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PubMed1985

Pen and field trials of flupropadine against the house mouse (Mus musculus L.).

Laboratory and field trials were conducted to determine the efficacy of the candidate rodenticide flupropadine against the house mouse (Mus musculus L.). In laboratory feeding tests, family groups of wild mice maintained in pens and conditioned to feeding on plain foods were offered flupropadine at either 0.10%, 0.15%, 0.18% or 0.20% in pinhead oatmeal bait. Overall mortalities in replicated 21-day treatments were 66/71 (93.0%), 71/79 (89.9%), 72/76 (94.7%) and 69/75 (92.0%) respectively. In 17 field trials carried out against mice infesting farm buildings, flupropadine was used at 0.10%, 0.15% and 0.18% in oatmeal bait. Mean treatment success, estimated from live-capture and mortality data, was 88.6%, 96.2% and 96.6% respectively. Flupropadine was found to be as near effective against mice as calciferol/warfarin and the second-generation anticoagulant rodenticides difenacoum, bromadiolone and brodifacoum. In further comparison with the anticoagulants, treatment with flupropadine bait achieved markedly quicker control.

Animals↗
PubMed2006

[Bromadiolone poisoning in foxes].

Bromadiolone is an anticoagulant rodenticide that inhibits the reactivation of vitamin K1 by the enzyme vitamin K1-epoxide reductase. The present case report originated from the application of bromadiolone against water voles (Arvicola terrestris) in northeastern Switzerland. At least 40 foxes (Vulpes vulpes) were found dead after the inappropriate use of a bait that contained 0.02 % bromadiolone. Anticoagulant rodenticide poisoning was suspected on the basis of the postmortem examination and subsequently confirmed by the detection ofbromadiolone both in the blood and in samples from thoracic and abdominal fluids.

4-Hydroxycoumarins↗
PubMed2000

Long-acting anticoagulant overdose: brodifacoum kinetics and optimal vitamin K dosing.

Ingestion of long-acting anticoagulant rodenticides such as brodifacoum can lead to prolonged and life-threatening coagulopathy. A paucity of conflicting information is available on brodifacoum's half-life and elimination pharmacokinetics. In addition, the optimal dose, duration, and route of administration of vitamin K(1) therapy are unknown. We report the case of a 52-year-old man who ingested eight 43-g boxes of a rodenticide (d-Con Mouse-Prufe II; 0.005% brodifacoum; Reckitt & Colman, Wayne, NJ). This case demonstrates that after stabilization with fresh frozen plasma, high-dose oral vitamin K(1) therapy ( congruent with 7 mg/kg per 24 hours divided every 6 hours) was effective in treating brodifacoum-induced coagulopathy. The concentration of vitamin K(1) required for normal coagulation in this case was less than the accepted value of 1 microg/mL, which is derived from a rabbit model. In this case, brodifacoum appears to follow zero-order elimination pharmacokinetics. In future cases of patients with ingestions of long-acting anticoagulants who present with coagulopathy, it may be useful to obtain serial brodifacoum concentrations to determine elimination curves to help predict the duration of oral vitamin K(1) therapy.

4-Hydroxycoumarins↗
PubMed1995

Combined superwarfarin and ethylene glycol ingestion. A unique case report with misleading clinical history.

A markedly elevated prothrombin time (PT) and activated partial thromboplastin time (APTT) were observed in a 24-year-old man who was admitted with a history of ethylene glycol ingestion. Further laboratory evaluation suggested that the coagulopathy was related to acquired factor deficiencies. The PT and APTT improved transiently on usual doses of vitamin K, but rapidly became abnormal again. The coagulopathy was controlled only after large doses of vitamin K for at least 37 days. On further questioning, the patient admitted to consuming a large quantity of a rodenticide. The second generation anticoagulant rodenticides (superwarfarins) result in a potent and prolonged anticoagulant effect by reducing the activity of the vitamin K dependent factors (II, XII, IX, and X). To our knowledge, this is the first reported concomitant ingestion of both ethylene glycol and a superwarfarin compound. This case serves to illustrate how a logical laboratory evaluation can lead to the proper diagnosis, despite a misleading clinical history.

