Poisoning Persons in Print


Vision 10

Poisoning Persons in Print


Alison Sinclair

Copyright © 2002, Alison Sinclair, All Rights Reserved

"All substances are poisons … The right dose separates a poison from a remedy." 

One of your characters has murder in mind, but is not disposed to direct confrontation with sword, knife or morningstar, having neither the skill nor the temperament, perhaps (the psychology of poisoners is beyond the scope of this article). I hope in this article to hit some high points, point up some patterns and offer some possibilities on the menu. I have tended to describe natural poisons, because that is my interest, although the references at the end of the article also cover chemical poisons. Partly because this is an article, not a textbook, and partly to help inventors of poisons, I have kept to broad outlines and general principles, though I've given examples which may be used directly or as models for invented poisons, under four rough headings: origins of poisons, various possibilities and patterns, how poisons cause sudden death, and psychotropic poisons.  

Where Does It Come From? 

If a poison is from a natural source, then where it comes from will determine its repertoire of effects. 

If an animal envenoms its prey, then its venoms will make the prey easier to catch or easier to digest, or both. Any animal at a disadvantage for mobility will tend to favour paralytic venoms - neurotoxins. As an example, there are a number of species of snails that live on fish. They spear the fish with a tethered harpoon containing a paralytic venom that works almost instantaneously. Each species produces a different cocktail of venoms, tailored to its own needs. A creature that does not have teeth or a similar, effective rending apparatus may produce enzymes which pre-digest its prey prior to ingestion: In March Upcountry, John Ringo and David Weber use this to horrible effect when their marooned marines encounter a predatory alien maggot. They're stretching enzyme kinetics with the speed of action, I think, but the effect fits with the origin. 

(Click pictures for larger versions)

LionfishIf an animal manufactures its venom for defense, then its poison is likely to be paralytic or extremely painful, so it will disable or deter a predators before it eats or damages the animal. Creatures which use venom for defense may be flamboyant in their colouring (left) or effectively camouflaged  (stonefish). 




StonefishThe stonefish (left), one of the world's most poisonous fishes, has short, thick spines which are embedded  in venom sacs. Pressure on one of those spines will compress the sac and inject the venom. Jellyfish poisons are immediately effective and extremely painful. Given the jellyfish's fragility, it needs to make its presence and deterrent known. 



PufferfishToxins are often bacterial or plant in origin. Even animal toxins may be borrowed from bacteria. Tetrodotoxin is the poison found in puffer fish, source of the delicacy fugu, which when eaten in small doses causes tingling of the lips and extremities and in large doses, paralysis and death. It has been touted as the voodoo poison; this the experts find implausible, but it does make a good story (see link below "Eye of Toad, Skin of Newt, Bile of Pufferfish"). The puffer fish (left) carries tetrodotoxin in its body without ill-effect because it has a mutation in the molecule which is the poison's site of action. However, if a puffer fish is reared without contact with wild puffer fish, its flesh has no poison. The poison is from a bacterial source; without contact, it cannot be transmitted. Batrachotoxin, which has been found on the skin of some species of toad and the feathers of a few species of bird, and is very poisonous – people have had toxic symptoms after merely handling one of those creatures – is another likely bacterial product. 

Plants are the Borgias of the living world. Unable to run away, they wage chemical warfare on insects, herbivores, and ruminants. Numerous plants produce cyanide in their seeds or their young leaves, often attached to other molecules in the form of cyanogenic glycosides, such as amygdalin (found in apricot and cherry pits). In this form, cyanide is nontoxic to the plant; only in the breakdown of cyanogenic glycosides, during animal consumption or digestion, is hydrogen cyanide gas released. Plant alkaloids, organic molecules noted for their bitter taste, include poisons which are paralytic (curare), hallucinogenic, and cardiotoxic (atropine); they have also given rise to medications such as the cancer drugs vinblastine and vincristine. Trees will produce caustic or cloying sap (latex) to kill insects. And then there are the poisons which are addressed to one particular pest: African bungleweed produces a substance that resembles a normal hormone but that causes caterpillars to develop into bicephalic butterflies – a lethal mutation. Milkweed contains a poison which causes heart attacks in caterpillars. Cotton grass contains a poison that inhibits lemmings' digestion (remember the tribbles?).  

