Case Studies on Second-Generation Anticoagulant Rodenticide Toxicities in Nontarget Species

DuVall, Michael D.; Murphy, Michael J.; Ray, Allen C; Reagor, John C.

doi:10.1177/104063878900100118

Cited by 66 publications

(54 citation statements)

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“…Hemorrhage in major organs and vessels was likely to be a contributor to death, if not the definitive cause of mortality. However, histopathological observations alone are generally not considered diagnostic of anticoagulant intoxication [24]. Although the half-life of diphacinone in birds has yet to be reported, data from the present study indicate that it is rapidly cleared from liver, and presumably other tissues.…”

Section: Lethality and Overt Toxicitymentioning

confidence: 55%

Acute toxicity, histopathology, and coagulopathy in American kestrels (Falco sparverius) following administration of the rodenticide diphacinone

Rattner

Horak

Warner

et al. 2011

Enviro Toxic and Chemistry

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The acute oral toxicity of the anticoagulant rodenticide diphacinone was found to be over 20 times greater in American kestrels (Falco sparverius; median lethal dose 96.8 mg/kg body weight) compared with Northern bobwhite (Colinus virginianus) and mallards (Anas platyrhynchos). Modest evidence of internal bleeding was observed at necropsy, although histological examination of heart, liver, kidney, lung, intestine, and skeletal muscle revealed hemorrhage over a wide range of doses (35.1-675 mg/kg). Residue analysis suggests that the half-life of diphacinone in the liver of kestrels that survived was relatively short, with the majority of the dose cleared within 7 d of exposure. Several precise and sensitive clotting assays (prothrombin time, Russell's viper venom time, thrombin clotting time) were adapted for use in this species, and oral administration of diphacinone at 50 mg/kg increased prothrombin time and Russell's viper venom time at 48 and 96 h postdose compared with controls. Prolongation of in vitro clotting time reflects impaired coagulation complex activity, and generally corresponded with the onset of overt signs of toxicity and lethality. In view of the toxicity and risk evaluation data derived from American kestrels, the involvement of diphacinone in some raptor mortality events, and the paucity of threshold effects data following short-term dietary exposure for birds of prey, additional feeding trials with captive raptors are warranted to characterize more fully the risk of secondary poisoning.

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Section: Lethality and Overt Toxicitymentioning

confidence: 55%

Acute toxicity, histopathology, and coagulopathy in American kestrels (Falco sparverius) following administration of the rodenticide diphacinone

Rattner

Horak

Warner

et al. 2011

Enviro Toxic and Chemistry

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“…In the absence of frank external bleeding, observations of depression, weakness and pallor were noted in DPN-dosed kestrels and screech-owls, and are considered key signs of potential rodenticide poisoning (Mount 1988). Heptaocellular vacuolation and necrosis were present in the most severely affected individuals, and have been previously reported in FGAR and SGAR poisoning cases in both birds and mammals (DuVall et al 1989;Shivaprasad and Galey 2001). Such hepatocellular lesions are suggestive of a metabolic disturbance and hypoxia possibly as a result of anemia.…”

Section: Pathological Lesions and Clotting Timementioning

confidence: 84%

Assessment of toxicity and potential risk of the anticoagulant rodenticide diphacinone using Eastern screech-owls (Megascops asio)

Rattner

Horak²,

Lazarus

et al. 2012

Ecotoxicology

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In the United States, new regulatory restrictions have been placed on the use of some second-generation anticoagulant rodenticides. This action may be offset by expanded use of first-generation compounds (e.g., diphacinone; DPN). Single-day acute oral exposure of adult Eastern screech-owls (Megascops asio) to DPN evoked overt signs of intoxication, coagulopathy, histopathological lesions (e.g., hemorrhage, hepatocellular vacuolation), and/or lethality at doses as low as 130 mg/kg body weight, although there was no dose-response relation. However, this single-day exposure protocol does not mimic the multiple-day field exposures required to cause mortality in rodent pest species and non-target birds and mammals. In 7-day feeding trials, similar toxic effects were observed in owls fed diets containing 2.15, 9.55 or 22.6 ppm DPN, but at a small fraction (<5%) of the acute oral dose. In the dietary trial, the average lowest-observed-adverse-effect-level for prolonged clotting time was 1.68 mg DPN/kg owl/week (0.24 mg/kg owl/day; 0.049 mg/owl/day) and the lowest lethal dose was 5.75 mg DPN/kg owl/week (0.82 mg/kg owl/day). In this feeding trial, DPN concentration in liver ranged from 0.473 to 2.21 μg/g wet weight, and was directly related to the daily and cumulative dose consumed by each owl. A probabilistic risk assessment indicated that daily exposure to as little as 3-5 g of liver from DPN-poisoned rodents for 7 days could result in prolonged clotting time in the endangered Hawaiian short-eared owl (Asio flammeus sandwichensis) and Hawaiian hawk (Buteo solitarius), and daily exposure to greater quantities (9-13 g of liver) could result in low-level mortality. These findings can assist natural resource managers in weighing the costs and benefits of anticoagulant rodenticide use in pest control and eradication programs.