4-Hydroxycoumarins↗
PubMedDate not supplied

GC/MS identification of tetramine in samples from human alimentary intoxication and evaluation of artificial carbonic kidneys for the treatment of the victims.

One day in July 1991, 78 people became victims of accidental alimentary intoxication in a factory in Hebei Province, China. Related samples, including rodenticide bait, the artificial carbonic kidneys used for the treatment of the victims, and the victims' blood, were analyzed by GC/MS. Tetramine [80-12-6], a highly toxic rodenticide, was identified as the toxicant. The effectiveness of artificial carbonic kidneys was evaluated. The analytical results revealed that detoxification of the patients was effective 48 hours after intoxication by percolating their blood through artificial carbonic kidneys.

Bridged-Ring Compounds↗
PubMed1997

Surreptitious superwarfarin poisoning with brodifacoum.

Because of the emergence of warfarin resistance in rodents, second-generation anticoagulants named "superwarfarins" were developed and marketed in over-the-counter rodenticide products. The availability of these compounds has resulted in accidental or intentional human ingestions, which cause severe bleeding. The methods for diagnosis and treatment of patients using superwarfarins are different from those for patients taking the regular warfarins. We report a case of intentional superwarfarin ingestion that caused petechiae and hematuria. Although the patient denied taking anticoagulant, the persistence of vitamin K-dependent factor deficiency led us to investigate the serum for anticoagulant rodenticides. We found high levels of brodifacoum, a superwarfarin compound. This case emphasizes the need for suspicion of superwarfarin poisoning in patients who show unexplained bleeding due to deficiency of vitamin K-dependent factors and resistance to treatment.

4-Hydroxycoumarins↗
PubMed2006

Fatal bromethalin poisoning.

Bromethalin is a neurotoxin found in some rodenticides. A delusional 21-year-old male presented to a hospital with altered mental status the day after ingesting a bromethalin-based rodenticide. He died 7 days after his self-reported exposure to c. 17 mg bromethalin (equivalent to 0.33 mg bromethalin/kg). His clinicopathologic course was characterized by altered mental status, obtundation, increased cerebrospinal fluid pressure, cerebral edema, death, and diffuse histologic vacuolization of the white matter in the central nervous system seen on microscopic examination at autopsy. The presence of a demethylated form of bromethalin in the patient's liver and brain was confirmed by gas chromatography with mass spectrometry. Clinical signs and lesions observed in this patient are similar to those seen in animals poisoned with bromethalin. This case illustrates the potential for bromethalin ingestion to result in fatal human poisoning.

Adult↗
PubMed1982

Bladder tumours among rodent operatives handling ANTU.

The rodenticide ANTU (alpha-naphthylthiourea) was used in the United Kingdom mainly in the late 1940s and early 1950s. The product then contained up to 0.2% of beta-naphthylamine as an impurity, and it was finally withdrawn in 1967 as a suspected carcinogen. Fourteen cases of urothelial tumours among rodent operatives exposed to ANTU are reported: in one district four out of 27 staff were affected, and in another area two out of 10. These cases strongly suggest that the early ANTU manufactured in the United Kingdom posed a cancer hazard to users. ANTU is still made or used in various countries, though the current product may be relatively pure and no longer contaminated by beta-naphthylamine. Recent laboratory evidence shows that even pure ANTU is mutagenic in the Ames test, and the safety of this rodenticide may need review.

Adult↗
PubMed2000

Unintentional pediatric superwarfarin exposures: do we really need a prothrombin time?

OBJECTIVE: To determine whether routine follow-up coagulation studies are useful in children with accidental exposures to rodenticides containing superwarfarin compounds. DESIGN: Retrospective review of poison center charts involving pediatric superwarfarin exposures occurring in two 2-year periods. SETTING: An American Association of Poison Control Centers-certified regional poison control center with an annual call volume of 55 000 calls per year from a 2-state area with a combined population of 4 million people. OUTCOME MEASURES: Prothrombin times and/or international normalized ratios and reported clinical signs of excessive anticoagulation after exposure. RESULTS: Of 542 children in 4 years of data collection, follow-up prothrombin times and/or international normalized ratios measurements did not detect any significant coagulation abnormalities. No child developed bleeding complications. No child required or received antidotal treatment with vitamin K. CONCLUSION: Normal preschool-aged children with unintentional acute exposures to superwarfarin rodenticides do not require any routine follow-up laboratory studies and do not require any medical intervention.

