Poison
|
|
Strychnine
What it is:
Strychnine is an odorless, colorless crystalline powder that is found in both naturally occurring alkaloid forms (from seeds of the nux vomica tree (S. nux-vomica) and related plants of the genus Strychnos),
as well as commercially produced salts. A 0.5-1% strychnine sulfate bait may be purchased over the counter in the United States and Canada for use in rodent burrows. A 2% liquid formulation of strychnine is also available in Canada. Strychnine is a strong poison with only a small amount being needed to produce severe effects and fatality. Read more below: 
Effects of strychnine:
Strychnine is absorbed into the blood stream within minutes of ingestion and clinical signs may occur in 10 to 30 minutes.
Strychnine acts by antagonizing the neurotransmitter glycine. Once the inhibitory effect of glycine is gone, persistent and uncontrollable excitement of the spinal reflex occurs. This excitation of the central nervous system leads to uncontrollable muscle contractions and convulsions. Strychnine produces some of the most dramatic and painful symptoms of any known toxic reaction. Death by strychnine ingestion is inhumane. Early signs consist of apprehension, nervousness, rapid breathing, drooling, tenseness, and stiffness. Vomiting is possible but uncommon. Severe tetanic seizures begin and may appear spontaneously or may be initiated by stimuli such as touch, sound, or bright lights. These tetanic convulsions may last from a few seconds to one min. An extreme and overpowering rigidity causes the animal to assume a “sawhorse” stance - a pulling of the animals neck and head back in a high arch, and front legs stiffened to point forward. Animals will often display a ‘sardonic grin’ due to spasm of the facial muscles and jaw. The animal remains conscious during these early stages of toxicity. As more strychnine is absorbed, seizures become more severe and prolonged, hyperthermia (increase in body temperature) occurs. Breathing becomes impaired due to spasms of the diaphragm and respiratory muscles. Respiration may stop momentarily. Intermittent periods of relaxation are seen during convulsions but become less frequent as the clinical course progresses. The mucous membranes become cyanotic (blue in color) and the pupils become dilated. Frequency of the seizures increases, and death eventually occurs from exhaustion or asphyxiation (suffocation) during seizures. Sometimes, because of prolonged convulsions before death, agonal (distress) hemorrhages of heart and lungs and cyanotic congestion from low tissue oxygenation may be seen. Death typically occurs within 1–2 hours of the onset of clinical signs, however, death can take up to 24 hours or longer if the dose is low. 
The typical "sawhorse" stance of an animal that has suffered the fatal effects of strychnine.
|
| ||||||
| kill_wolves_to_help_caribou_cjz-2014-0142-2.pdf |
| 129_-_2015_-_strychnine_is_unacceptable_ec2015-1.pdf |
Compound 1080 (sodium fluoroacetate)
|
What it is:
|
Potassium fluoroacetate occurs naturally as an anti-herbivore metabolite in various plants but can also be produced synthetically.
Sodium fluoroacetate, known in pesticide form as 1080, is an odorless, colourless, and tasteless toxin used as a metabolic poison. It is highly soluble in water and is categorized at a level 1 by the Environmental Protection Agency (EPA), indicating the highest degree of acute toxicity. It is highly toxic to all mammals (including humans) and birds. A single teaspoon can kill up to 100 adult human beings. 1080 is slow to decompose in soil and water in low temperatures, resulting in continued persistence in the environment. Due to its high toxicity and slow decomposition in soil and water, it poses serious environmental risks. Thus, like strychnine, it is banned in a number of countries and states such as California, South Africa and China. 1080 can be absorbed through inhalation, mucus membranes/eyes, breaks in skin and ingestion. There is no antidote. Read more about this poison below:
Effects of 1080:
Carnivores are the most sensitive to fluoroacetate poisoning, followed by ruminants, rabbits,horses, primates, rodents, and birds.
