Rodenticide

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RodenticideFrom Wikipedia, the free encyclopedia

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A wildrat

"Rat poison" redirects here. For the window manager, seeratpoison.

Rodenticides are a category ofpest controlchemicalsintended to killrodents.

Single feed baitsare 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 asscavengers. 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.

Contents

[hide]

1 Poisonous chemicals

o 1.1 Anticoagulants

o 1.2 Rodenticide in dogs

o 1.3 References

o 1.4 Metal phosphides

o 1.5 Hypercalcemia

o 1.6 Other

o 1.7 Combinations

2 List of rat eradications
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3 References

4 External links

[edit]Poisonous chemicals

[edit]Anticoagulants

A warning sign in a Chicago neighborhood advises that a dose of poison has recently been set out.

Anticoagulants are defined as chronic (death occurs after one to two weeks after ingestion of the lethal dose,

rarely sooner), single-dose (second generation) or multiple-dose (first generation) rodenticides, acting by

effective blocking of the vitamin K cycle, resulting in inability to produce essential blood-clotting factors

mainly coagulation factors II (prothrombin), VII (proconvertin), IX (Christmas factor) and X (Stuart factor).

In addition to this specific metabolic disruption, massive toxic doses of4-hydroxycoumarinor4-

hydroxythiacoumarinandindandioneanticoagulants 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

bothwarfarinpoisoning andhaemophiliacommonly cause moderate to severe pain from bleeding into muscles

and joints.[1]

In the final phase of the intoxication, the exhausted rodent collapses in hypovolemic

circulatoryshockor severeanemiaand dies calmly. However, because of the duration of discomfort and pain

before death it has been suggested that the use of rodenticides can be considered as inhumane.[2]
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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 the damage with their feeding habits.

First generation rodenticidal anticoagulants generally have shorter elimination half-lives,[3]require 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.

Second generation agents are far more toxic than first generation. They are generally applied in lower

concentrations in baits usually on the order of 0.001% to 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".[4]

Class Examples

Coumarins/4-

hydroxycoumarins

First generation:warfarin,coumatetralyl

Second generation:difenacoum,brodifacoum,[5]flocoumafenandbromadiolone.

1,3-indandiones

diphacinone,chlorophacinone,[6]

pindone

These are harder to group by generation. According to some sources, the indandiones are

considered second generation.[7]

However, according to the

, examples of first generation agents includechlorophacinoneanddiphacinone.[5]

Other Difethialoneis considered a second generation anticoagulant rodenticide .[8]

Indirect

Sometimes, anticoagulant rodenticides are potentiated by anantibioticorbacteriostatic agent,

most commonlysulfaquinoxaline. The aim of this association is that the antibiotic suppresses

intestinalsymbioticmicroflora, which are a source of vitamin K. Diminished production of

vitamin K by the intestinal microflora contributes to the action of anticoagulants.

Addedvitamin Dalso has a synergistic effect with anticoagulants.

Vitamin K1has been suggested, and successfully used, as antidote forpetsor humans accidentally or

intentionally (poison assaults on pets, suicidal attempts) exposed to anticoagulant poisons. Some of these

poisons act by inhibitingliverfunctions 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.

[edit]Rodenticide in dogs

Rodenticide, also known as rat bait, is an anticoagulant used to kill rodents. This product is also lethal to many

other species, specifically, dogs. Even in small doses this pest control substance can be fatal if not treated

immediately.
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Clinical signs for canine rodenticide toxicosis include lethargy, epistaxis, melena, bruising, acute blindness,

seizures, dyspnea, depression, weakness, pallor, paresis or paralysis, gingival bleeding, profuse bleeding from

wounds, hematemesis and hematuria. The vet may notice prolonged bleeding from venipuncture sites,

hematomas and hemorrhaging into body cavities. If any of these signs are noticed and rodenticide ingestion is

a probable cause, the pet should be taken to an animal hospital immediately.

This drug works by inhibiting an enzyme that uptakes and reuses vitamin K. Vitamin K is critical in the

production of coagulation factors and thus when ceased it reduces the production of vitamin K dependent

factors 2,7, 9 and 10. The body is then unable to activate vitamin K. Coagulation pathways are affected and

can lead to coagulopathy. This is why external and internal bleeding are major signs that the patient has been

exposed to rodenticide. It can take up to 5-7 days for signs to develop depending on the half-life of the active

ingredient. The half-life of Warfarin is only 14.5 hours while others like second generation hydroxycoumarins

and indanediones are between 4-6 days.