4-Hydroxycoumarins↗
PubMed2001

Effect of dietary protein on zinc phosphide toxicity in albino rats (Rattus norvegicus).

Adult male and female albino rats (R. norvegicus) were administered rodenticide, zinc phosphide ranging from 4, 2, 1, 0.5, 0.25 and 0.125% in the diet containing 10(A), 17(B) and 24%(C) protein. Zinc phosphide induced 100% mortality at 4, 2, 1, 0.5% in diet A; 4 and 2% in diet B; and 4% in diet C. The results reveal influence of dietary protein in modulating the toxicity of zinc phosphide, suggesting that greater caution should be exercised while formulating its baits for effectiveness. The results also suggest that baits having 10% protein are more suitable to carry the rodenticide from view point of acceptability and efficacy towards the target species.

Animals↗
PubMed2003

Intentional poisoning of animals in southeastern Spain: a review of the veterinary toxicology service from Murcia, Spain.

Data of toxicological analyses carried out over a 10-y period for suspected cases of wild and domestic animal poisonings are summarized. Of the 123 cases suspected as deliberate, 102 were be analyzed and 50 of them were positive to intentional poisoning, a total of 107 dead animals. Pesticides, especially insecticides (72%) and rodenticides (26%), were frequently involved. Aldicarb (n=15), anticoagulant rodenticides (n=8) and strychnine (n=4) were the most common toxins in baits prepared for intentional poisonings; carbofuran, methomyl, endosulfan and paraquat were also used. A coordinated Veterinary Toxicology Services network of collaboration should be set up in Spain to improve the quality of the services provided.

Aldicarb↗
PubMed1992

[Poisoning with long-acting anticoagulants].

Until last year, all rodenticides that could be marketed freely in Norway contained anticoagulants. In recent years rodenticide manufacturers have replaced warfarin by so-called "superwarfarins" as the active substances in their products. The latter are more toxic, also in a human context. One single intake can produce an anticoagulatory effect which may last for 50 to 60 days, and the intake of larger quantities over a period of time can induce the same effect for close to seven months. We describe two patients who were poisoned with bromadiolone. One of them had to be treated with vitamin K1 for six months. Reference is further made to similar casuistics described in the literature. Finally, the authors outline a recommended method of treatment.

4-Hydroxycoumarins↗
PubMed1991

Elevated 25-hydroxy and normal 1,25-dihydroxy cholecalciferol serum concentrations in a successfully-treated case of vitamin D3 toxicosis in a dog.

A 4-y old, 27 kg spayed female German Shepherd dog was observed to ingest one 1-oz package of a rodenticide containing cholecalciferol. An initial serum calcium concentration of 15.7 mg/dl was successfully reduced to normal during 10 d using calcitonin and prednisolone. During that time, the serum 25-hydroxy and 1,25-dihydroxy cholecalciferol concentrations ranged from 637 to 315 ng/ml (normal 32 +/- 6 ng/ml) and 64 to 29 pg/ml (normal 34 +/- 19 pg/ml), respectively. Serum mid-molecule parathyroid hormone concentrations (76 to 97 pcmol/L) were within the normal range (85-140 pcmol/L). These data indicate that hypercalcemia seen in dogs following field exposures to cholecalciferol-containing rodenticides may be associated with elevated 25-hydroxy rather than 1,25-dihydroxy cholecalciferol. Consequently, serum 25-hydroxy cholecalciferol concentrations may be the most conclusive method for diagnosing hypervitaminosis D3 toxicosis in the live dog.

Animals↗
PubMed1990

Salmon calcitonin as adjunct treatment for vitamin D toxicosis in a dog.

Calcitonin was used in conjunction with saline diuresis, furosemide, and prednisone in treatment of a dog that consumed a rodenticide that contained cholecalciferol and has been touted as safe for nontarget species. This report shows that the rodenticide is toxic to dogs and that salmon calcitonin is a useful treatment for the often refractory hypercalcemia induced by vitamin D toxicosis.

