Single feed baits are chemicals sufficiently dangerous that the first dose is sufficient to kill.
Rodents are difficult to kill with poisons because their feeding habits reflect their place as scavengers. They will eat a small bit of something and wait, and if they don't get sick, they continue. An effective rodenticide must be tasteless and odorless in lethal concentrations, and have a delayed effect.
In addition to this specific metabolic disruption, massive toxic doses of 4-hydroxycoumarin or 4-hydroxythiacoumarin and indandione anticoagulants cause damage to tiny blood vessels (capillaries), increasing their permeability, causing diffuse internal bleedings (haemorrhagias). These effects are gradual, developing over several days, but claims that they are painless are unfounded: in humans both warfarin poisoning and haemophilia commonly cause moderate to severe pain from bleeding into muscles and joints. In the final phase of the intoxication, the exhausted rodent collapses in hypovolemic circulatory shock or severe anemia and dies calmly. Rodenticidal anticoagulants are either first generation agents (4-hydroxycoumarin type: warfarin, coumatetralyl; indandione type: pindone, diphacinone, chlorophacinone), generally requiring higher concentrations (usually between 0.005 and 0.1%) and consecutive intake over days in order to accumulate the lethal dose, and less toxic than second generation agents, which are derivatives of 4-hydroxycoumarin (difenacoum, brodifacoum, bromadiolone and flocoumafen) or difethialone (4-hydroxy-1-benzothiin-2-one, sometimes incorrectly referred to as 4-hydroxy-1-thiocoumarin, see heterocyclic compounds).
Second generation agents are far more toxic than first generation. They are generally applied in lower concentrations in baits (usually in order 0.001 - 0.005%), are lethal after a single ingestion of bait and are also effective against strains of rodents that became resistant to first generation anticoagulants; thus, the second generation anticoagulants are sometimes referred to as "superwarfarins".
Sometimes, anticoagulant rodenticides are potentiated by an antibiotic or bacteriostatic agent, most commonly sulfaquinoxaline. The aim of this association is that the antibiotic suppresses intestinal symbiotic microflora, which are a source of vitamin K. Diminished production of vitamin K by the intestinal microflora contributes to the action of anticoagulants. Added vitamin D also has a synergistic effect with anticoagulants.
In some countries, fixed three-component rodenticides, i.e. anticoagulant + antibiotic + vitamin D, are used. Associations of a second-generation anticoagulant with an antibiotic and/or vitamin D are considered to be effective even against most resistant strains of rodents, though some second generation anticoagulants (namely brodifacoum and difethialone), in bait concentrations of 0.0025 - 0.005% are so toxic that resistance is unknown, and even rodents resistant to other rodenticides are reliably exterminated by application of these most toxic anticoagulants.
Vitamin K1 has been suggested, and successfully used, as antidote for pets or humans accidentally or intentionally (poison assaults on pets, suicidal attempts) exposed to anticoagulant poisons. Some of these poisons act by inhibiting liver functions and in advanced stages of poisoning, several blood-clotting factors are absent, and the volume of circulating blood is diminished, so that a blood transfusion (optionally with the clotting factors present) can save a person who has been poisoned, an advantage over some older poisons.
The main benefit of anticoagulants over other poisons is that the time taken for the poison to induce death means that the rats do not associate death with eating the poison.
Zinc phosphide is typically added to rodent baits in amount of around 0.75-2%. The baits have strong, pungent garlic-like odor characteristic for phosphine liberated by hydrolysis. The odor attracts (or, at least, does not repulse) rodents, but has repulsive effect on other mammals. Birds (notably wild turkeys) are not sensitive to the smell, and will feed on the bait, and thus become collateral damage.
The tablets or pellets (usually aluminium, calcium or magnesium phosphide for fumigation/gassing) may also contain other chemicals which evolve ammonia which helps to reduce the potential for spontaneous ignition or explosion of the phosphine gas.
Phosphides do not accumulate in the tissues of poisoned animals, therefore the risk of secondary poisoning is low.
