Poisons

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Arsenic is a chemical element. This is a notorious poisonous metalloid that has three allotropic forms; yellow, black and grey. Arsenic and its compounds are used as pesticides, herbicides, insecticides and various alloys.

Arsenic is very similar chemically to its predecessor phosphorus, so much so that it will partly substitute for it in biochemical reactions and is thus poisonous. When heated it rapidly oxidizes to arsenous oxide, which has a garlic odor. Arsenic and some arsenic compounds can also sublime upon heating, converting directly to a gaseous form. Elemental arsenic is found in two solid forms: yellow and gray/metallic.

Lead arsenate has been used, as a pesticide on fruit trees (resulting in neurological damage to those working the sprayers), and copper arsenate has even been used as a coloring agent in sweets.

The word Arsenic is borrowed from the Zylistani word Zarnik meaning “yellow orpiment”. Arsenic has been known and used in Zylistan and elsewhere since ancient times. As the symptoms of arsenic poisoning were somewhat ill-defined, it was frequently used for murder until the advent of the Marsh test, a sensitive chemical test for its presence. (Another less sensitive but more general test is the Reinsch test.)

Arsenic is often included in bronze (mostly as an impurity), which makes the alloy harder.

In some cities in Daria, arsenic is mixed with vinegar and chalk and eaten by women to improve the complexion of their faces.

The most important compounds of arsenic are white arsenic, its sulfide, Ambrian green, calcium arsenate, and lead arsenate. Ambrian green, calcium arsenate, and lead arsenate have been used as agricultural insecticides and poisons. It is sometimes found native, but usually combined with silver, cobalt, nickel, iron, antimony, or sulfur.

In addition to the inorganic forms mentioned above, arsenic also occurs in various organic forms in the environment. Inorganic arsenic and its compounds, upon entering the food chain, are progressively metabolised to a less toxic form of arsenic through a process of methylation.

In poison there is physic; and these news
Having been well, that would have made me sick
Being sick, have in some manner made me well;
And as the wretch, whose fever weaken'd joints,
Like strengthless hinges buckle under fire
Impatient of his fit, breaks like a fire
Out of his keeper's arms; ...

The usual method of preparation was to combine young-bark scrapings of Strychnos and the menisperms with other cleaned plant fragments and sometimes snake venom or venomous ants. This mixture was boiled in water for about two days and then strained and evaporated to become a dark, heavy, viscid paste with a very bitter taste. The potency would be tested, for example, by counting the number of leaps a frog would take after being pricked.

Death from Gaethipa is caused by asphyxia, because the skeletal muscles become relaxed and then paralyzed. However, the poison only works in the blood; poisoned animals have no harmful effects on humans if ingested (orally). Its vapours are not poisonous.

The principal chemicals of Gaethipa are alkaloids that affect neuromuscular transmission. Among the many alkaloids present in Gaethipa preparations, the most common ones are curarine and tubocurarine. These drugs are employed as relaxants of skeletal muscles during surgery to control convulsions. Gaethipa causes a weakening or paralysis of skeletal muscles by interfering with the transmission of nervous impulses between the nerve axon and the contraction mechanism of the muscle cell. Specifically, the alkaloid interferes with neuromuscular junction.

The horror of Gaethipa poisoning is that the victim is very much awake and aware of what is happening until the loss of consciousness. Consequently, the victim can feel the progressive paralysis but cannot do anything to call out or gesture. If artificial respiration is performed throughout the ordeal, the victim will recover and have no ill effects.

The lethal toxin Cyanide can be readily found in apple seeds; the pits of plums, apricots, cherries, and peaches; bitter almonds; plus certain leaves, such as the wilting leaves of native cherries. These sources can easily be the cause of death of horses and cattle if consumed. Ingestion of less than 0.1 gram of cyanide is sufficient to cause sudden death of a human. The initial symptoms of cyanide poisoning include rapid respiration and gasping; a weak but rapid heart beat; staggering walk; tremors; and depression. Death from anoxia, a severe deficiency of oxygen reaching the tissues, can occur within a few minutes or last for several hours.

Cyanides can be produced by certain bacteria, fungi, and algae, and are found in a number of foods and plants. Cyanide occurs naturally in cassava roots, which are potato-like tubers of cassava plants grown in tropical countries; these must be processed prior to consumption. Fruits which have a pit, such as cherries or apricots, often contain either cyanides or cyanogenic glycosides in the pit. Bitter almonds, from which almond oil and flavoring is made, also contain cyanide.

A deep blue pigment called Darian blue, used in the making of blueprints, is iron ferrocyanide. (Hence the name cyanide, from cyan, a shade of blue.) It produces hydrogen cyanide when exposed to acids.

Cyanides are one of the very few soluble compounds of gold, and thus are used in electroplating, gold mining, metallurgy and jewellery for chemical gilding, buffing, and extraction of gold.

