A case of infantile star anise toxicity.

Chinese star anise (Illicium verum) is a popular herbal remedy for infantile colic. Contamination with a related species of Japanese star anise (Illicium anisatum) has been related to cases of toxicity in infants. We report the case of a 3-month-old infant girl who presented to the emergency department with signs and symptoms of toxicity after recent star anise ingestion. Her presentation is consistent with other reports of toxicity that include particular gastrointestinal and neurological findings. A discussion of the clinical aspects of star anise toxicity, differential diagnosis, and management follows.

Norsesquiterpene glycosides in bracken ferns (Pteridium esculentum and Pteridium aquilinum subsp. wightianum) from Eastern Australia: reassessed poisoning risk to animals.

Austral bracken Pteridium esculentum contains three unstable norsesquiterpene glycosides: ptaquiloside, ptesculentoside, and caudatoside, in variable proportions. The concentration of each of the glycosides was determined in this study as their respective degradation products, pterosin B, pterosin G and pterosin A, by HPLC-UV analysis. Samples of P. esculentum collected from six sites in eastern Australia contained up to 17 mg of total glycoside/g DW, with both ptaquiloside and ptesculentoside present as major components accompanied by smaller amounts of caudatoside. Ratios of ptaquiloside to ptesculentoside varied from 1:3 to 4:3, but in all Australian samples ptesculentoside was a significant component. This profile differed substantially from that of P. esculentum from New Zealand, which contained only small amounts of both ptesculentoside and caudatoside, with ptaquiloside as the dominant component. A similar profile with ptaquiloside as the dominant glycoside was obtained for Pteridium aquilinum subsp. wightianum (previously P. revolutum ) from northern Queensland and also P. aquilinum from European sources. Ptesculentoside has chemical reactivity similar to that of ptaquiloside and presumably biological activity similar to that of this potent carcinogen. The presence of this additional reactive glycoside in Australian P. esculentum implies greater toxicity for consuming animals than previously estimated from ptaquiloside content alone.

[An epidemic of epileptic seizures after consumption of herbal tea]. / Een epidemie van epileptische aanvallen na drinken van kruidenthee.

UNLABELLED: At the end of September 2001 the Inspectorate for Health Protection and Veterinary Public Health and the National Poisons Control Centre (NPCC) were informed about adverse health effects after consumption of a herbal tea. During consultations it was suggested that Japanese star anise (Illicium anisatum L.), which is known to contain a neurotoxin, may have been inadvertently mixed into the herbal tea. In view of the severity of the adverse health effects and the clear association with consumption of a specific herbal tea, the supplier was urgently advised to withdraw the suspected herbal tea from the market. A total of 63 persons reported symptoms of general malaise, nausea and vomiting 2-4 hours following consumption of the herbal tea. Twenty-two persons required hospitalisation, of whom 16 due to generalised tonic-clonic seizures. Medical investigations revealed no underlying pathology and after supportive treatment, the patients were discharged in good health. Morphologic and organoleptic investigations of the suspected herbal tea indicated that this possibly contained Japanese star anise. NMR analysis of the herbal tea confirmed the presence of the neurotoxin anisatin, a non-competitive GABA-antagonist which can cause hyperactivity of the central nervous system and tonic-clonic seizures. CONCLUSION: Ingestion of a herbal tea containing anisatin caused the reported serious adverse health effects. Close cooperation between clinicians, the Inspectorate for Health Protection and Veterinary Public Health and the NPCC played a vital role in preventing further harm to public health.

Intoxication with huperzine A, a potent anticholinesterase found in the fir club moss.

BACKGROUND: Herbs from Lycopodium are generally reputed to be nontoxic and are occasionally used for preparing a salubrious tea. In Europe, the common Lycopodium clavatum can be easily confused with Lycopodium selago, the fir club moss. CASE REPORT: We report 2 patients who drank a tea, erroneously prepared from dried herbs of Lycopodium selago, which resulted in sweating, vomiting, diarrhea, dizziness, cramps, and slurred speech. These symptoms were suggestive of a cholinergic mechanism. To elucidate the active principle, aqueous extracts of Lycopodium selago were checked for their suspected anticholinesterase activity using human erythrocytes as an enzyme source in a modified Ellman assay. The extracts did exhibit significant anticholinesterase activity. The anticholinesterase(s) were most effectively extracted with dichloromethane and isolated by high-performance liquid chromatography. The major compound with anticholinesterase activity co-chromatographed with authentic huperzine A, but had a 2-3-fold higher inhibitory potency than the racemic standard. The amount of huperzine A found in the Lycopodium selago sample used for the tea preparation was calculated to be sufficient for a relevant acetylcholinesterase inhibition. CONCLUSION: The signs and symptoms of Lycopodium selago poisoning are consistent with the anticholinesterase activity of huperzine A and should favorably respond to atropine therapy. This report demonstrates once more that laymen should not be encouraged to gather their remedies from "Mother Nature" without advanced botanical knowledge.

Status spongiosis, optic neuropathy, and retinal degeneration in Helichrysum argyrosphaerum poisoning in sheep and a goat.