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“…However, considering that the serum half-life of brodifacoum in adult dogs is 6 Ϯ 4 days 22 and that serum concentrations of brodifacoum are much lower than liver concentrations, 7 it is unlikely that brodifacoum would be detectable in samples taken from the dam 4 weeks after subclinical ingestion of rodenticide.…”

mentioning

confidence: 99%

Brodifacoum Toxicosis in Two Neonatal Puppies

Munday¹,

Thompson²

2003

Vet Pathol

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Abstract. Eight out of a litter of 13 puppies were either born dead or died within 48 hours of birth. Three puppies that died shortly after birth were necropsied. Two puppies had hemorrhage in the thoracic and peritoneal cavities, intestinal serosa, and meninges. The third puppy was smaller than the other two puppies but did not have detectable hemorrhage. Brodifacoum, a second-generation coumarin anticoagulant, was detected in livers from the two puppies with hemorrhage. The dam did not have clinical signs of coagulopathy before or subsequent to whelping. The owners were confident that the dog had not been exposed to rodenticide for at least 4 weeks before whelping. A presumptive diagnosis of in utero brodifacoum toxicity was made. To the authors' knowledge this is the first time a second-generation coumarin anticoagulant has been detected in the liver of a newborn animal. This case is also unique because the dam was unaffected, suggesting that fetuses are more susceptible to brodifacoum toxicity than adult animals.Key words: Anticoagulant; brodifacoum; canine; coagulopathy; coumarin; transplacental; vitamin K.A 1-year-old Great Pyrenees bitch that was housed at a breeding kennel gave birth to 13 puppies after 63 days of gestation. Whelping was observed and was considered normal. However, two puppies were born dead, three died within 6 hours, and three died between 6 and 48 hours of birth. Four of the six puppies that died postpartum had variable hemoptysis or epistaxis before death. Two puppies were reported to have died suddenly without previous clinical signs of disease. The birth weight of the eight puppies that were born dead or died was 280 Ϯ 107 g (mean Ϯ 1 SD), whereas the birth weight of the five puppies that survived was 502 Ϯ 57 g (mean Ϯ 1 SD).The three puppies that were born alive but died within 6 hours of birth were necropsied. The abdominal cavities of two puppies (puppy Nos. 1 and 2) each contained approximately 40 ml of uncoagulated blood. Both puppies also had approximately 15 ml of uncoagulated blood within the thoracic cavity. However, one (puppy No. 3) did not have visible hemorrhage. Representative tissue samples from all three puppies were fixed in 10% buffered formalin and routinely processed for histologic examination. Histologic examination of tissues from puppy Nos. 1 and 2 revealed microscopic hemorrhage within the intestinal serosa and meninges. No significant lesions were observed by histologic examination of tissues from puppy No. 3. No histologic evidence of any infectious process was present in tissues from any of the puppies. Aerobic cultures of lung, liver, small intestine, and kidney from all three puppies did not yield pathogenic bacteria. Direct fluorescent antibody (American Bioresearch, Seivierville, TN) examination of kidney, lung, and liver did not reveal canine herpes virus antigen in any of the puppies.Liver samples from all three puppies were analyzed by high performance liquid chromatography (HPLC) for warfarin, bromadiolone, and brodifacoum. 17 Briefly, liver samp...

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Case Studies on Second-Generation Anticoagulant Rodenticide Toxicities in Nontarget Species

Cited by 66 publications

References 1 publication

Acute toxicity, histopathology, and coagulopathy in American kestrels (Falco sparverius) following administration of the rodenticide diphacinone

Acute toxicity, histopathology, and coagulopathy in American kestrels (Falco sparverius) following administration of the rodenticide diphacinone

Assessment of toxicity and potential risk of the anticoagulant rodenticide diphacinone using Eastern screech-owls (Megascops asio)

Brodifacoum Toxicosis in Two Neonatal Puppies

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