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In the early morning hours of July 9, 2008, six adult family members were admitted to a hospital emergency department in Maryland with hallucinations, confusion, mydriasis, and tachycardia of approximately 3-4 hours duration. Approximately 4-5 hours earlier, all six family members had shared a meal of homemade stew and bread. Subsequent investigation by the Montgomery County Department of Health and Human Services (MCDHHS) and the Maryland Department of Health and Mental Hygiene (MDHMH) determined that the stew contained jimsonweed (Datura stramonium), a plant in the nightshade family that contains atropine and scopolamine1 and has been associated with anticholinergic-type poisoning.1 This report describes the poisoning incident, which resulted in six hospitalizations, and the subsequent multidisciplinary investigation. Health-care providers and public health officials should be aware that jimsonweed poisoning can occur among many age groups, including younger persons, who typically consume the plant material for recreational purposes, or persons of any age group who might unknowingly ingest the plant. A prompt diagnosis of jimsonweed poisoning is complicated by the difficulties in eliciting exposure histories in persons with altered mental status and the variable presentations of affected persons. Consultation with horticulturalists, poison control centers, and specialized laboratories might be necessary to investigate cases and outbreaks.
The six affected persons came from one family and included three men and three women ranging in age from 38 to 80 years (median age: 42 years). All six shared a meal of homemade stew and bread at approximately 9:00 p.m. on July 8, 2008. No one else was at the home when the meal was eaten. Approximately 1 hour later, another relative arrived at the home and discovered the six affected family members laughing, confused, and complaining of hallucinations, dizziness, and thirst. One of the family members vomited. The unaffected relative called emergency medical services, and all six were transported to the hospital by ambulance.
On admission to the emergency department, two of the six patients were unconscious. The other four were awake and had altered mental status; complete history of meal preparation and food exposures could not be obtained. Physical examinations revealed tachycardia and dilated, sluggishly reactive pupils in five of the six patients. Temperatures ranged from 98.0°F (36.7°C) to 99.4°F (37.4°C). Respirations ranged from 17 to 22 breaths per minute.
During the next 6 hours in the emergency department, the six patients continued to experience tachycardia, mydriasis, and altered mental status. One remained unconscious. The others demonstrated confusion, aggression, agitation, disorganized speech, incoherence, and hallucinations. All six were admitted to the hospital, five to the intensive-care unit. The unaffected relative reported to providers that pesticides had been sprayed on mint leaves that might have been incorporated into the stew. However, a treating physician consulted the poison control center hotline and established that the illnesses were not consistent with cholinergic poisoning, as would be expected with ingestion of organophosphate pesticides, but were consistent with anticholinergic poisoning.
Complete blood counts, basic metabolic panels, comprehensive metabolic panels, and urinalysis generally were within normal limits. Urine screenings for amphetamines, barbiturates, benzodiazipines, tetrahydrocannabinol, opiates, phencyclidine, and cocaine were negative among four patients tested.
Over the course of their hospitalizations, the patients' signs and symptoms of anticholinergic toxicity fluctuated. In addition to tachycardia, mydriasis, and altered mental status, two patients experienced urinary retention, and one had a small pleural effusion identified by computed tomography scan. The patients received supportive care, including cardiac monitoring and intravenous fluids. Four of six patients were administered lorazepam to control agitation. None were administered physostigmine. Their neurologic statuses improved during hospitalization and were normal by the time of discharge. Four were discharged on the third hospital day, one on the fourth hospital day, and one on the fifth hospital day, each with a final diagnosis of altered mental status secondary to food poisoning. The patient reported to have eaten the most stew was the slowest to recover and had the longest stay. All patients fully recovered.
On July 9, 2008, MCDHHS and MDHMH began an investigation. At that time, the patients were still too disoriented to provide reliable information. Investigators interviewed unaffected family members about meal preparation and asked them to collect samples of the plants they thought had been used in the stew. One plant was identified as mint. Interviews with the patients on July 10 confirmed that all patients had consumed the stew and no one else had eaten the stew. The preparer of the stew recalled that it consisted mainly of potatoes but also included garlic, onion, tomato, curry powder, and leaves from two plants growing in the yard. One plant was confirmed to be mint. The meal preparer did not know what the other plant was, only that it grew wild in the yard.