Animals↗
PubMed1990

Surreptitious ingestion of a long-acting vitamin K antagonist/rodenticide, brodifacoum: clinical and metabolic studies of three cases.

The vitamin K metabolism of three patients with factitious purpura due to brodifacoum ingestion was studied. These patients, who presented with bleeding disorders due to deficiency of the vitamin K-dependent blood clotting proteins, were refractory to vitamin K1 at standard doses and required fresh frozen plasma to control bleeding until large doses of vitamin K1 were used. Metabolic studies demonstrated a blockade in vitamin K utilization, consistent with the presence of a vitamin K antagonist, but the patients denied use of anticoagulants. Warfarin assays were negative. We show that the factitious purpura in each patient was due to the surreptitious ingestion of brodifacoum, a potent second generation long-acting vitamin K antagonist used as a rodenticide. The coagulopathies responded to long-term therapy with large doses of vitamin K1. The serum elimination half-time for brodifacoum ranged from 16 to 36 days in these patients. The anticoagulant effect is of long duration, requiring chronic vitamin K treatment. With increasing availability of new rodenticides, factitious purpura due to surreptitious ingestion of these potent vitamin K antagonists is emerging as a new problem, previously associated with warfarin, with important implications for diagnosis and treatment.

4-Hydroxycoumarins↗
PubMed1990

The effect of some anticoagulants against three commensal rodents under laboratory conditions.

Eight anticoagulant rodenticides were used against Rattus norvegicus, R. r. frugivorous and Muss musculus. Phenal proved to be the most suitable against R. norvegicus, while Redentin 75 was less effective. However, males accepted Super-Caid as bait. On the other hand, Klerat Super was more effective than Storm against R. r. frugivorous and M. musculus, in choice feeding and V.V. in no choice feeding. It was concluded that more than one anticoagulant rodenticide being recommended with interval between application in a large rodent infested area.

Animals↗
PubMed1989

[Prolonged hypocoagulability following the ingestion of anticoagulant raticides].

Voluntary ingestion of concentrated anticoagulant rodenticides leads to prolonged hypocoagulability sometimes accompanied by haemorrhage. The authors report 11 cases referred to the Paris Anti-Poisons Centre. The products implicated were chlorophacinone, bromadiolone, and warfarin. The time interval before medical intervention ranged from 90 minutes to 3 weeks. The absence of early clinical signs probably explains the number of late admissions. Haemorrhage of variable severity was observed in 8 cases. The prothrombin time varied with the administered dose of Vitamin K and/or coagulation factors. Three patients were lost to follow-up at days 9, 24 and 68. The other patients were treated for several weeks (27 to 82 days). Massive overdose with these rodenticides justifies stomach washout when the patients are seen early, daily check-ups of coagulability and treatment with Vitamin K at a dosage adapted to the biochemical abnormalities. Severe haemorrhage requires transfusion and the administration of factors of coagulation. The duration of the abnormalities is unpredictable; the prothrombin time should therefore be checked 48 hours after stopping Vitamin K therapy to detect any recurrence.

4-Hydroxycoumarins↗
PubMed1988

[Prolonged anticoagulation following chlorophacinone poisoning].

In 1985 and 1986 the Swiss Toxicologic Information Center registered 152 cases of rodenticide poisoning. Among those substances chlorophacinone, an indanedione derivative, has a prolonged antivitamin K effect. We report here the case of an eighteen-year-old female hospitalized 3 days after deliberately ingesting some 100 mg chlorophacinone. Her Quick time at admission was less than 10% (Prothrombin time 79 sec., normal control 12 sec.). Under high dose vitamin K therapy the Quick was rapidly corrected but fell again on each vitamin K withdrawal. In a search for a relation between the variations of prothrombin time and chlorophacinone plasma levels, these were assessed by HPLC. Prothrombin time (and vitamin K dependent factors VII and X) finally normalized only 7 weeks after chlorophacinone ingestion. Clinical condition remained satisfactory throughout and other biological parameters unaffected. This case emphasizes the need for prolonged clinical and laboratory follow-up for rodenticide intoxications and for vitamin K administration for several weeks.

Adolescent↗