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At least 19 recordsLinked to original sources

PubMed1978

Laboratory evaluation of pyriminyl used as a rodenticide against the lesser bandicoot rat, Bandicota bengalensis.

The properties of pyriminyl (N-3-pyridylmethyl-N'-p-nitrophenyl urea) as a rodenticide against the lesser bandicoot rat (Bandicota bengalensis) in Rangoon, Burma, were investigated in the laboratory. The acute LD 50 and LD 95 dose of orally administered pyriminyl for B. bengalensis were found to be 6.7 mg/kg and 23.0 mg/kg of body weight respectively. When caged bandicoots were given a choice between plain and poisoned baits, the optimum rodenticidal concentration in the bait was found to be 0.25-0.5%. Symptoms of pyriminyl poisoning appear from 1 to 4 h after feeding starts, giving individual animals time to consume from 2 to over 30 LD 50 doses of 0.5% pyriminyl before feeding stops. Deaths occurred from 4 to 96 h after either oral dosing or free-choice feeding. There appeared to be no significant aversion to the poison at 0.25% or 0.5% concentration in foods. The potential hazards and use of pyriminyl as a field bait against populations of B. bengalensis are discussed.

Administration, Oral↗

PubMed1975

Laboratory evaluation of gophacide as a rodenticide for use against Rattus norvegicus and Mus musculus.

Laboratory tests were carried out to assess the efficacy of gophacide as a rodenticide against the Norway rat (Rattus norvegicus) and the house mouse (Mus musculus). Results of feeding tests with wild animals suggest that the compound would be more useful against mice than rats, and that 0.3% would be a near optimal concentration for field trials for both species. The hazards of using gophacide as a rodenticide are discussed.

Amidines↗

PubMed1975

Laboratory evaluation of difenacoum as a rodenticide.

The efficacy of difenacoum as a new anticoagulant rodenticide was evaluated by blood coagulation studies and laboratory feeding tests using warfarin-resistant and non-resistant common rats (Rattus norvegicus), ship rats (R. rattus) and house mice (Mus musculus). Prothrombin assays indicated that the compound had as marked an activity with warfarin-resistant common rats as coumatetralyl had with non-resistant animals. Feeding tests confirmed that 0-005% would be a near-optimal concentration for field use, although there was some evidence of unpalatability. Results with ship rats and house mice were less favourable. Trials with enclosed colonies of warfarin-resistant mice confirmed the laboratory finding that although difenacoum was more effective than all other currently used anticoagulants, it was unlikely to give complete control. It is concluded that difenacoum is a valuable new rodenticide, especiaaly for controlling warfarin-resistant common rats.

4-Hydroxycoumarins↗

PubMed1976

Trials of the anticoagulant rodenticide WBA 8119 against confined colonies of warfarin-resistant house mice (Mus musculus L.).

The efficacy of the newly developed anticoagulant rodenticide WBA 8119 was evaluated against the house mouse (Mus musculus L.) using individual and family groups of warfarin-resistant animals. WBA 8119 at 0-002%, 0-005% and 0-01% in pinhead oatmeal bait gave complete kills of mice in 'no-choice' feeding tests carried out in cages and small pens. In replicated 21-day treatments on families of mice confined in larger pens conditioned to feeding on plain foods, the overall mortalities obtained using the three formulated poison baits were 71/72, 62/63 and 57/57 respectively. The results of the WBA 8119 toxicity tests are considered in relation to previous findings on other anticoagulant rodenticides, particularly difenacoum. In equivalents tests, WBA 8119 performed better than difenacoum. The data thus suport the laboratory findings that WBA 8119 is the most active anticoagulant so far tested for the control of warfarin-resistant house mice.

4-Hydroxycoumarins↗

PubMed1976

Trials of the anticoagulants rodenticide WBA 8119 against confined colonies of warfarin-resistant house mice (Mus musculus L.).