On July 10, the public health investigators and a horticulture expert visited the home, located in a suburban Maryland neighborhood, to verify the stew ingredients and identify any ingredients that could cause anticholinergic poisoning. They found leftover stew, which was green in color with cooked leaves visible in the bottom of the pot. They also discovered plant material in the kitchen trash, identified by the horticulture expert as jimsonweed. In the outdoor location described by the stew preparer, the horticulture expert identified jimsonweed plants with recent cutting marks. They collected plant samples and leftover stew from the home for testing at the Maryland Department of Agriculture Laboratory. Atropine and scopolamine were detected in leftover stew by liquid chromatography-tandem mass spectrometry. Chaconine and solanine, glycoalkaloids normally present in potatoes, also were detected.
J Russell, C Edwards, C Jordan, Montgomery County Dept of Health and Human Svcs; E Luckman, A Chu, D Blythe, J Krick, Maryland Dept of Health and Mental Hygiene.
Jimsonweed grows wild and is used as an ornamental plant in much of the United States. It contains alkaloids such as atropine and scopolamine, which can cause anticholinergic toxicity. The concentration of anticholinergics can vary over time and in different parts of a plant, with the seeds having the highest concentration, containing approximately 0.1 mg of atropine per seed.1 A dosage of ≥10 mg of atropine can be fatal.1 Among the patients described in this report, those who ate more of the stew had more severe illness; however, the quantity of jimsonweed ingested could not be estimated. Cooking does not substantially affect the potency of the leaves, and atropine and scopolamine remain intact during baking.2 In this incident, chaconine and solanine, glycoalkaloids normally present in potatoes, were detected in the stew along with atropine and scopolamine. Green or sprouting potatoes can contain levels of glycoalkaloids high enough to cause toxicity in humans.3 However, only qualitative testing was performed, and no indication that the potatoes used in the stew were green or sprouting was noted.
Jimsonweed poisoning causes dry mucous membranes and skin, thirst, flushing, fever, blurred vision, altered mental status, mydriasis, urinary retention, tachycardia, coma, and, in rare cases, death.1,4 Treatment with physostigmine is indicated only in severe cases to reverse anticholinergic toxicity.1 Jimsonweed is sometimes consumed intentionally by persons seeking to experience its hallucinogenic effects,1,4 often in a jimsonweed tea.1* Because previous reports of toxicity have involved adolescents and young adults using jimsonweed to experience its hallucinogenic effects,1,4 health-care providers might be less likely to suspect ingestion of jimsonweed in older adults with signs and symptoms of anticholinergic toxicity.
The diagnosis of jimsonweed poisoning can be difficult because of the wide range of signs and symptoms associated with anticholinergic toxicity and the inability to obtain an accurate history of exposures.1,6,7 No clinical laboratory tests are routinely available to detect anticholinergic toxicity. The diagnosis generally is based on history, physical findings, and symptoms. The signs and symptoms among the patients described in this report varied over time. All patients reported thirst, hallucinations, and dizziness when first examined by emergency medical technicians; however, after arrival at the hospital, the clinical course for the six patients diverged. Clinicians might not suspect jimsonweed poisoning in a lone patient with coma or altered mental status, tachycardia, and mydriasis,6 especially if no specific exposure history is available. However, in this incident, health-care providers quickly suspected toxicity associated with the shared meal. Although the initial history of pesticide application to the mint caused providers to briefly consider organophosphate poisoning as the cause of the illnesses, consultation with the poison control center assisted quickly in determining that the illnesses instead were consistent with anticholinergic toxicity.
Health-care providers and public health officials should be aware of the signs of anticholinergic toxicity and should consider jimsonweed poisoning as a cause of any compatible food-related outbreak of anticholinergic toxicity. A thorough history of food consumption and drug exposures should be obtained, if possible, for all persons with anticholinergic toxicity. Health departments might have limited experience investigating the types of noninfectious foodborne illnesses, as described in this report. Consultation with horticulturalists, poison control centers, and specialized laboratories can be an important component of such investigations.
This report is based, in part, on contributions by W Bontoyan, K McManus, T Phillips, and S Audino, Maryland Dept of Agriculture; C Schuster, Univ of Maryland Extension; and The National Capital Poison Center.
*Jimsonweed historically was used by American Indians for medicinal and religious purposes. It is also known as thorn apple, angel's trumpet, and Jamestown weed (because the first record of physical symptoms after ingestion occurred in Jamestown, Virginia, in 1676).5
Jimsonweed Poisoning Associated With a Homemade Stew—Maryland, 2008. JAMA. 2010;303(11):1028–1030. doi:
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