Anticholinesterase Poisoning of Birds: Field Monitoring and Diagnosis of Acute Poisoning

Abstract

Organophosphorus and carbamate pesticides are cholinesterase (ChE) inhibiting chemicals that have been responsible for avian die‐offs. Identification of chemicals implicated in these die‐offs is difficult and sometimes conclusions are solely circumstantial. However, when marked depression (inhibition) of brain ChE activity accompanies organophosphorus or carbamate residues in body tissues or ingesta, cause‐effect diagnosis is enhanced. To achieve this end, normal brain ChE activity is estimated for controls of the affected species and then die‐off specimens are individually evaluated for evidence of ChE inhibition. This approach to evaluation of antiChE poisoning may also be used to monitor exposure of vertebrates to field application of organophosphorus or carbamate pesticides. Problems associated with this kind of evaluation, and the main topic of this report, include variability of brain ChE activity among species, postmortem influences of ambient conditions (storage or field) on ChE activity, and differential patterns of ChE activity when inhibited by organophosphorus or carbamate compounds. Other topics discussed are the ChE assay procedure, example case reports and interpretation, and research needed for improving the diagnostic utility of ChE activity in a field situation.

Survival and behaviour of captive Mallard broods exposed to carbofuran-sprayed vegetation: a field experiment

“…These ducklings exhibited severely depressed AChE (75 and 73% below mean control activity, respectively), indicating that incapacitation or death was caused by carbofuran poisoning. The duckling that died during exposure on day 1 in replicate 4 of the low spray-rate experiment exhibited a degree of AChE depression less than the level of 20% usually associated with exposure to anticholinesterase compounds (Hill and Fleming, 1982), however. Although the 2 h delay in recovery of the carcass (Table 1) may have resulted in reactivation of AChE to some extent, it is unlikely that activity would have recovered from the levels normally associated with death from carbofuran poisoning (<20% of control activity: Martin et al, 1991a) during this time.…”

“…Waterfowl exhibit particular intolerance to carbofuran with LDsos of 0.48 and 0.24 mg per kg body weight to Mallards and fulvous Whistlingducks (Dendrocygna bicolor), respectively (Hudson et al, 1984). Many die-offs of adult waterfowl wintering in the southern United States have been attributed to carbofuran 0963-9292 © 1993 Chapman & Hall use (Stickel, 1975;Flickinger et al, 1980;Hill and Fleming, 1982). No documentation of poisoning on the breeding grounds exists, however.…”

Effects of Methyl Parathion on Reproduction in the Japanese Quail

“…The extent of the inhibition of brain and plasma cholinesterase is regarded as a useful indicator of organophosphate and carbamate exposure in both humans and birds (Hill and Fleming 1982;Fossi et al 1992). In addition, effects on eggshell thickness are useful biomarkers for monitoring environmental contaminants.…”

Effects of insecticide use on breeding birds in Christmas tree plantations in Quebec

“…According to Hill and Fleming (1982), the measurement of inhibition of this enzyme is one of the best available methods to show the exposure of a subject to one of these insecticides. For each bird species under study and for each organophosphorus insecticide, we have matched up cholinesterase results for the period prior to spraying in a plantation and compared them to the results obtained in that plantation the second day (for security reasons) after the pesticide applications.…”

“…The brains of captured birds were immediately removed by decapitating the bird and placing the whole head on dry ice while awaiting transfer to a freezer at -80°C. Analyses of ChE activity were made with the methodology used by Ellman et al (1961) and modified by Hill and Fleming (1982) at the laboratory of the National Wildlife Research Centre (NWRC). For samples that showed a reduction in ChE activity, two cholinesterase reactivation tests (spontaneous reactivation and 2-PAM, cf.…”