Rodenticides

Pesticides designed to kill rodents, such as mice or rats, are called rodenticides. There are inherent difficulties in killing scavenging rodents with poison. Rodents display a pattern of nibbling and waiting to determine if something is safe to eat. A good rodent poison must have a time lapsed effect and remain tasteless and odorless at the necessary deadly dosage.

Anticoagulants
Anticoagulants are rodenticides which have a delayed effect, usually lethal between 1 to 2 weeks after a fatal dose is consumed. They come in first and second generation types. The first type requires multiple doses to kill rodents, while the second only needs a single dose to be effective. Anticoagulants, as the name implies, work by blocking the ability of the rodent's blood to coagulate or clot.

Furthermore, certain types of anticlotting agents destroy capillaries, resulting in internal bleeding. This happens gradually over a period of days. It is known from human conditions, such as haemophilia and warfarin poisoning, that conditions like these cause moderate to debilitating pain due to hemorrhaging into muscles and joints. The same is expected in rodents. For this reason, many view anticlotting poisons as an inhumane method of mice control. As the last stage of poisoning is reached, advanced anemia or severe bloodloss occurs and the rodent collapses and dies calmly.

Anticlotting agents have the benefit that, due to the lapse in time from the dose consumption to death, rodents will fail to connect ingesting the poison with death. This insures that rodents in a litter will not begin to avoid the bait that killed their fellow rodents.

First generation poisons of this type usually metabolize more quickly and need greater dosages with multiple feedings to reach fatal levels, as well as have less toxicity than second generation poisons. Because of their far greater toxicity, second generation anticlotting agents or superwarfarins kill after a single dose and remain deadly to rodent strains resistant to first generation warfarins.

In case of acidental or deliberate consumption (whether by suicide attempt or by intentional poisoning) of anticlotting agents, vitamin K1 has served to successfully counteract the poison. Liver function inhibited by certain poisons and at later stages bloodloss can be treated with blood transfusions and so save a victim of poisoning. This is advantageous over some older types of poisons.

Metal phosphides
Metal phosphides were the prefered rodenticide before anticoagulants came into favor. A strychnine shortage in the United States, caused by Japanese occupation of American strychnine-producing territories, during WWII, led to their widespread usage. These fast acting rodentiticides lead to rodents dying quickly out in the open as opposed to the places they infest.
Common phosphides are: aluminium phosphide (fumigant), calcium phosphide (fumigant), magnesium phosphide (fumigant), zinc phosphide (baits)

Baits made from phosphides (often zinc phosphide) mixed with food become effective after a single doseage and act quckly, usually within 1 to 3 days after a single feeding. Phosphides work by reacting with the rodent's stomach acid to produce phosphine gas. This rodent control method still finds use where rodents have developed anticlotting agent resistance. As they are cheaper than second generation anticoagulants, especially zinc phosphide baits, severe infestations can be treated with fast acting phosphide baits and as their population reduces, survivors finished off with anticlotting agents. This also works in the reverse where anticoagulants have failed to eniterly exterminate vermin populations. Using bait and switch tactics to adapt the rodents to the new bait, poison is then applied until all feeding has stopped.

Zinc phosphide baits give off a strong pungent garlic-like stench, which rodents find attractive, but other animals, except birds, find repulsive. In tablet and pellet form, other chemicals may be added to its mixture to prevent phosphine gas explosions. Secondary poisoning from afflicted animals remains low risk due to the nonaccumulation in the tissues of poisoned vermin.


Hypercalcemia Causing Vitamins
Another type of substance used as rodent poison are calciferols or vitamin D, cholecalciferol or vitamin D3, and ergocalciferol or vitamin D2. Ironically, the reason these vitamins promote well-being in humans are the same reasons rodents find them poisonous. These fat soluable vitamins affect the body's equilibrium of calcium and phosphate and so remain essential at small doses only becoming toxic in larger quantities. High enough doseage causes death through a condition of hypercalcemia. This is accomplished in rodents through an increase in calcium absorbtion from the ingestion of food. At sufficient levels calcification of blood vessels and vital tissues occurs, leading to heart problems, internal hemorrhaging, and even kidney failure. This bait works in single dosage and is accumulative with death occuring within a few days to one week after bait consumption.

Another consideration with calciferols is their synergistic reaction with anticoagulants. Anticlotting agent / calciferol mixtures exhibit more toxicity than simply adding the toxicity of each substance. A pronounced hypercalcimia and advanced hemorrhaging results from lesser quantities of each substance when combined together. This mixture is used most often with low calciferol dose baits due to the greater expense of calciferols over anticoagulants.

Clinical experience demonstrates that cholecalciferol rodenticides present a solid health threat to pets, such as dogs and cats. This threat includes, but are not limited to system wide soft tissue calcification, renal failure, abnormal cardiac symptoms, CNS depression, high blood pressure, and GI upset. These signs usually present within 18 to 36 hours after consumption. These signs will worsen in severity and result in anorexia, vomiting and constipation in the pet.