The efficacy of the newly developed anticoagulant rodenticide WBA 8119 was evaluated against the house mouse (Mus musculus L.) using individual and family groups of warfarin-resistant animals. WBA 8119 at 0-002%, 0-005% and 0-01% in pinhead oatmeal bait gave complete kills of mice in 'no-choice' feeding tests carried out in cages and small pens. In replicated 21-day treatments on families of mice confined in larger pens and conditioned to feeding on plain foods, the overall mortalities obtained using the three formulated poison baits were 71/72, 62/63 and 57/57 respectively. The results of the WBA 8119 toxicity tests are considered in relation to previous findings on other anticoagulant rodenticides, particularly difenacoum. In equivalent tests, WBA 8119 performed better than difenacoum. The data thus support the laboratory findings that WBA 8119 is the most active anticoagulant so far tested for the control of warfarin-resistant house mice.

4-Hydroxycoumarins↗

PubMed1979

Laboratory test of seven rodenticides for the control of Mastomys natalensis.

Laboratory feeding tests were carried out to assess the efficacy of seven rodenticides against Mastomys natalensis. The poisons (warfarin, coumatetralyl, difenacoum, brodifacoum, bromadiolone, calciferol and zinc phosphide) were all toxic at the concentrations normally used against Rattus norvegicus (Berk.), although several were unpalatable. Trials are now needed to demonstrate the relative efficacy of these poisons in the field, but it is likely that, given suitable bait formulations, they would all be useful as practical control agents.

4-Hydroxycoumarins↗

PubMed1975

Field trials of the rodenticide gophacide against wild house mice (Mus musculus L.).

The acute rodenticide gophacide was tested against urban infestations of the house mouse (Mus musculus L.) and treatment success was assessed from the results of census baitings conducted before and after each treatment. Seven of eight populations of mice living in premises where alternative food supplies were limited were successfully controlled when medium oatmeal bait containing gophacide at 0.1% was laid directly for 4 days. In further treatments against mice inhabiting more complex environments and having greater access to other foods, the performance of gophacide at 0.1% and at 0.25% in a wholemeal flour/pinhead oatmeal/corn oil bait was compared with that of zinc phosphide at 3.0% in the same bait-base. The poison treatments were conducted for 1 or 4 days and always after 3 days pre-baiting. Treatment success varied considerably irrespective of the type of treatment or of the poison used. In general, however, gophacide proved to be as effective as zinc phosphide for the control of mice.

Amidines↗

PubMed1978

Trials of the rodenticide pyriminil against wild house mice (Mus musculus L.).

Pen field trials were conducted to assess the performance of the acute rodenticide pyriminil against the house mouse (Mus musculus L.). Four types of poison treatment were carried out using penned family groups of warfarin-resistant mice supplied with alternative plain foods. In each treatment pyriminil was included at 2% in a wholemeal flour/pinhead oatmeal/corn oil bait. Mortality was highest (46/54; 85.2%) when poison bait was offered for 4 days following 3 days of pre-baiting. The same pre-baiting and poisoning technique was adopted in five field trials carried out against mice infesting farm buildings. The efficacy of each poison treatment was estimated from the results of pre- and post-treatment census baitings; treatment success ranged between 53.7% and 96.7%, mean 80.5%. It is concluded that pyriminil treatments are best carried out after a period of pre-baiting and that when pyriminil is used in this manner it is about as effective as zinc phosphide for the control of mice.

Animals↗

PubMed1976

Laboratory evaluation of WBA 8119 as a rodenticide for use against warfarin-resistant and non-resistant rats and mice.

Feeding tests were carried out in the laboratory to evaluate WBA 8119 as a potential new rodenticide against wild common rats (Rattus norvegicus), ship rats (R. rattus) and house mice (Mus musculus). The results obtained are compared with data previously obtained for difenacoum, another member of the same series of 4-hydroxycoumarin anticoagulants. With warfarin-resistnat and non-resistant common rats, complete kills were obtained using a concentration of 0-0005% for 2 days, or 0-001% for 1 day: a 1-day test at 0-0005% killed 6 out of 10 and 17 out of 20 of the two types respectively. At 0-0005% complete kills of resistant ship rats were obtained after 2 days exposure and of resistant house mice after 1 day, but at 0-002% for 2 days there was some survival. Non-resistant ship rats and house mice were all killed after 2 days feeding on 0-002% bait. In 2-day palatability tests, R. norvegicus showed no significant aversion to the poison at 0-002% and 100% mortality was obtained. The poison was significantly unpalatable to R. rattus at 0-005% and to M. musculus at 0-005% and 0-002%, although with the last species these concentrations gave complete kills. It is concluded that WBA 8119 has greater activity than other known anticoagulants against the three commensal species examined. The laboratory results suggest that concentrations between 0-0005% and 0-002% would be suitable for field use against common rats, and between 0-002% and 0-005% for ship rats and house mice.