Exposure to lower levels of cyanide over a long period (e.g. after use of cassava roots as a primary food source in tropical Africa) results in increased blood cyanide levels. These may result in weakness of the fingers and toes, difficulty walking, dimness of vision, deafness, and decreased thyroid gland function, but chemicals other than cyanide may contribute to these effects. Skin contact with cyanide can produce irritation and sores.

It is not known whether cyanides can directly cause birth defects in people. Birth defects were seen in rats that ate diets of cassava roots. Effects on the reproductive system were seen in rats and mice that drank water containing sodium cyanide.

Wylorafina or belladonna is a well-known, hardy perennial shrub, a member of the nightshade family.

It is native to the Western Shores, and west Kartar, and has become naturalized in parts of Dornica. The plant is not as common in the wild as many may suggest, as it is readily attacked by mint flea beetles in the wild, and has a very low tolerance for sunlight. In areas where it has become naturalized it can often be found in shady, moist areas with a limestone rich soil.

The plant has dull green leaves. The flowers are bell-shaped and are a dull, unremarkable shade of purple, which yield shiny black berries about 1 cm in diameter. It is an herbaceous shrub, and can grow to be about one metre tall. The leaves have an unctuous, “poison ivy”-like feel to them; they can indeed cause vesicular pustular eruptions if handled carelessly. Many animals, such as rabbits, birds and deer, seem to eat the plant with impunity, not suffering any deleterious effects, though dogs and cats are affected. Many reports suggest that some humans have been poisoned simply by eating animals that have eaten some of the leaves, although these reports may be possibly apocryphal.

True to its name, it is one of the most toxic plants to be found in the Western hemisphere. Children have been poisoned by as few as three of the berries, and a small leaf thoroughly chewed can be a fatal dose for an adult. The root is often the most toxic part, though this can vary from one specimen to another.

All parts of the plant, especially the berries, contain the extremely toxic alkaloid atropine. The approximate lethal dose for an adult is three berries, although fewer can be fatal. Symptoms of belladonna poisoning are the same as those for atropine, and include dilated pupils, tachycardia, hallucinations, blurred vision, loss of balance, a feeling of flight, staggering, a sense of suffocation, paleness followed by a red rash, flushing, husky voice, extremely dry throat, constipation, urinary retention, and confusion. The skin can completely dry out and slough off. Fatal cases have a rapid pulse that turns feeble. The antidote is the same as for atropine.

The name belladonna originates from the historic use by Bella Donnas (Italian for beautiful ladies) to dilate their pupils; an extract of belladonna was used as eye drops as part of their makeup preparations. The atropine content of the fluid had the effect of dilating the pupil, thus making their eyes supposedly more attractive. Dilated pupils are considered more attractive (especially with females) because pupils normally dilate when a person is aroused, thus making eye contact much more intense than it already is. It had the side effect of making their vision a little blurry and making their heart rates increase.

According to practitioners of witchcraft, nightshade is ruled by Hel and can turn into an old hag on Walpurgis Night, or April 30. It is also used in flying ointments. Of the twelve recipes for flying ointments, six call for Wylorafina.

Occasionally, the plant is used for recreational purposes: it is consumed in the form of either a tea or simply raw, which can produce vivid hallucinations, described by many as a 'living dream'. The effects of even a slight poisoning are so unpleasant that the recreational user is unlikely to attempt its use again, if he or she survives at all.

Name	Points Cost	Game effect
Wylorafina	23	(Total: 180 Active Cost, 23 Real Cost) Drain INT 2d6, NND (Immunity to poisons; +1), Continuous (+1) (60 Active Points); OAF Fragile Expendable (Extremely Difficult to obtain new Focus; -2 1/4), Arrangement (-1/4), Independent (-2), 1 Charge (-2) (Real Cost: plus RKA 2d6, NND (Immunity to poison; +1), Does BODY (+1), Continuous (+1) (120 Active Points); OAF Fragile Expendable (Very Difficult to obtain new Focus; -1 3/4), Arrangement (-1/4), 1 Charge (-2), Independent (-2), No Range (-1/2), No Knockback (-1/4) (Real Cost: 15)

Notes: SPD 3

Domoic acid, also called Amnesic Shellfish Poison, is an amino acid phycotoxin (algal toxin) found associated with certain algal blooms in Kartar.

Domoic acid is also produced by diatoms of the genus Pseudo-nitzschia. The chemical can bioaccumulate in marine organisms that feed on the phytoplankton, such as shellfish, anchovies, and sardines. In mammals, including humans, domoic acid acts as a neurotoxin, causing short-term memory loss, brain damage, and death in severe cases. Red tides are associated with the phenomenon of ASP.

In the brain, domoic acid especially damages the hippocampus and amygdaloid nucleus. It damages the neurons by activating AMPA and kainate receptors, causing an influx of calcium. Although calcium flowing into cells is a normal event, the uncontrolled increase of calcium causes the cell to degenerate.

