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SHORT COMMUNICATION |
1 Avian Disease Division, National Veterinary Research and Quarantine Service, Anyang, Kyunggi 430824, Korea;
2 Veterinary Epidemiology Division, National Veterinary Research and Quarantine Service, Anyang, Kyunggi 430-824, Korea
3 Corresponding author (email: kwonyk{at}nvrqs.go.kr)
ABSTRACT:
We describe cases of pesticide poisoning of wild birds diagnosed at the National Veterinary Research and Quarantine Service (Kyunggi, Korea) from 1998 to 2002. Forty-one mortality events (759 birds) of 87 incidents (2,464 birds) investigated were associated with pesticide poisoning, and six organophosphates or carbamates were identified as being responsible for the poisoning. Phosphamidon was most frequently identified as the cause of poisoning, accounting for 23 mortality events. Other pesticides identified as poisons for birds were organophosphates monocrotophus, fenthion, parathion, EPN, and diazinon, and the carbamate carbofuran. Pesticide poisoning is a problem in wild birds in Korea.
Key words: Carbamate, Korea, organo-phosphates, pesticide, phosphamidon, poisoning, wild birds.
Organophosphate (OP) and carbamate pesticides are used to control pests in the agricultural industry, home gardening, and veterinary medicine. These toxic compounds are capable of disrupting the avian nervous system by inhibiting cholinesterase (ChE; Ludke et al., 1975; Hill and Fleming, 1982; Quick, 1982).
This short communication reports the relative likelihood of poisoning by various pesticides and gives an indication of the wild birds most affected in Korea. This report is based on wild bird mortalities submitted to the Avian Disease Division, National Veterinary Research & Quarantine Service (Anyang, Kyunggi, Korea) from 1998 to 2002 and diagnosed as pesticide poisonings.
Although some birds were submitted alive with neurologic signs such as convulsions, lethargy, and paralysis, most birds were dead. At the time of necropsy, no specific gross lesions were observed in most birds. Ingested grains were commonly found in the upper digestive tracts of waterfowl and cranes, and feathers, flesh, or other animal parts were frequently observed in the esophagus and stomach of raptors and scavengers.
OP or carbamate poisoning was confirmed by identifying pesticide residues in stomach contents and tissuesincluding liver, kidney, fat, and brainof wild birds using gas chromatography/mass spectrometry (Hewlett Packard, Palo Alto, California USA) or high-performance liquid chromatography (Pickering, Mountain View, California). The detection limits of pesticides by these analyzers were lower than 1 ng.
Among 87 mortality events investigated from 1998 to 2002, 41 were diagnosed as being attributable to pesticide poisoning (Table 1
). Six OPs or a carbamate were identified as being responsible for poisoning the wild birds. The compound most frequently identified as the cause of poisoning was phosphamidon, which accounted for poisoning in 23 of 41 cases. Other compounds identified as poisons were the OPs monocrotophus, fenthion, parathion, EPN, and diazinon and the carbamate carbofuran. More than 10 to 1,000 times the minimum toxic dose of pesticide was commonly detected in the stomach contents of wild birds.
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Although we were fortunate in identifying the causative pesticides in many cases, a diagnosis of pesticide poisoning in wild birds can be difficult, and not all cases are solved. The changes in birds affected due to OP and carbamate toxicity are mostly biochemical, and gross and microscopic lesions are not present. These compounds may be undetectable in dead birds because of the rapid breakdown of the chemicals. Alternately, analysis of brain ChE activity is widely used as a diagnostic technique. However, diagnostic interpretation of ChE data always requires knowledge of the normal value for each species (Blakley and Skelley, 1988), and it may be confounded as well by changes in ChE levels caused by post mortem decomposition. Therefore, findings reported by field investigators and complete histories for avian mortality events are very important in the diagnosis of pesticide poisoning.
BLAKLEY, B. R., AND K. W. SKELLEY. 1988. Brain cholinesterase activity in animals and birds. Veterinary and Human Toxicology 30: 329331.[Medline]
HENNY, C. J., E. J. KOLBE, E. F. HILL, AND L. J. BLUS. 1987. Case history of bald eagles and other raptors killed by organophosphorus insecticides topically applied to livestock. Journal of Wildlife Diseases 23: 292295.
HILL, E. F., AND V. M. MENDENBALL. 1980. Secondary poisoning of barn owls with famphur, an organophophate insecticide. Journal of Wildlife Management 44: 676681.
, AND W. J. FLEMING. 1982. Anticholinesterase poisoning of birds: Field monitoring and diagnosis of acute poisoning. Environmental Toxicology and Chemistry 1: 2738.
LUDKE, J. L., E. F. HILL, AND M. P. DIETER. 1975. Cholinesterase (ChE) response and related mortality among birds fed ChE inhibitors. Archives of Environmental Contamination and Toxicology 3: 121.[Medline]
PRIJONO, W. B., AND F. A. LEIGHTON. 1991. Parallel measurement of brain acetylcholinesterase and the muscarinic cholinergic receptor in the diagnosis of acute, lethal poisoning by anticholinesterase pesticides. Journal of Wildlife Diseases 27: 110115.[Abstract]
QUICK, M. P. 1982. Pesticide poisoning of livestock: A review of cases investigated. The Veterinary Record 111: 57.[Abstract]
REECE, R. L., AND P. HANDSON. 1982. Observations on the accidental poisoning of birds by organo-phosphate insecticides and other toxic substances. The Veterinary Record 111: 453455.[Abstract]
WOO, H. J., AND M, B, YOON. 1989. Wild birds of Korea (In Korean). Academic Press, Seoul, Korea, pp. 1012.
Received for publication 26 January 2004.
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