4-Hydroxycoumarins↗

PubMed1977

The susceptibility of Tatera indica, Nesokia indica and Bandicota bengalensis to three anticoagulant rodenticides.

Three South-Asian rodent past species were tested for susceptibility to anticoagulant rodenticides. Wheat fluor containing 0-025% warfarin 0-0375% coumatetralyl or 0-005% difenacoum was fed to 260 Tatera indica, 140 Nesokia indica and 81 Bandicota bengalensis for 1-56 days. Tatera was about as susceptible to anticoagulants as Rattus has been reported to be. Nesokia and Bandicota were extremely variable: though the majority were highly susceptible, the slopes of the dose-mortality curves were close to zero. The difenacoum diet appeared to be more toxic than the warfarin diet to all three species, but less toxic than the coumatetralyl diet to Tatera and Nesokia. All of the anticoagulants were eventually lethal to all of the animals tested.

Animals↗

PubMedDate not supplied

TLC-spectrophotometric assay of the main glycosides of red squill, a specific rodenticide.

Red squill bulbs, with reported specific rodenticidal properties, have been assayed for their content of the two main glycosides, scilliroside and scillaren A, by a method depending on the separation of the glycosides from purified plant extracts by tlc followed by spectrophotometric (uv and visible) determination of the individual glycosides in the eluates. The method was found convenient for assessment of the potency of red squill bulbs.

Bufanolides↗

PubMed1975

Role of illness in producing learned taste aversions in rats: a comparison of several rodenticides.

Several toxic agents were compared in order to test the effect of various types of illness in producing learned taste aversions. After a 10-min sucrose drinking trial, groups of rats were injected intraperitoneally with lithium chloride or with a strong, near lethal dose of a rodenticide. Strong sucrose aversions were acquired by groups injected with lithium chloride, copper sulfate, sodium fluoroacetate, or red squill, and very weak or no aversions were learned by groups injected with thallium, warfarin cyanide, or strychnine. The results were discussed in terms of onset of symptoms, duration of symptoms, and kinds of physiological effects necessary to produce aversions. It was concluded that the effects of different drugs may be mediated by different physiological systems learned taste aversions.

Animals↗

PubMed1977

Effects of a new rodenticide, benzenesulfonic acid hydrazide, on prenatal mice.

Benzenesulfonic acid [(3-amino-2,4,6-trichlorophenyl)methylene] hydrazide, a candidate rodenticide coded as DRC-4575, was administered by gavage to pregnant female BALB/c mice. Each dose (5.5, 28.0, 42.0, 62.0 and 94.0 mg/kg) was given to one of five groups of ten mice on day 8 of gestation, making a total of five different dose groups on day 8. This same procedure was followed for days 9, 10, 11, 12, and 13. This made a total of 30 dose-day treatment groups. Six control females were dosed each day. Dam survival to day 18 declined as the dose increased; only 2% of the dams survived at 94 mg/kg. When the surviving females were killed at day 18, no significant differences were found between treatment and control animals in the number or weight of live fetuses, or in the ratio of male to female fetuses. However, the percentage of live fetuses was significantly lower and the number of resorptions was significantly higher for the treated dams at the 62 mg/kg dose level than for the control dams. Skeletal anomalies were limited primarily to unossified phalanges, which were probably related to the lower weights of those fetuses. Slight hydrocephalus occurred infrequently at all dose levels and in the controls, and was not dose-related. These data indicate that DRC-4575 would be embryotoxic only at doses of 62 mg/kg or higher and would not be teratogenic.

Animals↗

PubMed1992

Confirmation of indandione rodenticide toxicoses by mass spectrometry/mass spectrometry.