To diagnose rodenticide toxicosis, veterinarians use blood testing to find abnormal values to assess the

patients clotting time and other related issues. Baseline testing includes pack cell volume (PVC), total protein

(TP), complete blood count (CBC), platelet estimate and activated clotting time (ACT). From these values the

veterinarian will be able to know if the patient is anemic, if the platelet count is within normal limits and if the

clotting time is delayed. Further testing if time allows would include a coagulation screen (PT, PTT, fibrinogen,

and FDPs), PIVKA (proteins induced by vitamin K absence), complete serum biochemical profile, urinalysis,

fecal exam, blood gas analysis and chemical analysis of heparinized plasma.

Treatment begins with identifying the specific toxic agent. This will significantly affect the depth and length of

treatment needed for the patient and the prognosis. If the product was ingested within 1 hour upon presentation

to the hospital then emesis will be utilized by administering an IV medication called apomorphine. If it has been

between 2-4 hours of ingestion, gastric lavage will be performed. Activated charcoal should then be given by

mouth every 3-4 hours and continued depending on the time of ingestion. Finally the antidote, vitamin K should

be administered and repeated again depending on the time of exposure.

The prognosis of the patient all depends on what kind of rodenticide was ingested, the amount, the time lapse

between ingestion and treatment, the severity of the symptoms, underlying diseases that may bring about

further complications and the correct treatment and diagnosis. It is very important to bring your pet into a

veterinarian as soon as you suspect ingestion and dont wait for clinical signs. You will be saving their life the

quicker you act upon it.

[edit]References

Plunkett, Signe J. (2001). Emergency Procedures for the Small Animal Veterinarian. Harcourt Publishers.

pp. 289292.ISBN0-7020-2487-2.
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Gfeller, Roger W.; Shawn P. Messonnier (2004). Small Animal Toxicology and Poisonings. Mosby.. pp. 321

326.ISBN0-323-01246-9.

[edit]Metal phosphides

Rat poison vendor's stall at a market inLinxia City, China

Metal phosphides have been used as a means of killing rodents and are considered single-dose fast acting

rodenticides (death occurs commonly within 1-3 days after single bait ingestion). A bait consisting of food and a

phosphide (usuallyzinc phosphide) is left where the rodents can eat it. The acid in the digestive system of the

rodent reacts with the phosphide to generate the toxicphosphinegas. This method of vermin control has

possible use in places where rodents are resistant to some of the anticoagulants, particularly for control of

house and field mice; zinc phosphide baits are also cheaper than most second-generation anticoagulants, so

that sometimes, in the case of large infestation by rodents, their population is initially reduced by copious

amounts of zinc phosphide bait applied, and the rest of population that survived the initial fast-acting poison is

then eradicated by prolonged feeding on anticoagulant bait. Inversely, the individual rodents, that survived

anticoagulant bait poisoning (rest population) can be eradicated by pre-baiting them with nontoxic bait for a

week or two (this is important to overcome bait shyness, and to get rodents used to feeding in specific areas by

specific food, especially in eradicating rats) and subsequently applying poisoned bait of the same sort as used

for pre-baiting until all consumption of the bait ceases (usually within 2-4 days). These methods of alternating

rodenticides with different modes of action gives actual or almost 100% eradications of the rodent population in

the area, if the acceptance/palatability of baits are good (i.e., rodents feed on it readily).

Zinc phosphide is typically added to rodent baits in a concentration of 0.75% to 2.0%. The baits have strong,

pungent garlic-like odor characteristic forphosphineliberated byhydrolysis. The odor attracts (or, at least, does

not repulse) rodents, but has repulsive effect on other mammals. Birds, notablywild 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 evolveammonia, which helps to reduce the potential for

spontaneousignitionorexplosionof the phosphine gas.
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Phosphides do not accumulate in the tissues of poisoned animals, so the risk ofsecondary poisoningis low.

Before the advent of anticoagulants, phosphides were the favored kind of rat poison. During World War II, they

came into use in United States because of shortage ofstrychninedue to the Japanese occupation of the

territories where strychnine-producing plants are grown (Strychnos nux-vomica, in southeast 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:

aluminium phosphide(fumigantonly)

calcium phosphide(fumigantonly)

magnesium phosphide(fumigantonly)

zinc phosphide(in baits)

[edit]Hypercalcemia

Calciferols (vitamins D),cholecalciferol(vitamin D3) andergocalciferol(vitamin D2) are used as rodenticides.