Poisonous Possibilities 

Symptoms of poisoning come in clusters which are consistent with the organ or body system affected by the poison. Poisons which affect receptors in the nervous system can have wide-ranging effects. "Red as a beet, blind as a bat, mad as a hatter, dry as a bone" or alternately "can't see, can't pee, and dammit, I drink all day," are two mnemonics medical students acquire while learning the effects of atropine. Atropine (also known as belladona) affects the receptors which are common to nerves which control pupil dilatation, salivation, heartbeat, urination, and blood flow to the skin; it also causes psychosis. Some other possible clusters of symptoms from poisons which affect widely distributed receptors (with examples) are:  

Dry mouth; large pupils; difficulty with focusing the eyes; rapid heart beat; hot, dry, flushed skin; agitation and delirium

Belladona alkaloids

Sweating; diarrhea; lowered blood pressure; lowered heartbeat; small pupils; urination; difficulty breathing; vomiting; muscle twitches; tearing; salivation; seizures

Mushrooms, nicotine

Low body temperature; slow heartbeat; low blood pressure; slow, shallow breathing; pupils may be large or small (opiates); drowsy or unconscious

Alcohol and other sedatives

Raised temperature, rapid heartbeat, raised blood pressure, dilated pupils, nausea and vomiting; sweating

Amphetamines, cocaine

Difficulty speaking; difficulty swallowing; muscle rigidity; shakes; muscle spasms

[No examples]

 Poisons can be photoactivated: a harmless precursor can be converted into a poison by the action of sunlight on the skin. A number of medications are notorious for making people intolerant to sunlight. Poisons can also enhance each others' effect: alcohol and tetrachloromethane, both poisonous to the liver, cause far more damage in combination than could be predicted from the separate effect of each. And what might be a harmless substance to one person – such as a trace of peanut butter - can be lethal to someone who is severely allergic to it (which has been used in a number of mystery novels, and requires foreknowledge of the vulnerability).

Sudden Death 

The quickest acting poisons - those which bring about sudden death or death within minutes - affect the cardiovascular or respiratory system, both of which are required for the delivery of oxygen to the tissues. Next comes the clotting system, and after that (over days) the body's detoxification systems, the liver and kidneys, and then the bone marrow. 

The heart is an electrical organ. A bundle of cells (the sinoatrial node) in the wall of the right atrium sends out an electrical pulse through nerve pathways that branch throughout the heart. The muscles of the heart walls contract in response to the signal, forcing blood out into the arteries. There are two principal mechanisms for poisoning heart action: block the electrical signal at some point along the pathway, or desynchronize the muscles so that the heart cannot effectively contract. Unsynchronized contraction of the atria (the filling chambers)  is problematic, increasing the risk of stroke, but not generally fatal in itself. Unsynchronized contraction of the ventricles is ventricular fibrillation (aka Vfib) and is fatal within minutes. 

Digoxin (foxglove, and also the drug) acts by blocking the electrical signal. Any number of drugs and poisons can induce arrythmias - from antiarrythmic drugs through to over-the-counter antihistamines (for people who have a susceptibility) through to the venoms of carnivorous invertebrates. Generally, any venom that produces paralysis in the prey could plausibly produce sudden death.  

Interruption of respiration is, likewise, rapidly fatal. Five minutes is the oft-quoted limit - but brain damage occurs in less time. And it's possible to last longer, particularly in intense cold and with good resuscitation afterwards. But say five minutes. Any step along the pathway between nose and mitochondria (respiratory organelles of the cell) can be interrupted. Breathing requires nerve input and muscle effort; either can be blocked by neurotoxins. Incidentally, paralysis need not necessarily lead to immediate loss of consciousness. The lining of the airsacs is exquisitely thin when healthy; poison can inflame or damage it, and that cuts down the ability of oxygen to cross it. Hemoglobin can be blocked from carrying oxygen to the tissues (carbon monoxide). The metabolic pathways within the cell that convert oxygen to metabolic energy can be inhibited (cyanide). 