Mass spectrometry/mass spectrometry (MS/MS) with collision-activated dissociation (CAD) was utilized to unequivocally distinguish 1,3-indandione rodenticides in 2 cases of anticoagulant toxicosis. Anecdotal evidence provided by the veterinarian in a case involving feedlot cows and physical evidence at the site of occurrence in a similar case involving lambs strongly implicated diphenadione (diphacinone; DP) in both instances. However, high performance liquid chromatography indicated chlorophacinone (CP), not DP, was present in the blood samples obtained from both cows and lambs. Intact 1,3-indandiones exhibit poor gas chromatographic properties, so procedures were developed for analysis by MS/MS using a direct exposure probe for sample introduction. The EI mass spectra of DP and CP contained a base peak at m/z 173, with molecular ions (M+) at m/z 340 and m/z 374 (Cl isotope cluster), respectively. Corresponding MS/MS CAD parent ion spectra of m/z 173 showed an ion of m/z 340 for DP and 374 (Cl cluster) for CP. CAD analysis of the blood extracts showed a parent ion scan of m/z 173 identical to that of CP, with the m/z 374 (Cl cluster). (Additional evidence was obtained by MS/MS examination of the CAD daughter ion spectrum of m/z 374.) Blood extracts from the affected animals revealed CAD daughter ion spectra for m/z 374 identical to that of reference CP. Positive confirmation of CP in both cases led to identification of the source of the toxicant and prevention of further animal exposures.

Animals↗

PubMedDate not supplied

Diabetes mellitus and autonomic dysfunction after vacor rodenticide ingestion.

A case of N-3 pyridylmethyl-N' 4 nitrophenyl urea (Vacor) rodenticide poisoning in a 52-year-old man is presented. Vacor is structurally related to alloxan and streptozotocin, agents that have been used extensively to produce diabetes mellitus in laboratory animals. Seven days after ingestion of Vacor, the patient presented in diabetic ketoacidosis complicated by postural hypotension and adynamic ileus. The patient recovered from ketoacidosis but has continued to require insulin. With infusion of arginine, glucagon rose from 185 to 650 pg./ml. and C-peptide from 0.5 to 3.4 ng./ml. Six weeks after onset of diabetes, no anti-islet-cell antibodies were detected. Muscle capillary basement membrane thickness on electron microscopy was found to be 1,918 +/- 194 A. The absence of hyperglycemia after Vacor ingestion should not lead to complacency on the part of the attending physician. The patient must be observed closely for development of ketoacidosis and treated prophylactically with nicotinamide, the suggested antidote.

Autonomic Nervous System↗

PubMed1991

Cholecalciferol rodenticide intoxication in a cat.

A 4-month-old 2.5-kg sexually intact female domestic shorthair cat was referred to the teaching hospital because of suspected cholecalciferol intoxication after ingestion of a cholecalciferol-containing rodenticide. At referral, the cat was hypercalcemic, hyperkalemic, and acidotic. Despite management of hypercalcemia and preservation of renal function with physiologic saline solution, furosemide, dopamine, and calcitonin, the cat died, apparently as a result of extensive pulmonary mineralization.

Animals↗

PubMed1978

Diabetes mellitus following rodenticide ingestion in man.

Ketotic, insulin-requiring diabetes mellitus and a severe peripheral neuropathy developed in a previously healthy 25-year-old man several days after he attempted suicide with rat poison containing N-3-pyridylmethyl N'-p-nitrophenyl urea. Study of islet-cell function ten months after ingestion showed a reduced disappearance rate of intravenous glucose and depressed C-peptide response to intravenous glucose when compared with a normal control but no impairment of glucagon release after intravenous arginine stimulation. Nerve conduction studies demonstrated severe sensory and mild motor neuropathy. Quadriceps capillary basement membrane thickness was in the diabetic range. Because at least 15 similar occurrences have been reported to the manufacturer, this agent appears to be diabetogenic in man, probably causing beta-cell destruction. Niacinamide, which can prevent glucose intolerance in both streptozocin- and alloxan-treated animals and prevents death in rats given this rodenticide, may be a useful antidote.

Adult↗

PubMed1979

[Intoxication with anticoagulant rodenticides (author's transl)].

Generally the ingestion of rodenticides containing anticoagulant substances is not dangerous. Following accidental ingestion, 9 out of 77 children, and 7 out of 13 adults who had taken such substances in attempted suicide had slight or moderate increases of thromboplastin time, but no serious alteration of plasmatic blood coagulation. Vitamin K1 should be given as an antidote in all cases; gastric lavage or induced emesis are often unnecessary.

Anticoagulants↗