Often referred to as sago palms, cycads are hardy evergreen yard plants that grow in warm states, such as Florida, North Carolina, and Georgia, and are also
used as ornamental houseplants.1 Lately, their increased use as houseplants has made them available all over the world.2 Cycads, such as Zamia floridana, Cycas revoluta, and Cycas circinalis, arose from vegetation that dominated in the Mesozoic era.
Cycad leaves are one-pinnately divided and glossy green (Figure 1). The leaflets are narrow, with a sunken midrib, and the margins roll downward. These palmlike plants are dioecious (separate
male and female plants in the same species). The female plant has a cone-shaped middle that produces seeds.3-5 The pollen cone is large and erect; the seeds are loosely arranged with leaves around the stem. Each seed is large, plumlike,
and pale-yellowish-tan.1 Male cones are elongated and do not produce seeds.
1. The glossy green leaves of Cycas revoluta. (Photo courtesy of Dr. Safdar Khan, APCC, ASPCA.)
Cycad toxicosis has been described in people and many animals, including dogs, sheep, and cattle. In this article, I focus
on the clinical signs, diagnosis, and treatment of cycad toxicosis in dogs.
TOXICITY AND MECHANISM OF ACTION
Cycad palms produce three toxins: cycasin, beta-methylamino-L-alanine, and an unidentified toxin.3-6
Cycasin, which is converted to its aglycone, methylazoxymethanol, may cause centrilobular and midzonal coagulative hepatic
necrosis and gastrointestinal irritation. In addition, cycasin is carcinogenic, mutagenic, and teratogenic.3,5,6
Beta-methylamino-L-alanine, a neurotoxic amino acid, causes ataxia in rats and is implicated in Guam disease in people. Guam
disease is characterized by symptoms similar to those of Alzheimer, Parkinson, and Lou Gehrig (amyotrophic lateral sclerosis)
The unidentified toxin, a high-molecular-weight compound, may cause hindlimb paralysis in cattle because of axonal degeneration
in the central nervous system.3,5,6
All parts of the plant are toxic, but the seeds contain higher amounts of cycasin than do other parts of the plant. Dogs usually
ingest the seeds. Although toxic, the young leaves are palatable.7-9
In one study, the most common signs in dogs ingesting cycad plants were gastrointestinal, hepatic, and neurologic.10 In cases reported to the American Society for the Prevention of Cruelty to Animals (ASPCA) Animal Poison Control Center
and recorded in the AnTox database between 1988 and 1998, the most common signs of cycad toxicosis in dogs were vomiting (with
or without blood), depression, diarrhea (with or without blood), and anorexia.11 AnTox data from 2000 through 2007 show the same common signs of cycad toxicosis in dogs as mentioned above.
Gastrointestinal signs may develop within 24 hours, but bilirubin concentrations and serum alanine aminotransferase and alkaline
phosphatase activities may not become elevated for 24 to 48 hours.10 Signs may last from 24 hours to nine days.11
Gastrointestinal abnormalities in dogs with cycad poisoning include hemorrhage and mucosal necrosis. Histologic abnormalities
in the livers of these dogs include cirrhosis with marked focal centrilobular and midzonal coagulation necrosis.2
Cycad toxicosis is diagnosed based on a history of known exposure (e.g. observed ingestion, identification of chewed plants, identification of plant material in vomitus) and compatible clinical
signs. Although cycasin and beta-methylamino-L-alanine can be found in the livers of animals that ingest cycad palms, no diagnostic
laboratories routinely test for these compounds.2