Lily Robinson and the Art of Secret Poisoning: Recollections

Recollections

I hoped to confuse my dinner companions’ analysis of the events by providing a diverse meal that included mussels, parsley and watercress. I anticipated that the dinner guests would assume that the likely cause of death would be saxitoxin, the toxin responsible for paralytic shellfish poisoning, given that there were contaminated shellfish beds in New England. This was not the case. I chose to use the poison aconitine. Aconitine poisoning presents with similar symptoms to paralytic shellfish poisoning. The high concentration of aconitine I put in the tea ensured that my victim would die in the shortest period of time.

Aconite, Monkshood, or Wolfsbane (Aconitum species, e.g. Aconitum napellus) is a perennial plant originally native to Europe. It has deeply divided palmate leaves and flowers that are borne off a long stalk. Each flower contains 5 petaloid septals, one in the shape of a monkshood or helmet with blooms that vary in color from purple and blue, to combinations of color.

One of the most powerful plant-derived toxins, aconite can produce severe poisoning with as little as 0.2 mg of aconitine, 5 ml of the tincture, or 1 gram of the cured plant. Gastrointestinal manifestations of toxicity include the early onset of nausea, hypersalivation, and vomiting while neurotoxic symptoms include peri-oral paresthesias, numbness, dysarthria, weakness in the extremities, ataxia, and fading consciousness leading to seizures and coma.

Cardiac symptoms consist of characteristic bradydysrhythmias and hypotension with life-threatening ventricular ectopy. Ventricular tachycardia and/or fibrillation precedes asystole. QRS widening, a prolonged QT interval, and bundle branch block are illustrative of cardiac conduction disturbances. Toxicity advances rapidly, and life-threatening cardiotoxicity may be apparent within 2 hours of the ingestion. Death results from a malignant dysrhythmia or from direct myocardial depression and cardiovascular collapse.

Compounds are primarily derived from the tubers or root stock of Aconitum species and are classified as diterpenoid alkaloids, i.e., a nitrogenous base formed from some C20-terpenoid precursors. Aconitine, mesaconitine and 3-acetylaconitine are the most toxic alkaloids. It is the benzoylester side chain at carbon fourteen that produces the arrhythmic effects ascribed to these three alkaloids. The alkaloid content within the plant varies with the species, the geographic location and the time of harvest. Aconitine alkaloids can be detected by LC-MS/MS, as well as other chromatographic and mass spectrometric methods.

Aconitine is considered an “activator” agent that opens sodium channels and it binds within the transmembrane region known as “neurotoxin receptor site 2.” This binding generates continual activation of the voltage-gated Na⁺ channel at the resting membrane potential, and simultaneous inhibition of channel inactivation. These activators affect both the autonomic nerves innervating the heart and the cardiac conduction tissues and both actions contribute to the clinical presentation.

Hypotension and bradycardia are most likely caused by activation of autonomic reflexes by specific Aconitum diterpenoid alkaloids. This activation produces reflex stimulation of vagal tone seen primarily as decreased heart rate and atrioventricular block.

My next assignment takes me to Washington DC.

© 2008 Lily Robinson

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