Page 765 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

724 SECTION | X Avian and Aquatic Toxicology

VetBooks.ir formulations, including sprays, dusts, dips, shampoos, exposed. The second-generation anticoagulant rodenti-
cides (brodifacoum, bromodiolone, difenacoum, and
spot-ons, foggers, ear tags, wettable powders, granules,
difethialone) are acutely toxic and have longer tissue half-
soluble powders, and emulsifiable concentrates. They are
often combined with synergists such as piperonyl butox- lives resulting in bioaccumulation and risk of secondary
ide to enhance their insecticidal activity. poisoning. Soon after the introduction of second-
Pyrethrins and pyrethroids are neurotoxic as a result of generation anticoagulants, the potential for secondary
their ability to alter sodium, chloride, and calcium chan- intoxication of raptor species such as owls and hawks was
nels and cause repetitive nervous discharges or membrane investigated and residues have been measured in a num-
depolarization. At relatively high concentrations, they ber of bird species (Thomas et al., 2011). Although anti-
also have effect on GABA-gated chloride channels coagulant intoxication has been documented in a number
(Anado ´n et al., 2009). Clinical signs associated with acute of individual birds, population impacts are less clear.
intoxication are related to nervous system stimulation Anticoagulant rodenticides bind and inhibit vitamin K
such as restlessness, pecking feathers, and abrupt move- epoxide reductase and halt the recycling of vitamin K
ments (Zwart, 1988). There does not appear to be any thereby affecting both intrinsic and extrinsic pathways of
reports on adverse behavioral effects on avian wildlife the coagulation system. Initial clinical signs are nonspe-
following sublethal exposures to pyrethrins/pyrethroids, cific, and coagulopathies develop as vitamin K dependent
similar to those reported for OPs or carbamates, which clotting factors deplete. Observable clinical signs of poi-
would cause mortality due to increased predation or soning are depression, mucous membrane pallor, increased
inability to obtain food. Gross and histopathological find- capillary refill time and bleeding from superficial wounds.
ings are usually absent. On postmortem, extensive subcutaneous, intramuscular,
The diagnosis of pyrethrin and pyrethroid toxicosis is pulmonary, pericardial and intracoelomic hemorrhages, and
dependent on exposure history and development of com- pallor of internal organs are noted (Murray, 2011).
patible clinical signs. Serum samples antemortem and Diagnosis of intoxication is dependent on antemortem
gastrointestinal contents, brain or liver postmortem can and/or postmortem evidence of a coagulopathy and the
confirm exposure but not necessarily intoxication. detection of an anticoagulant in blood, serum, or liver
samples. Merely finding a residue of an anticoagulant in
Neonicotinoids an animal is not sufficient for a diagnosis of intoxication
because residues are often found in the absence of a
Neonicotinoids, a new class of insecticide, are nicotinic
coagulopathy.
receptor agonists. They initially stimulate the receptor and
Vitamin K 1 is antidotal treatment, although there is
cause a depolarizing blockade later leading to death as a
some delay before coagulopathy resolves. Dosing regi-
result of paralysis. This class includes acetamiprid,
mens have not been well defined in avian species, but
clothianidin, dinotefuran, imidacloprid, nitenpyram, thia-
vitamin K 1 at 2.5 mg/kg given subcutaneously every 12 h
cloprid, and thiamethoxam. They are considered to have
along with oxygen therapy has been found to be curative
low toxicity for vertebrates because of relatively low
in a red-tailed hawk (Murray and Tseng, 2008). Once sta-
affinity for vertebrate nicotinic receptors compared to
bilized, vitamin K 1 given at similar doses once daily for 2
insect nicotinic receptors (Tomizawa and Casida, 2011).
weeks or longer is indicated.
However recent studies have shown decline in insectivo-
rous bird populations in association with widespread
usage of the neonicotinoid drug imidacloprid possibly due Avicides
to depletion of insect food resource though a less
A number of chemicals have been investigated for their
possible-direct consumption toxicity has also been pro-
ability to repel birds (Clark, 1998). Avicides are marketed
posed (Hallmann et al., 2014).
primarily to control pest bird species such as blackbirds,
pigeons, and grackles. Two commonly used avicides are
Rodenticides
4-aminopyridine (4-AP, Avitrol) and 3-chloro-4-
Anticoagulants methylbenzenamine hydrochloride (Starlicide). 4-AP is
Anticoagulant rodenticides are widely used to control designed to be placed on grain for baiting in such a way
rodent pests in urban and agricultural settings. Avian spe- as to only affect a few individuals in a flock. The clinical
cies that feed primarily on small rodents are at greatest signs exhibited by affected birds (distress cries and aerial
risk of poisoning. Wild birds and raptors have likelihood distress displays) are such that unaffected birds are scared
of exposure following ingestion of baits and exposed and/ away. Repellants such as methyl anthranilate are gener-
or intoxicated prey. Commercial poultry have a less ally not associated with lethal intoxication.
chance of exposure due to their controlled environments 4-AP is rapidly absorbed from gastrointestinal tract
whereas free-roaming poultry are more likely to be and clinical signs develop within a short duration of