Before the advent of anticoagulants, phosphides were the favored kind of rat poison. During the World War II, they came in use in United States because of shortage of strychnine due to the Japanese occupation of the territories where strychnine-producing plants are grown (Strychnos nux-vomica, in south-east Asia). Phosphides are rather fast acting rat poisons, resulting in the rats dying usually in open areas instead of in the affected buildings.
Phosphides used as rodenticides are:
Although this rodenticide was introduced with claims that it was less toxic to nontarget species than to rodents, clinical experience has shown that rodenticides containing cholecalciferol are a significant health threat to dogs and cats. Cholecalciferol produces hypercalcemia, which results in systemic calcification of soft tissue, leading to renal failure, cardiac abnormalities, hypertension, CNS depression and GI upset.
Signs generally develop within 18-36 hours of ingestion and can include depression, anorexia, polyuria and polydipsia. As serum calcium concentrations increase, clinical signs become more severe, manifesting often via anorexia, vomiting and constipation in the pet. Inability of the kidneys to concentrate urine is a direct result of hypercalcemia. As hypercalcemia persists, mineralization of the kidneys results in progressive renal insufficiency.
Additional anticoagulant renders the bait more toxic to pets as well as human. Upon single ingestion, solely calciferol-based baits are considered generally safer to birds than second generation anticoagulants or acute toxicants. A specific antidote for calciferol intoxication is calcitonin, a hormone that lowers the blood levels of calcium. The therapy with commercially available calcitonin preparations is, however, expensive.
Other chemical poisons include:
Newer rodenticides have been developed to work by reducing the sperm count in males to deprive them of the ability to procreate rather than to kill rodents outright. They are usually administered in the breeding seasons of most rodents.
NATURAL RODENT CONTROL
Several wildlife rehabilitation organizations encourage natural form of rodent control through exclusion and predator support and preventing secondary poisoning altogether.
The EPA agrees, noting in its Proposed Risk Mitigation Decision for Nine Rodenticides that “without habitat modification to make areas less attractive to commensal rodents, even eradication will not prevent new populations from recolonizing the habitat.” Rodents play an important role in nature. Removing rodent food sources and habitat, while encouraging natural predators, is the only permanent solution.
Eliminate Food Sources: Keep bulk food, seed, and dry pet food in metal cans with secure lids. Pick up fallen fruit. Take birdfeeders inside at night.
Remove potential rodent homes like yard debris, trash, construction waste, etc.
Exclude rodents from your home. Seal openings 1/2 inch or larger around the outside of your house with metal, concrete, or Copper Mesh Wool, which can be found online or at hardware stores.
Include natural rodent predators in your solution. A family of five owls can consume up to 3000 rodents in breeding season. Placing a nest box to encourage a family of owls to make your property home can be a great alternative to commercial pest control methods.
Use catch-and-release traps as a safe, sanitary, and humane solution. Catch-and-release traps will allow you to remove rodents from inside your home, but you must prevent their return by sealing entrance and exit holes and removing attractants (see above). Do not release the animal in an area that is unkown to the animal.
If you exhaust all the above efforts and as a last resort decide to kill the rodents, please consider purchasing a rat zapper or snap traps.
It has also been found that the breed raticus tompkinus can be killed with kiwi fruit.
G.A. Morriss; C.E. O'Connor; A.T. Airey; P. Fisher (2008) Factors influencing palatability and efficacy of toxic baits in ship rats, Norway rats and house mice. Science for Conservation 282. p 26. Published by Department of Conservation, New Zealand.
QUANTITATIVE DETERMINATION OF RODENTICIDE RESIDUES AND THE SUBSEQUENT EVALUATION OF POTENTIAL ECO-TOXICOLOGICAL RISK TO BIRDS OF PREY
Oct 01, 2011; Abstract Hromada R., Ondrasovicová S., Kudríková D., Harkabus J., Legáth J., Kosco J., Ondrasovic M.: Quantitative determination...