm long and contain many cylindrical, brown seeds. (1)

Crown vetch contains nitroglycosides, the most toxic of which, [beta]-nitropropionic acid, is poisonous to nonruminants. (9) Toxicity of the milk vetches is primarily attributed to the nitro-compounds. The pathophysiology of plant nitrotoxin poisoning in animals is not fully understood. The proposed pathophysiology of plant nitrotoxin poisoning in animals is summarized (Fig 3). Ingested fresh plants are toxic, but toxicity gradually declines as the plant dies. (9) The toxin is absorbed from the alimentary tract and enters the portal blood where it passes into the liver before circulating to the rest of the body. The toxicity of the nitrotoxin is influenced by the amount ingested and the rate of absorption, metabolism, excretion, and delivery to the target molecule. (10)

[FIGURE 3 OMITTED]

Little is known about how most plant toxins are absorbed from the alimentary tract. Once absorbed, the liver is typically the major organ for the metabolism of foreign compounds; however, plant toxins can be metabolized in extrahepatic locations, such as the lung, kidneys, and intestine. (9) [beta]-Nitropropionic acid and perhaps other unidentified metabolites from crown vetch affect the brain and spinal cord, causing muscle weakness and collapse. (1) The toxin also inhibits enzymes of the tricarboxylic acid cycle. (9) Metabolism of [beta]-nitropropionic acid produces nitrites that can also result in methemoglobin formation.

Chickens experimentally fed crown vetch exhibited signs of incoordination and staggering gait, leading to collapse and an inability to right themselves. (11) These signs are very similar to those observed in this budgerigar. Vomiting was not reported in the chickens, and the cause of the initial vomiting in the budgerigar is not known but is presumed to be associated with irritation of the intestinal tract.

In 1991, an aviary housing budgerigars, cockatiels, and lovebirds was reported to experience 80% mortality after the birds were fed a type of vetch. (12) The plant in that report was of the genus, Vicia, not Coronilla, and the toxic compound was suspected to be cyanide, not a nitrotoxin, leaving the reader puzzled as to what plant was involved. The birds in that incident exhibited clinical signs of muscle tremors, opisthotonus and seizures. Necropsy findings of two of the birds revealed focal areas of cerebral necrosis.

Specific antidotes for crown vetch toxins are not available. The general treatment for plant-related toxicosis involves reducing or eliminating exposure to the plant, detoxification, and symptomatic treatment. Detoxification begins by promptly causing emesis or performing gastric lavage. Induction of emesis in birds can be difficult and risky; therefore, crop lavage may be the preferred method of detoxification. This is followed by treatment with oral activated charcoal and osmotic cathartics. Activated charcoal administered orally may inhibit absorption of the toxin. In this case, the bird had vomited before being presented to the veterinary emergency clinic. It was not treated with liquid activated charcoal because of the possibility that all the plant had already been vomited and concern about aspiration of the activated charcoal. However, apparently the bird did not vomit all of the plant and absorbed some of the ingested toxin later, as indicated by the development of the neurological signs. If the bird had been treated with activated charcoal at the time of original presentation, the neurologic signs may have been prevented. By the time activated charcoal was administered, the toxin, most likely, had been maximally absorbed.

Because a blood sample was not obtained from this bird at the time of presentation, it is not known if methemoglobinemia was present. If methemoglobin formation is a manifestation of crown vetch toxicity in birds, then part of the treatment for crown vetch poisoning would be intravenous methylene blue. (13) The safety of using methylene blue in such a small bird is not known.

References

(1.) Knight AP, Walter RG. A Guide to Plant Poisoning. Jackson, WY: Teton NewMedia; 2002.

(2.) Peckham MC. Poisons and toxins. In: Hofstad MS, Barnes HJ, Calnek BW, Reid WM, Yoder HW, eds. Diseases of Poultry. 8th ed. Ames: Iowa State University Press; 1986:738-818.

(3.) Jackson ARB, Runnegar MTC, Cumming RB, Brunner JF. Experimental acute intoxication of young layer and broiler chickens with the cyanobacterium [blue-green algae] Microcystis aeruginosa. Avian Pathol. 1986;15:741-748.

(4.) Humphreys DJ. Poisoning in poultry. World's Poult Sci J. 1979;35:161-176.

(5.) Calnek BW, ed. Diseases of Poultry. 10th ed. Ames: Iowa State University Press; 1997:996-998.

(6.) Frazier DL. Avian toxicology. In: Olsen GH, Orosz SE, eds. Manual of Avian Medicine. St. Louis, MO: Mosby; 2000:228-263.

(7.) Bauck L, LaBonde J. Toxic diseases. In: Altman RB, Clubb SL, Dorrestein GM, Quesenberry K, eds. Avi an Medicine and Surgery. Philadelphia, PA: WB Saunders Co; 1997:612.

(8.) Hargis AM, Stauber E, Casteel S, Eitner D. Avocado (Persea americana) intoxication in caged birds. J Am Vet Med Assoc. 1989;194:64-66.

(9.) Pass MA. Toxins and mechanisms of intoxication. In: James LE Keeler RF, Bailey EM Jr, Cheeke PR, Hegarty MP, eds. Poisonous Plants: Proceedings of the Third International Symposium. Ames: Iowa State University Press; 1992:407-413.

(10.) Osweiler GD. The National Veterinary Medical Series for Independent Study: Toxicology. Philadelphia, PA: Williams & Wilkins; 1996:361-407.

(11.) Shenk JS, Wangsness PJ, Leach RM, et al. Relationship between [beta]-nitropropionic acid content of crown-vetch and toxicity in nonruminant animals. J Anita Sci. 1976;42:616-621.

(12.) Lutz ME. In my experience: crown vetch intoxication. J Assoc Avian Vet. 1991;5:73.

(13.) Dumonceaux G, Harrison GJ. Toxins. In: Ritchie BW, Harrison GJ, Harrison LR, eds. Avian Medicine: Principles and Application. Lake Worth, FL: Wingers Publishing Inc; 1994:1030-1052.

From the Colorado State University, College of Veterinary Medicine and Biomedical Sciences, Department of Clinical Sciences, 300 West Drake Road, Fort Collins, CO 80523, USA.
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Article Details
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Title Annotation:Clinical Reports
Author:Campbell, Terry W.
Publication:Journal of Avian Medicine and Surgery
Article Type:Case study
Geographic Code:1USA
Date:Jun 1, 2006
Words:2133
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