Page 764 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Avian Toxicology Chapter | 53 723

VetBooks.ir general, have long environmental and body half-lives. intoxication is generally completed within 2 or 3 days.
Gross and histopathologic lesions in dead birds are usu-
Because of their lipophilic and persistent nature, they bio-
ally minimal and nonspecific.
magnify within food webs. They were banned due to their
environmental persistence, concern about their impact on Some OPs, including insecticides such as leptophos,
human health and wildlife health, and widespread insect mipafox, and cyanofenphos and industrial chemicals such
resistance. as tri-ortho-cresyl-phosphate, cause a delayed neurotoxic
effect referred to as OP-induced delayed neuropathy
(OPIDN) or OP-induced delayed polyneuropathy
Cholinesterase Inhibitors (Organophosphorus (OPIDPN). OPIDN occurs as a result of inhibition of neu-
and Carbamate Insecticides) rotoxic esterase (NTE), an enzyme found in peripheral
Due to their more rapid breakdown in the environment, nerves. OP insecticides are tested for their ability to cause
OP and carbamate insecticides replaced the OC pesticides OPIDN in adult hens as a result of their unique sensitivity
as the latter were banned for use in North America and to this effect. Also, pheasants and mallard ducklings are
Europe in the 1960s and 1970s. A number of different highly susceptible to delayed neurotoxicity (Brown and
formulations are available for use either in the environ- Julian, 2003). Most OPIDN-inducing insecticides are no
ment (e.g., agricultural or residential use) or on animals longer on the market.
(e.g., livestock dips or sprays). The more toxic insecti- A diagnosis of intoxication is dependent on measuring
cides of each group are generally restricted to agricultural reduced activity of cholinesterase along with identifica-
uses, whereas less-toxic members are approved for use on tion of a specific insecticide in suitable antemortem or
animals or in residential environments. postmortem samples. In birds, plasma is suitable for cho-
Birds are exposed to cholinesterase inhibitors in differ- linesterase activity determinations. Brain cholinesterase
ent ways. Pet and production birds can be exposed via activity can be measured in dead birds. It is important to
their diets, via home or premise use, or via direct applica- note that because carbamate-induced inhibition of cholin-
tion. Inhalation exposure is also possible from the use of esterase activity is readily reversible, even after death,
dichlorvos-impregnated pest strips or premise spraying or care must be taken when interpreting laboratory results.
fogging. Acute OP and carbamate intoxications are com- In general, cholinesterase activity less than 70% of nor-
mon in wild birds, and exposures can occur via ingestion mal suggests significant exposure to an OP or carbamate
of treated seeds or vegetation (accidental, intentional, or (activity is often ,20% of normal following lethal expo-
misuse of a product), poisoned insects or animals sures) (Hill, 1988). Normal plasma/whole blood and brain
(impaired live animals or carcasses), product (especially cholinesterase activities are quite variable among bird
granular formulations), or contaminated water (Friend and species, and interpretation of cholinesterase activity
Franson, 1999). Inhalation or dermal exposure is also should be based on species-specific and, when possible,
possible from spraying or spills. With avian wildlife, laboratory-specific reference ranges. Gastrointestinal con-
there can be some degree of seasonality to OP or carba- tents should be examined carefully because the presence
mate intoxications as a result of seasonal patterns of of granules or dye may suggest pesticide exposure. Often,
insecticide use. given the rapidity of death, there is freshly ingested food
The acute oral toxicity of individual OPs and carba- in the upper GI tract.
mates vary considerably within classes and between spe- Fortunately, the overall adverse impact of agricultural
cies. A number of other factors can influence toxicity, pesticide use in general, and OPs and carbamate use more
including age, sex, diet, body condition, and product specifically, on avian wildlife has lessened during approx-
formulation. imately the past decade due primarily to the replacement
Although chemically distinct, the OPs and carbamates of older, more toxic insecticides with newer, less-toxic
have a common mechanism of toxic action, namely the ones such as pyrethrins/pyrethroids and neonicotinoids.
inhibition of cholinesterase enzymes. Inhibition of acetyl-
cholinesterase (AChE) is primarily responsible for the
clinical signs associated with intoxication. The onset of Pyrethrins/Pyrethroids
clinical signs and death can be rapid; birds are often Naturally occurring pyrethrins (derived from chrysanthe-
found dead. Death is most often due to respiratory failure mum flowers) and synthetic pyrethroid insecticides are
and hypoxia. OP inhibition of AChE activity can be irre- currently estimated to make up more than 25% of insecti-
versible, thus necessitating synthesis of new enzyme cide use worldwide. Their popularity is due to their lack
before recovery can occur. Carbamates do not irreversibly of environmental persistence and relatively low toxicity
inhibit AChE, and spontaneous regeneration of enzyme for birds and mammals (they are highly toxic for fish).
activity is rapid. Clinical signs can persist for days in OP They are used to control a variety of agricultural, home,
intoxicated animals, whereas recovery from carbamate and animal pests and are available in a large number of