The clinical spectrum and outcome of accidental wildfowl-mediated nicotinic plant poisoning.

Sir,

I read with much interest the case report by Bellomo et al. [1]. I would like to make two comments: (i) a toxicological analysis on biological specimens, such as urine and serum, should have been done in order to increase the diagnostic accuracy [2] and (ii) the description of the clinical spectrum and outcome of the disease made by the authors is misleading because it can induce the readers to consider it a mild disease. Actually, the clinical spectrum and outcome of accidental wildfowl-mediated (quails, skylarks, chaffinches, robins) nicotinic plant poisoning are very large and variable. Plants containing nicotine and nicotine-like alkaloids that have been reported to be poisonous to humans include Conium maculatum, Nicotiana glauca and Nicotiana tabacum, Laburnum anagyroides and Caulophyllum thalictroides [3]. They contain the toxic alkaloids nicotine, anabasine, cytosine, n-methylcytisine, coniine, n-methylconiine and gamma-coniceine [3]. These alkaloids act agonistically at nicotinic-type acetylcholine (cholinergic) receptors. The nicotinic-type acetylcholine receptor can vary both in its subunit composition and in its distribution within the body (the central and autonomic nervous systems, the neuromuscular junctions and the adrenal medulla). Agonistic interactions at these variable sites may explain why alkaloids have diverse effects depending on the administered dose and duration of exposure [3]. Twenty years ago, we reported the largest series ever published of accidental hemlock poisoning [4]: it included 17 patients poisoned in Apulia (South Italy) between 1972 and 1990: in 14 of them, toxicological analysis was performed on the same day of hospital admission which detected coniine. Neurotoxic effects were observed in all cases: in six coniine-poisoned patients, flaccid paralysis involved respiratory muscles following the typical curare progression. In others of our coniine-intoxicated subjects, muscle hypotonia without loss of voluntary movements was observed, probably because of the smaller amounts of poison ingested. Nicotinic effects of coniine were also present: stimulation (sialorrhoea, nausea, vomiting, abdominal cramps, diarrhoea) being followed by mucosal dryness, gastrointestinal hypotonia and mydriasis [4]. The 17 patients intoxicated by coniine experienced muscle pains, which started some hours after the ingestion of the poison (rhabdomyolysis). Five patients developed the clinical features of acute kidney injury from the first day of intoxication. Ten patients were simply treated on forced diuresis sometimes with gastrolavage; six patients were transferred to the intensive care unit and required artificial respiration; the five subjects who suffered acute kidney injury were treated with haemodialysis or peritoneal dialysis; in one patient, plasmaphaeresis seems to have improved an initially severe clinical picture. The outcome was favourable in 13 cases: 4 patients (∼24%) died, 3 of them from complications linked to the acute kidney injury; the last one died 36 h after the poisoning because of respiratory muscle paralysis [4].

In conclusion, the clinical spectrum of accidental wildfowl-mediated nicotinic plant poisoning is very large and the outcome is variable, ranging from complete recovery to death.