Cocklebur toxicosis results from ingestion of the dicotyledonary stage or seedling stage of the common cockleburs. Cocklebur are ubiquitous throughout North America and can be fatal when consumed by livestock via pasture, feed contamination with bur seeds, in hay, or while grazing crop residues. Cases of cocklebur poisoning have been reported from cattle, sheep, swine and poultry.
Plant characteristics: The common cocklebur belongs to the genus Xanthium, with the most common species in the Midwest being Xanthium strumarium. Cocklebur is an annual plant that grows in many soil types including floodplains, moist rich soils such as shorelines of ponds and reservoirs, and disturbed soils of feedlots. Variation in morphology is common among cocklebur species, and they grow to an approximate mature size of 3-5 feet (1-1.5 cm) and usually have dark brown to purple spotted, stout stems. The plants have large, rough, glandular,triangular to shovel-shaped leaves with three main veins from the leaf base and; measure 2-14” (5-35.5 cm) long and 1-8” (2.5-20 cm) wide. The female flowers are larger than the male flowers, and form a 3/4” (1.5 cm) egg-shaped bur near the base of the plant. Each bur contains two seeds which can stay dormant in the soil for many years. Intoxications with cocklebur are most common in the spring and summer following periods of rain coupled with warmer temperatures that encourage germination of the seeds. Pigs, ruminants, and horses are all susceptible to cocklebur toxicosis, especially in the early spring following germination of seeds and grazing in fields where the highly palatable young plants may be present.
Toxic principle: Carboxyactractyloside (CAT), sulfated glycoside, is the principle toxin in cocklebur plants. CAT is structurally similar to adenosine diphosphate and, therefore, inhibits ADP translocase on the cytosolic side of the mitochondrial membrane. Inhibition of ADP translocase activity leads to diminished transport of ADP into the mitochondria and, hence, decreased oxidative phosphorylation and ATO formation. CAT is concentrated in embryonic and cotyledonary tissues of the cocklebur plant, resulting in the seed and two leaf cotyledonary stage of the plant being the most poisonous. While the toxin remains potent when these portions of the plant are preserved in hay, CAT is not present in the four-leaf stage and mature plant. Witte et al reported death in 6 of 70 yearling calves that had been fed round bale hay of foxtail and mature cocklebur plants. Cocklebur seeds can also contaminate grains used in concentrate rations fed to livestock.
Clinical signs: Consumption of as little as 0.75% of body weight of cotyledonary portions can cause death, with clinical signs occurring a few hours post cocklebur sprout or seed ingestion.The most commonly reported clinical signs of cocklebur intoxication in pigs and cattle include depression, weakness, anorexia, reluctance to move, opisthotonus, ataxia, hyperexcitability,spasmodic muscular activity, and an unusual gait with erect ears and head held high. Recumbency, paddling of limbs, convulsions followed by coma, and death can occur within hours to days of consumption. Onset of clinical signs is usually delayed in cattle with a functional rumen as compared to non-ruminants.
Pathology: Burrows and Tyrl report that distinct clinical pathology changes include a ten-fold or greater increase in the serum concentration of the liver enzymes AST and SDH accompanied by a marked hypoglycemia to as low as 10 mg/dl, especially in calves. Grossly,serosanguinous ascites, proteinaceous pericardial and pleural effusions, a swollen and congested liver, edema of the gall bladder wall, hepatic capsule, and subserosa of the small intestine along with fibrin tags on visceral surfaces are commonly present.
The most characteristic histologic lesion is severe, diffuse, centrilobular hepatocellular necrosis. Other lesions include para-central hepatic necrosis, renal tubular necrosis, and inconsistent neuronal degeneration and cerebral edema.
Prior to discovery of the CAT toxin and its related signs, reported lesions from cocklebur consumption included oral ulcers and other mechanical injury along with excessive salivation. As long haired dogs, cattle and sheep groomed burs out of their coats, spines or other parts of the bur would break off and traumatize oral mucosa resulting in ulcers similar to those caused by grass awns. Additionally, the bur remnants could become embedded in granulation tissue, making visualization of the foreign particles difficult and potentiating subsequent distant draining wounds or abscesses.
Diagnosis: Diagnosis of cocklebur intoxication is based on the combination of evidence of consumption of cocklebur cotyledonary tissues and/or burs in stomach contents, clinical signs, characteristic histopathologic lesions, and clinical pathology findings. Conklin and Hooser both report that diagnostic tests, including assays for CAT such as thin layer chromatography (TLC) reported in literature, have not produced reliable, repeatable results and, thus, no practical diagnostic test for cocklebur intoxication exists at this time.
