Carbofuran: Toxicity, diagnosing poisoning and rehabilitation of poisoned birds - Carbofuran and Wildlife Poisoning: Global Perspectives and Forensic Approaches - page 33

over a 28 day period during which 164 mm of rain fell. No apparent postmortem loss of residue
was recorded. Otieno and colleagues (2010) have also recently extracted residues from the beaks
and talons of poisoned vultures. Based on their fi ndings, they suggest that the two main breakdown
products (3-hydroxycarbofuran and 3-ketocarbofuran) should be analysed in addition to the par-
ent material (carbofuran proper). These metabolites were present in certain cases, even when the
parent compound had completely disappeared.
Whether residues are detected within gastrointestinal contents, in feet, or in the beak, converting
these fi gures into lethal-dose equivalents (for the purposes of proving causation) is often not simple
or perhaps even useful. Unfortunately, pathology reports often state that the gastrointestinal residue
level was below the LD 50 value, and that therefore the pesticide probably did not kill the animal. For
many reasons, this is scientifi cally unsound. Gastrointestinal tract contents are pre-absorptive (i.e.,
they do not indicate the amount that has already entered the animals' circulatory system and target
organs) and, different parts of the gastrointestinal tract can present very different residue load values
(as described above).
Much of the above discussion assumes that a bird will die quickly after carbofuran ingestion.
However, delayed mortality is also possible. Birds that are sub lethally exposed to cholinesterase
inhibitors, for example, are known to be more susceptible to predation (Galindo, Kendall, Driver
et al. 1985; Buerger, Kendall, Mueller et al. 1991; Hunt, Bird, Mineau et al. 1992). There is also
anecdotal evidence which suggests that sub lethal exposure may make animals more vulnerable to
collision with objects, either moving (e.g., vehicles) or stationary (e.g., power lines, fences, build-
ings). Upon arriving at a rehabilitation centre, a raptor for example, may often be diagnosed as a
victim of 'collision'. The suggestion that pesticides may well be involved in at least some such cases
is two-fold: (1) there is anecdotal evidence available (from rehabilitation centres) when cholinester-
ase measurements are taken as a matter of routine (e.g., Porter 1993); and (2) a wealth of human
based evidence shows that various visual/motor effects can be recorded in humans (see Gallo and
Lawryk 1991 for a review) after they are occupationally exposed to organophosphorus and carba-
mate insecticides. Blurred vision is a common complaint, and unequal miosis can also lead to a phe-
nomenon called the 'Pulfrich Stereo Effect' where depth perception/the ability to compute trajectory
is affected. Assuming that these physiological effects can extend to birds, one may imagine that birds
could thus suffer more collisions in fl ight.
2.8 Rehabilitation of poisoned wildlife
Normally, the treatment of choice is to remove all food contents from the upper gastrointestinal
tract. If the bird being treated has an engorged crop, this must be emptied. The crop contents can be
gently manipulated toward the pharynx and then removed manually, or the bird may be anaesthe-
tised for this procedure. Alternatively, the bird may be anaesthetised but if manual manipulation is
not possible, an ingluviotomy (an incision made to the crop of the bird) can be performed and the
crop contents carefully removed. This is then followed by intravenous or intramuscular (i.e., IV or
IM) atropine administration. The recommended dose is usually within the 0.5 to 5.0 mg/kg range.
However, Shlosberg and colleagues (1997) argued for a much higher dose (of 50 mg/kg) after work-
ing with young chickens and the carbamate insecticide methomyl. They attributed this requirement
for a higher dose to the presence of hydrolytic enzymes in chicken blood (atropine esterase), and,
recommended that an appropriate atropine esterase regimen should be developed for various wild
bird species. Atropine will only alleviate the clinical signs of toxicity, and will not affect cholineste-
rase levels. If the only obvious sign is depression, no improvement may be noted. The antispasmodic
drug diphenhydramine (at 15 mg/kg) is often used if a bird is exhibiting tremors or twitching.
There is a long-standing belief that oximes (such as 2-PAM - pralidoxime chloride)
should not be used in cases of carbamate poisoning. Oximes are very effective at breaking the