Animals that are poisoned by 1080 do not die a humane and quick death. 1080 poison is a slow killer. When ingested (usually through baited food) the animal suffers a prolonged and horrific death. Herbivores take the longest to die - up to 44hrs, while carnivores can take up to 21hrs before finally succumbing to the final effects of the poison. The speed of death is dependent on the rate of the animals metabolism. Once absorbed, 1080 stops the energy cycle of living cells. It blocks the body’s muscle and organs ability to absorb energy from its food, causing cell death as acid accumulates in the blood and results in a slow and inhumane death. Clinical signs occur 30 minutes to 2-4 hours after ingestion of fluoroacetate. Signs of toxicity do not appear immediately because fluoroacetate must be metabolized in the liver first. Approximately one hour after exposure, canids show anxious behaviour, hyper-excitability, followed by vomiting and diarrhea, frothing from the mouth, excessive salivation, and abrupt bouts of vocalization. This is followed by difficulty breathing, elevated body temperature, heart arrhythmia and sudden bouts of violent activity. All affected animals fall to the ground in teranic seizure, with hind limbs or all four limbs and sometimes the tail extended rigidly from their arched bodies. At other times the front feet are clasped together, clenched or used to scratch frantically at the cage walls. This tonic phase is then followed by a clonic phase in which the animals lie and kick or 'paddle' with the front legs and sometimes squeal, crawl around and bite at objects. During this phase the tongue and penis may be extruded, their eyes rolled back so that only the whites show and the teeth ground together. Breathing is rapid but laboured, with some animals partly choking on their saliva. Finally the animal begins to relax, breathing more slowly and shallowly and lying quietly with the hind legs still extended but apparently semiparalysed. Death occurs 2-12 hours after exposure, usually due to failure of the heart and lungs. |
History and locations of use:
This pesticide was discovered in the 1940s as a naturally occurring compound in plants from Africa, Australia, and South America. The effectiveness of sodium fluoroacetate as a rodenticide was reported in 1942. Fluoroacetate has since been used worldwide to control ‘pest’ species, including wolves. Access to fluoroacetate is tightly controlled due to its high toxicity and lack of species specificity. The only licensed use of fluoroacetate in the United States is a ‘predator protection collar’ for sheep and goats. In Canada, Alberta is the only province which licenses fluoroacetate for use in pest control. Compound 1080 is used in Alberta mainly to poison coyotes. Compound 1080 is widely used in Australia & New Zealand, as well as in Japan, Isreal, Korea and Mexico. In Alberta 1080 is available in tablets and in livestock collars. The poison is held in a ‘bladder’ fixed to the collar, which poisons a predator that punctures it if attacking. These collars can also burst and puncture on barbed wire, bushes, and can fall off which can lead to the leaking of poison into the environment and subsequently secondary poisoning of non target species, including pets. Despite having to be licensed to use 1080 poison, control can and has been an issue. Past patterns of abuse include overloading ‘single bait’ stations (increasing by-kill and partial poisoning), stockpiling and illegal poisonings of wild animals and dogs. Much has been written about the availability, and sloppy control of poisons of this toxicity. Read an article from 2011 about 1080 concern. The Alberta government has a coyote predation control manual & study guide that outlines the use of poisons.
Another article from 2013 about the wolf poison program:
A sheep wearing a predator protection collar.
| ||||||
The video below illustrates some of the effects of 1080. Please note that the video does contain some disturbing footage.
Cyanide
What it is:
Cyanide is a general term for a group of chemicals containing carbon (C) and nitrogen (N). Cyanide compounds include both naturally occurring and human-made chemicals. Naturally, cyanide can be produced by certain bacteria, fungi, algae, and it is found in a number of foods and plants. The principal human-made cyanide forms
are hydrogen cyanide (HCN), sodium cyanide (NaCN) and potassium cyanide (KCN). Hydrogen cyanide is a colorless gas with a faint, bitter, almond-like odor. Cyanide is acute toxic and is lethal if ingested or inhaled. Sodium cyanide is the form most used with regards to predator control programs. Effects of cyanide:
Sodium cyanide releases hydrogen cyanide gas, a highly toxic chemical asphyxiant that interferes with the body's ability to use oxygen. It has whole-body (systemic) effects, particularly affecting those organ systems most sensitive to low oxygen levels: the central nervous system (brain), the cardiovascular system (heart and blood vessels), and the pulmonary system (lungs).
Depending on the animal and exposure amount, poisoned animals can die within minutes or can suffer for as long as 8 hours. Victims initially suffer excitement/panic and rapid respiratory rate. Loss of balance, weakness, and rapid breathing, which may start and stop, follow. Salivation, foaming at the mouth, excess lacrimation (tearing), and voiding of urine and feces may occur. Vomiting may also occur. Muscle contractions/twitching is common and progresses to generalized spasms, convulsions and coma before death. Animals may stagger and struggle before collapse and they eventually die due to respiratory failure -severe asphyxia/suffocation. Mucous membranes become bright red because of the high amount of oxygen that remains in venous blood. Amyl nitrite, sodium nitrite, and sodium thiosulfate are antidotes for cyanide toxicity. Use of the M44 device has been criticized by scientists, environmental groups and the public for many years, as the suffering they cause is not humane and because the devices have many unintended victims, including pets. ARTICLE about the use of M-44s in the USA |
History of use:
Sodium cyanide (NaCN) ejectors have been used in predator damage control programs in North America since the late 1930s.
The first model was the Humane Coyote Getter (HCG), more commonly known as the "coyote getter" (CG). It was used in federally supervised control programs for almost 40 years, until 1970 when it was replaced by the spring-activated M-44. The M-44, with many modifications over the years, remains in use today. An enlarged M-44, the ‘M-50’, also was used during 1979-1983. Where it is used:
In Alberta, cyanide is used in a mechanical devices called M-44s by licensed individuals and are primarily used at the request of private livestock owners to control "pest" animals and those that threaten livestock. A small cylinder containing the deadly dose of sodium cyanide is driven into the ground on a stake, and spring-loaded to deliver a deadly dose of sodium cyanide when an animal licks, bites or pulls on the wax fabric covering of the cylinder. These devices lure predators with an attractive smell, often from a small piece of bait, then uses a spring to propel a dosage of sodium cyanide into the predator's mouth. The sodium cyanide combines with water in the mouth to produce poisonous cyanide gas. The ejector can spray the cyanide granules up to 5 feet.
|