Damage to the blood vessel wall releases small molecules that signal the activation of a cascade of enzyme-activations - each enzyme in the sequence is activated by the last and activates the next; this leads after multiple steps to the formation of a clot. The process doesn't stop there; even as the clot is being formed, it is being broken down by another enzymatic cascade. Push the balance of the two processes towards excess clotting, and you get thrombosis of major vessels, which Michael Crichton used in The Andromeda Strain and James Herbert in his recent '48. Push it towards clot breakdown, or poor clot formation,  and you get uncontrollable bleeding, hemophilia being the example familiar to most. Dicoumarin, the poison from sweet clover, inhibits clotting. Run both processes too fast and you get disseminated intravascular coagulation (DIC), where microscopic clots are constantly being formed and broken down, consuming the clotting factors and leading to uncontrollable bleeding. DIC kills people with sepsis and hemorrhagic fever,  following massive blood loss and transfusion, and a variety of other medical catastrophes. And snakebite: snake venoms contain powerful procoagulants and anticoagulants. 

On a timescale of days, there are the fundamental detoxification and excretion pathways of the body, the liver and kidneys. Block either of those, and the body poisons itself with the byproducts of its own metabolism, notably the waste products of protein metabolism. Carbohydrates can be converted to carbon dioxide and water and exhaled, but protein metabolism, even from muscle breakdown, produces urea, which has to be excreted through the kidneys. Furthermore, if the kidneys shut down, water and ions can no longer be secreted and the fine electrical balance of the body is perturbed – with fatal consequences such as cardiac arrythmias (see above) or swelling of the brain. Kidney failure can also be a terminal consequence of myotoxins – muscle poisons. Widespread death of muscle releases muscle pigments, which poison the kidneys. The liver is responsible for breaking down protein wastes and clearing many drugs from the systems; it is also responsible for the synthesis of the coagulation factors described above.  

Finally, over the long term, there is the bone marrow, which produces the body's supply of red and white blood cells and platelets. If the bone marrow stops working, over a period of weeks, as the red and white cells and platelets already circulating in the bloodstream die off, the person becomes prone to severe bleeding, severe infection and severe anemia. 

You can play around with the timing of effect by modifying the delivery system, as, for instance, Dirk Wyle does in Pharmacology is Murder: packaging a rapidly acting toxin in a slow-release capsule can allow an assassin to be elsewhere at the time of death. However, a venom may not necessarily be active as an ingested poison, since it must not only survive the rigors of stomach acidity  and digestive enzymes, but be taken up by the cells of the intestinal mucosa.  

Poisoning the Mind 

There's probably no more dramatic way to affect a character than to drive him or her insane. Psychological effects of poisons range from the subtle – the slow mental deterioration of chronic heavy metal poisoning, for example – to the florid – hallucinations from the psychotropic alkaloids. Since prehistory, shamans have used hallucinogens such as mescaline, psilocybin, and ibogaine, derived from natural products, to extend their awareness, and native peoples have incorporated psychotropic drugs into social and religious rituals.  Ergot poisoning, from ergot mold infection of rye bread, has been offered as the cause of mass insanity (St. Vitis' Dance, St. Anthony's Fire) in medieval times, as an explanation for the belief in vampires and werewolves, and even for the witches of Salem. More than to other poisons, a person's response to psychotropic drugs and poisons is determined by their temperament and their culture. Hallucinations caused by a psychotropic alkaloid might be interpreted by one character as insanity, or a curse, or a visitation by demons, and by another as a gift of the divine.    


The single most useful print source I can suggest is:

Serita Deborah Stevens and Ann Klarner. Deadly Doses: A Writer's Guide to Poisons. Writers Digest Books; ISBN: 0898793718 

Michael J. Balick and Paul Allan Cox. Plants, People and Culture: The Science of Ethnobotany. W H Freeman & Co; ISBN: 0716760274  (has a chapter on the peyote cactus, but is also a fascinating look at natural products and material culture) 

Online, see:  

EMedicine.com, on-line textbook of emergency medicine: Toxicology http://www.emedicine.com/emerg/TOXICOLOGY.htm 

The Bad Bug Book. Foodborne Pathogenic Microorganisms and Natural Toxins Handbook from the US FDA http://www.cfsan.fda.gov/~mow/intro.html 

Colorado State College of Veterinary Medicine and Biomedical Sciences Guide to Poisonous Plants http://www.vth.colostate.edu/poisonous_plants/ 

Ethnobotanical Leaflets http://www.siu.edu/~ebl/ 

Cone Snails and Conotoxins Home Page  http://grimwade.biochem.unimelb.edu.au/cone/ 

On tetrodotoxin. "Eye of Newt, Skin of Toad and Bile of Pufferfish" http://www.calacademy.org/calwild/sum98/eye.htm