Cocklebur Poisoning

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Cockleburs (Xanthium spp.) are widely distributed in the midwestern US and grow as weeds in fencerows, ditches, and low or marshy areas. The toxic principle, carboxyatractyloside, is present in the seeds and young seedlings of the plant, especially during the cotyledonary (“two-leaf”) stage of growth. Seedlings may be ingested by pigs on pasture especially after spring rains when burs sprout in low-lying areas. Also, seeds may be ingested in mixed or ground feeds. Pigs may be found dead after consuming only modest number of seedlings. Because the clinical course of disease is only several hours, signs may not be observed and lesions may be absent from dead pigs. Mortality is sporadic unless plants are numerous.

In experimentally poisoned pigs, signs include depression, hypoglycemia, occasional nausea, incoordination, convulsions, and death. Lesions include serofibrinous effusions in body cavities and subcutaneous edema. There sometimes can be edema of the gall bladder wall and mild gastroenteritis. Microscopic lesions include centrilobular hepatotoxicosis with centrilobular accentuation of the liver pattern.

Diagnosis is often difficult unless cocklebur seedlings can be found in significant numbers in the pasture or seeds can be found in the feed. An “on-the-knees” search for the two-leaf stage sometimes reveals seedlings deep within lush pasture. Cocklebur poisoning must be differentiated from poisonings caused by ingestion of clay pigeons, aflatoxin, and gossypol.

In pigs showing clinical signs, mineral oil administered per os may delay absorption of the toxic principle until it can be eliminated. Injecting physostigmine has been reported to be of value in affected pigs.