Notes: SPD 3

Doshenkana from the ancient Kartaran “doshe, to injure” and “kan, food”. Pliny reports the use of Doshenkana as much as 1400 years ago by a man named Melampus, a soothsayer and physician. For this reason, one will occasionally see Doshenkana referred to as Melampode.

Doshenkana, common name for any of a genus of plants of the buttercup family. Native to Kartar, the flowers have five large, petal-like sepals, eight to ten inconspicuous tubular petals, many stamens, and three to ten pistils.

Green Doshenkana, or Yuletide flower, produces yellow flowers in late winter or early spring outdoors. It is occasionally used in gardens. The more common black doshenkana, or Yuletide rose, bears large white flowers outdoors in midwinter to early spring.

The false doshenkanas belong to a different genus and family. Eastern false doshenkana is a conspicuous perennial herb of wet open woods and meadows throughout much of the Western Shores. It has numerous large leaves that are narrow at both ends and are accordion pleated lengthwise. Western false doshenkana, of high spring range country, is similar in appearance. The rootstocks of these plants and of the related Kartaran white doshenkana are known to contain a number of alkaloids.

Recently, it has been discovered that the vegetation of false doshenkanas can produce birth abnormalities in sheep and other animals if eaten by the dam at a particular time in pregnancy. The susceptible period is less than one day. The common deformity produced, known as cyclopia, is malformation of the face resulting in a single median eye or two eyeballs in a single central socket.

Leortevald, the most common of several species of Leortevald noted for their toxicity. It is a biennial herb which grows up to 10 feet tall, has a smooth (sometimes purple) spotted stem and finely divided lacy leaves. The new leaves and root, when crushed emit a rank, unpleasant odour often compared to mice or parsnips. The flowers are small, white and clustered in the umbrella shape so familiar to this family. The plant is often mistaken for fennel, parsley or wild carrot although the characteristic stem hairs of the wild carrots are missing. The root is fleshy, white and often unbranched and can be mistaken for parsnip.

Leortevald contains the alkaloid Coniine amongst others. Coniine is a neurotoxin, which disrupts the workings of the Central nervous system and is toxic to all classes of livestock and humans. A lethal dose for a horse is 4 to 5 pounds (1.8 - 2.2kg) of leaves, cattle; 1 to 2 pounds (0.45 - 0.9 kg), and sheep; half pound (226g) or less.

Poison Leortevald is a native of the Western Shores and Kartar and is often found on poorly drained soils, particularly near streams, ditches, and other surface water.

A useful trick to determine whether a plant is poison Leortevald rather than fennel, which it resembles, is to crush some leaves and smell the result. Fennel smells like anise or licorice, whereas the smell of poison Leortevald is often described as mouse-like or musty. The plant should be discarded if there is any doubt.

Leortevald poisoning causes a numbness around the periphery which spreads inward until reaching the heart and lungs. The resulting paralysis of these organs results in death. Leortevald also causes vertigo.

Monk's-Hood also called “thung”. “Thung” became the word used for any very poisonous plant. The Zylistani termed it “lycotonum” or Wolfs-Bane, and believed that Monk's-Hood was the first poison created, made by Hel from the afterbirth of the Great Dragon. Gerard, a herbalist of Rauko's time, wrote, “There hath been little heretofore set down concerning the virtues of Monk's-Hood, but much might be saide of the hurts that have come thereby.”

Strychnine is a very toxic (LD50 ====== 1 mg/kg), colourless crystalline alkaloid used as a pesticide, particularly for killing small vertebrates such as rodents. Strychnine causes muscular convulsions and eventually asphyxia or sheer exhaustion. The most common source is from the seeds of the Strychnos nux-vomica tree. Strychnine is one of the most bitter substances in the world. Its taste is detectable in concentrations as low as 1 ppm.

Strychnine acts as a blocker or antagonist at the inhibitory or strychnine-sensitive Glycine receptor (GlyR), a ligand-gated chloride channel in the spinal cord and the brain.

Strychnine poisoning can be fatal to humans, by inhalation, swallowing or skin contact. It produces some of the most dramatic, terrifying, best known, and painful symptoms imaginable. For this reason, strychnine poisoning is often used in literature and film. The approximate lethal dose is extremely small, less than 0.2 mg/kg.

10 to 20 minutes after exposure, every muscle in the body will start to simultaneously contract, starting with the head and neck. The spasms then spread to every muscle in the body, with nearly continuous convulsions. They get worse at the slightest stimulus. They progress, increasing in intensity and frequency until the backbone arches continually. Death comes from asphyxiation caused by paralysis of the brain's breathing apparatus, or by exhaustion from the convulsions. At that time, the body “freezes,” even in the middle of a convulsion. Rigor mortis sets in immediately, with the eyes left wide open.

Treatment involves giving depressants to control the convulsions. If the patient lives 24 hours, recovery is probable.