Environmental Engineering Reference
In-Depth Information
2.5 Physiological effects and signs of intoxication
The following discussion is adapted from Mineau and Tucker (2002). Overstimulation of the somatic
nervous system (which controls voluntary muscle movement by a pooling of acetylcholine) typi-
cally results in tremors, muscle twitches and piloerection (erection of the contour feathers), as well
as paresis (slight or incomplete paralysis) resulting in ataxia (lack of coordination/stability). More
rarely, an animal may convulse. Cholinergic tracts are also important to both the parasympathetic and
sympathetic autonomic nervous systems, but especially to the former. They conduct impulses from
the neural ganglia to a multitude of organs such as the heart, the endocrine glands, and the digestive
system. Because the autonomic nervous system is subject to constant adjustment through feedback
mechanisms, intoxication with a cholinesterase inhibitor is rarely straightforward. For example,
individuals may show either constriction or dilation of the pupils, or a speeding up or slowing down
of the heartbeat, and so on. Also, because the somatic and autonomous systems react to different
levels of cholinergic stimulation, some doses of a cholinesterase inhibitor may produce apparently
opposite signs (e.g., contraction of the striated muscles involved in locomotion, and simultaneous
relaxation of the smooth musculature leading to a fl accid gut and food impaction). Poisoned raptors,
for example, are often found with very full crops.
The rate at which an individual is exposed to a cholinesterase-inhibiting pesticide is often as
important as the dose itself. Typically, gradual exposure allows the individual to compensate for,
and thus tolerate, a higher dose than if the exposure was due to a single large dose. This is especially
true for carbofuran and other carbamates because rapid spontaneous recovery from intoxication can
occur via the hydrolysis of the enzyme-pesticide moiety. Porter (1993) cautions that many 'classic
signs' of parasympathetic stimulation (as reported in standard toxicology texts) may not be seen in
carbamate poisoned raptors, and certainly not with any consistency. Often, clinical signs may be
non-specifi c and may only involve depression or ataxia. Shimmel and Snell (1999) also note that
it is often diffi cult to arrive at a conclusive diagnosis without chemical or biochemical laboratory
backup. Nevertheless, the following list (modifi ed from Grue, Hart and Mineau 1991) summarises
the signs noted by Hudson and colleagues (1984) following dosing using various bird species (in the
laboratory) with a variety of cholinesterase-inhibiting agents:
•
ataraxia (induced tranquility), lethargy
•
ataxia (incoordination of muscular action)
•
blindness
•
convulsions, particularly just prior to death
•
defecation, diarrhoea
•
dyspnea (diffi cult breathing)
•
epistaxis (bleeding from the nares [nostrils])
•
exophthalmia (protruding eyes)
•
hyperexcitability
•
lacrimation (secretion/discharge of tears)
•
miosis (contraction of pupils)
•
myasthenia (muscular weakness)
•
mydriasis (dilation of pupils)
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