They are toxic to rodents for the same reason they are important to humans: they affect calcium and

phosphatehomeostasisin the body. Vitamins D are essential in minute quantities (fewIUsper kilogram body

weight daily, only a fraction of a milligram), and like most fat solublevitamins, they are toxic in larger doses,

causinghypervitaminosis. If the poisoning is severe enough (that is, if the dose of the toxin is high enough), it

leads to death. In rodents that consume the rodenticidal bait, it causeshypercalcemia, raising the calcium level,

mainly by increasing calcium absorption from food, mobilising bone-matrix-fixed calcium intoionisedform

(mainly monohydrogencarbonate calcium cation, partially bound to plasma proteins, [CaHCO3]+), which

circulates dissolved in theblood plasma. After ingestion of a lethal dose, the free calcium levels are raised

sufficiently thatblood vessels,kidneys, thestomachwall andlungsare mineralised/calcificated (formation of

calcificates, crystals of calcium salts/complexes in the tissues, damaging them), leading further to heart

problems (myocardial tissue is sensitive to variations of free calcium levels, affecting both myocardial

contractibility and excitation propagation between atrias and ventriculas), bleeding (due to capillary damage)

and possibly kidney failure. It is considered to be single-dose, cumulative (depending on concentration used;

the common 0.075% bait concentration is lethal to most rodents after a single intake of larger portions of the

bait) or sub-chronic (death occurring usually within days to one week after ingestion of the bait). Appliedconcentrations are 0.075% cholecalciferol and 0.1% ergocalciferol when used alone.

There is an important feature of calciferols toxicology, that they aresynergisticwithanticoagulanttoxicants, that

means, that mixtures of anticoagulants and calciferols in same bait are more toxic than a sum of toxicities of

the anticoagulant and the calciferol in the bait, so that a massive hypercalcemic effect can be achieved by a

substantially lower calciferol content in the bait, and vice-versa, a more pronounced anticoagulant/hemorrhagic
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effects are observed if the calciferol is present. This synergism is mostly used in calciferol low concentration

baits, because effective concentrations of calciferols are more expensive than effective concentrations of most

anticoagulants.

The first application of a calciferol in rodenticidal bait was in the Sorex product Sorexa D (with a different

formula than today's Sorexa D), back in early 1970s, which contained 0.025% warfarin and 0.1% ergocalciferol.

Today, Sorexa CD contains a 0.0025% difenacoum and 0.075% cholecalciferol combination. Numerous other

brand products containing either 0.075-0.1% calciferols (e.g. Quintox) alone or alongside an anticoagulant are

marketed.

The Merck Veterinary Manual states the following:

Although this rodenticide [cholecalciferol] 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 calcificationof 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. ... GI smooth

muscle excitability decreases and is manifest by anorexia, vomiting and constipation. ... Loss of renal

concentrating ability is a direct result of hypercalcemia. As hypercalcemia persists, mineralization of the

kidneys results in progressive renal insufficiency."[9]

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 iscalcitonin, a hormone that lowers the blood levels of

calcium. The therapy with commercially available calcitonin preparations is, however, expensive.

[edit]Other
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Civilian Public Serviceworker distributes rat poison fortyphuscontrol in Gulfport Mississippi, ca. 1945.

Other chemicalpoisonsinclude:

ANTU(-naphthylthiourea; specific againstBrown rat,Rattus norvegicus)

Arsenic

Barium(atoxicmetal) compound

Barium carbonate

Bromethalin(which affects thenervous system, noantidote)

Chloralose(narcotic acting condensation product of chloral and glucose)

Crimidine(2-chloro-N, N,6-trimethylpyrimidin-4-amine; a synthetic convulsant poison, antivitamin B6)

1,3-Difluoro-2-propanol("Gliftor" in the former USSR)

Endrin(organochlorine cyclodiene insecticide, used in the past for extermination of voles in f ields during

winter by aircraft spraying)

Fluoroacetamide("1081")

Phosacetim(a delayed-action organophosphorous rodenticide)

Whitephosphorus

Pyrinuron(anureaderivative)

Scilliroside

Sodium fluoroacetate("1080")

Strychnine

Tetramethylenedisulfotetramine("tetramine")
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Thallium(a toxicheavy metal) compounds

Zyklon B(hydrogen cyanideabsorbed in an inert carrier)

[edit]Combinations

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% to 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
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