Lesions of natural Helichrysum argyrosphaerum poisoning were studied in eight sheep and one goat. Light microscopic examination revealed widespread, bilaterally symmetrical status spongiosis of the white matter of the brain consistently present in the subependymal area adjacent to the lateral ventricles, cerebellar peduncles, and brain stem in all animals. In three animals, the ultrastructural finding of intramyelinic vacuolation due to splitting of the myelin lamellae at the intraperiod lines indicated myelin edema. There was also mild distension of perivascular and extracellular spaces in the severely affected areas. Significant changes were absent in neurons, glial cells, axons, or blood vessel walls. Myelin edema associated with degeneration and loss of axons and myelin and astrocytic gliosis was present in the intraorbital and intracranial portions of the optic nerves. In the intracanalicular portions of the nerves in three animals that were studied, more chronic lesions consisting of fibrosis and atrophy of the nerve suggested that the optic neuropathy follows compression of the nerve in the optic canal as a result of myelin edema. The toxic principle of the plant also caused a degenerative retinopathy in five animals. The essential histopathologic change was degeneration and loss of the photoreceptor outer segments predominantly in the nontapetal retina. These retinal lesions were associated with hyperplasia and hypertrophy and with migration of the pigmented epithelium, focal retinal separation, and depletion and loss of the nuclear layers.

The effect of dietary supplements on chronic bitterweed (Hymenoxys odorata) poisoning in sheep.

Two experiments were designed to establish a chronic bitterweed dose in sheep and to study the prevention of chronic bitterweed poisoning with dietary supplements of high protein (20% crude protein) and sodium sulfate. The first experiment consisted of 5 lambs in each of 3 groups. The low dose received up to 5.0 g bitterweed/kg/day which was equivalent to 10 mg hymenoxon/kg bw. The high dose group received a maximum bitterweed dose of 1 g/kg/day or 20 mg hymenoxon/kg. The final average weights of the low (29 kg) and the high (30 kg) dose groups were significantly different from the control (40 kg) group. The prophylactic experiment consisted of 5 groups of 4 sheep each. Each group received a different combination of bitterweed, a basal ration, soybean meal, urea, or sodium sulfate. The soybean meal and urea were used to adjust the ration to 20% crude protein, and each animal received 1.2 g bitterweed/kg/day. The high protein-sodium sulfate diet did not prevent chronic bitterweed toxicity, but soybean meal-sodium sulfate combination had the greatest effect on the reduction of bitterweed toxicity. Urea potentiated the toxic effects of bitterweed.

Potential for dietary amino acid precursors of neurotransmitters to overcome neurochemical changes in acute T-2 toxicosis in rats.

Experiments were conducted to determine the potential for overcoming T-2 toxin-induced changes in brain neurotransmitter concentrations through dietary manipulation. Rats were fed either a tryptophan-deficient, gelatin-based diet or the same diet supplemented with a mixture of large neutral amino acids for 4 d. Rats were then dosed with 0 or 2.0 mg T-2 toxin/kg body weight and killed 4, 8 or 12 h after dosing. The large neutral amino acid supplements successfully reduced brain concentrations of tryptophan and serotonin in control rats, but this was not enough to overcome the acute effects seen in T-2 toxin-treated rats. A further experiment was then conducted to monitor the effect of T-2 toxin on the ratio of free to protein-bound tryptophan in plasma. Total plasma tryptophan increased in T-2 toxin-treated rats, although there were no significant differences in the ratio of free to protein-bound tryptophan. A final experiment was conducted to determine the specificity of the T-2 toxin effect on concentrations of plasma amino acids. Concentrations of amino acids that use the large neutral amino acid transport system into the brain were higher in T-2 toxin-treated animals. The only other amino acid that had a higher concentration was arginine. It was concluded that acute doses of T-2 toxin may selectively alter membrane transport of amino acids.

Assessment of a general therapeutic protocol for the treatment of acute T-2 toxicosis in swine.

T-2 toxin, a trichothecene mycotoxin suspected of being used as a chemical warfare agent, was administered iv to swine at a dose of 3.6 mg/kg body weight (iv LD50 approximately 1.2 mg/kg). Four different therapeutic protocols were assessed for their efficacy in the treatment of the resultant acute T-2 toxicosis syndrome. One therapeutic protocol included the combined use of metoclopramide, activated charcoal, magnesium sulfate, dexamethasone sodium phosphate, sodium bicarbonate and normal saline. The other 3 protocols utilized the same agents less 1 of the following: the combination of activated charcoal and magnesium sulfate, sodium bicarbonate, or normal saline. All 4 treatment groups showed improved survival times compared to a positive T-2 control group. Within the limits of the study, it would appear that the removal of activated charcoal and magnesium sulfate was most detrimental to the T-2 toxin-dosed swine.

Protective effects of antioxidants on bitterweed (Hymenoxys odorata DC) toxicity in sheep.

Antidotal effects of the 2 antioxidants butylated hydroxyanisole (BHA) and ethoxyquin (EQ) were evaluated in bitterweed (Hymenoxys odorata DC) toxicosis in sheep. Bitteerweed contains a toxic sesquiterpene lactone, hymenoxon, the toxicity of which is reduced by cysteine. Both BHA and EQ are known to induce hepatic glutathione production in rodents. Treatment of sheep with EQ (2.5 g/sheep/day for 9 days before poisoning) gave significant protection from toxic doses of bitterweed, but the protective effect of BHA was insignificant. Of 6 sheep given EQ in the feed, 5 survived 7 doses of bitterweed (4 g/kg/day or higher for 7 days), whereas 5 of 7 controls and 4 of 7 sheep given feed with added BHA died. The added EQ in the feed decreased the serum alkaline phosphatase activity and total protein, albumin, and calcium concentrations. Seemingly, EQ is the first protective agent with field application potential for bitterweed toxicity.