Treatment: Carboxyatractyloside is a potent toxin that disrupts cellular function, and no treatment exists to antagonize the ADP/ATP mitochondrial imbalance caused by CAT. Supportive treatments reported in the literature, while helpful, are not curative and include increasing GI motility and clearance of the toxin with mineral oil and neostigmine, offering fatty substances with milk and lard to prevent absorption, and giving activated charcoal as an absorbent (not in concert with fatty substances). IV glucose can be administered to counteract the severe hypoglycemia. Use of neostigmine or physostigmine IM has been reported to temporarily alleviate muscular problems and, as such, can be a diagnostic aid.
Populations of Xanthium spp. plants should be eliminated with mowing, cultivation, and/or herbicide use to most effectively prevent cocklebur intoxication.
Case Report: In July 2003, a case of cocklebur toxicosis was diagnosed at ADDL in a herd of cattle in Indiana where 29 of 98 yearling calves died. While some animals were found dead, others exhibited depression, anorexia, muscle tremors, ataxia, aggression, became recumbent and died within a few hours of showing clinical signs. Lesions reported included a swollen liver with acute diffuse centrilobular necrosis. Many intact burs, along with partially ruminated corn shucklage, were present in the rumen. Histologically, marked centrilobular necrosis, hemorrhage and congestion were evident in the liver. Diagnosis of cocklebur intoxication was made based on evidence of exposure found at necropsy along with characteristic clinical signs, clinical pathology, and histologic findings in affected cattle. Cocklebur plants with burs had contaminated the primarily corn shucklage ration fed to the animals. The producer reportedly continued to feed this ration to the remaining animals; however, prior to feeding, placed large tube socks over his boots and walked through the bur-contaminated shucklage. If burs were collected via attachment to the socks, that portion of the feed was discarded.
Sample collection with a suspected toxicosis: Recall that if a toxicosis of any kind is suspected and the toxin/toxicant is unknown, it is important to obtain a complete history and perform a thorough physical examination and/or necropsy. If the animal is alive freeze and save all available vomitus and urine, 5 ml of whole blood in both red top clot and purple top EDTA tubes. Serum should be collected and stored in a plastic tube. At necropsy, fix representative tissues in 10% neutral buffered formalin. Save samples for virology, bacteriology or other ancillary tests if appropriate, and freeze and save the following tissues: liver (100g), stomach/rumen contents (100g or all available), brain (1/2 if organophosphate toxicosis is suspected), kidney (1/2), urine (all available), and an eyeball or ocular fluid (if nitrate toxicosis is suspected). A minimum of one pound of feed and one quart of water should also be submitted for toxicologic examination.
-by Emily Blough, Class of 2007
-edited by Dr. Dinesh Singh, ADDL Graduate Student
References:
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Burrows GE and RJ Tyrl: 2001. Toxic Plants of North America. Iowa State Press, Ames, Iowa
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Conklin B: (undated): FSO Project: A Year in Review. Development of New Thin Layer Chromatography (TLC) Testing Methods for Diagnosing Cocklebur Poisoning in Livestock. Obtained from Dr. Steve Hooser, Purdue ADDL Toxicologist, June, 2006.
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Hooser SB: Fall, 2005. Applied Food Animal and Equine Toxicology Class Notes. CPB 518
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Hooser SB: 2006. personal communication
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Knight AP and RG Walter: 2001. A Guide to Plant Poisoning of Animals in North America. Teton NewMedia, Jackson, Wyoming
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McGavin MD et al: 2001. Thomson’s Special Veterinary Pathology, 3rd ed., St. Louis: Mosby
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Isweuker GD: 1996. The National Veterinary medical Series for Independent Study: Toxicology. Williams and Wilkins, Philadelphia, PA
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Purdue Extension: 2004. Forage Field Guide, West Lafayette, IN
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Radostits OM et al: 2000. A Textbook of the Diseases of Cattle, Sheep, Pigs, Goats and Horses, 9th ed., W.B. Saunders, New York.
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Smith BO: 2002. Large Animal Internal Medicine, 3rd ed, St. Louis, Mosby.
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Stiles PI: 2003. Investigation of Multiple Deaths in a Beef Cattle Herd. Purdue University School of Veterinary Medicine Research Seminar, November 6.
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Witte ST et al: 1990. Cocklebur toxicosis in cattle associated with the consumption of mature Xanthium strumarium. J Vet Diag Invest 2(4): 263-7.
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