Journal articles: 'Brodifacoum'

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&NA;. "Brodifacoum." Reactions Weekly &NA;, no. 425 (October 1992): 5. http://dx.doi.org/10.2165/00128415-199204250-00016.

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&NA;. "Brodifacoum overdose." Reactions Weekly &NA;, no. 1109 (July 2006): 8. http://dx.doi.org/10.2165/00128415-200611090-00023.

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&NA;. "Brodifacoum overdose." Reactions Weekly &NA;, no. 402 (May 1992): 6. http://dx.doi.org/10.2165/00128415-199204020-00016.

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Brooke, M. de L., R. J. Cuthbert, R. Mateo, and M. A. Taggart. "An experimental test of the toxicity of cereal pellets containing brodifacoum to the snails of Henderson Island, South Pacific." Wildlife Research 38, no. 1 (2011): 34. http://dx.doi.org/10.1071/wr10132.

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Context Cereal pellets containing the anti-coagulant poison brodifacoum at 20 ppm are routinely used to rid islands of invasive rodents. The impact, if any, of the poison on invertebrates is not well understood. This is problematic because many of the islands targeted for treatment harbour endemic invertebrate species, including snails where available information about brodifacoum impact is equivocal. Aims Combining field tests and subsequent laboratory analysis, the present study investigated the effect of brodifacoum on the snails of Henderson Island, South Pacific. Methods In the field, we housed snails in plastic boxes for up to 10 days to compare the survival of those kept with and without access to brodifacoum cereal pellets. Subsequently, we analysed brodifacoum levels in those kept with access to poisoned pellets, according to whether they survived or died. Key results There were no detectable differences in the survival between the captive snails kept with and those kept without access to brodifacoum. Among those with access, there were no significant differences in brodifacoum concentrations between the minority that died and the majority that survived. In fact, brodifacoum was detected in only a few samples. Conclusions Brodifacoum appears not to pose a risk to the snails of Henderson Island. Implications Although it would be prudent to test the impact of brodifacoum on the resident snails before proceeding with a rodent eradication on other islands, we suspect the Henderson results can be extended to other sites.

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Corke, P. J. "Superwarfarin (Brodifacoum) Poisoning." Anaesthesia and Intensive Care 25, no. 6 (December 1997): 707–9. http://dx.doi.org/10.1177/0310057x9702500622.

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A case of self-ingestion of brodifacoum that resulted in spontaneous intra-abdominal haemorrhage, circulatory shock, rhabdomyolysis and acute renal failure is reported. Current knowledge and management of superwarfarin poisoning are discussed.

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Anderson, Sarah L., Robbie S. Kattappuram, Joel C. Marrs, and Nicole M. Joseph. "Intentional Brodifacoum Ingestion." American Journal of Medicine 130, no. 1 (January 2017): e27-e28. http://dx.doi.org/10.1016/j.amjmed.2016.08.010.

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Littin, K. E., C. E. O'Connor, and C. T. Eason. "Comparative effects of brodifacoum on rats and possums." New Zealand Plant Protection 53 (August 1, 2000): 310–15. http://dx.doi.org/10.30843/nzpp.2000.53.3701.

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The anticoagulant brodifacoum is widely used overseas as a rodenticide and in New Zealand to control rodents and brushtail possums (Trichosurus vulpecula) The efficacy behavioural and pathological changes and times to death were compared between Norway rats (Rattus norvegicus) and brushtail possums poisoned with brodifacoum Caged animals were given brodifacoum in wax or cereal baits observed for signs of toxicosis and changes in behaviour then autopsied after death Brodifacoum caused haemorrhaging and death in both species and although each showed marked changes in behaviour and pathology they differed in character time of onset and duration Results may be explained in part by species differences in behaviour and halflives of blood clotting factors

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Booth, Karen. "Brodifacoum poisoning (a reply)." New Zealand Veterinary Journal 37, no. 4 (December 1989): 173. http://dx.doi.org/10.1080/00480169.1989.35599.

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Parshad, V. R., C. S. Malhi, N. Ahmad, and B. Gupta. "Rodent Damage and Control in Peanut Fields in India." Peanut Science 14, no. 1 (January 1, 1987): 4–6. http://dx.doi.org/10.3146/i0095-3679-14-1-2.

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Abstract Studies were made on the identification, damage and chemical methods of control of rodent pests in irrigated and nonirrigated fields of peanut (Arachis hypogaea L.) at Ludhiana, India. Peanut fields were infested with Bandicota bengalensis, Tatera indica, Rattus meltada and Mus spp., except that B. bengalensis was absent in nonirrigated fields. These rodents reduced peanut yield by an average 3.86%, a loss of 190.18 rupees/ha ($15.12 US). Severe rodent damage was sporadic with a maximum of 18.97% reduction in peanut yield. Rodents inflicted more damage between 80 to 120 days after planting, i. e. during the pod fill stage of crop growth. A single treatment with poison bait at 80 to 90 days after planting with 2.4% zinc phosphide, 0.005% brodifacoum and 0.005% bromadiolone in cereal baits at the rate of 1 kg/ha resulted in 58.07%, 42.26% and 40.88% rodent control, respectively, in nonirrigated fields. In irrigated fields, 58.70% and 67.02% rodent control was achieved with zinc phosphide and brodifacoum baits respectively. Significantly higher rodent control was obtained with 2 treatments of either brodifacoum or bromadiolone than with a single treatment of any rodenticide. Wax blocks containing 0.005% brodifacoum were less effective than cereal baits containing the same rodenticide. Two applications at 10 day interval of either 0.005% brodifacoum or bromadiolone between 80–100 days after planting is suggested for rodent control in peanut fields.

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J. Wedding, Chris, Weihong Ji, and Dianne H. Brunton. "Implications of visitations by Shore Skinks Oligosoma smithi to bait stations containing brodifacoum in a dune system in New Zealand." Pacific Conservation Biology 16, no. 2 (2010): 86. http://dx.doi.org/10.1071/pc100086.

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Brodifacoum is a highly toxic, second-generation anticoagulant developed for the control of rodent pests. However, information regarding the impacts of brodifacoum on non-target wildlife has been largely collected opportunistically and is generally avian biased. Reviews of non-target impacts of brodifacoum routinely regard reptiles and amphibians as low risk, despite there being no formal evidence supporting this assumption. Recent evidence suggests that some native lizard species will consume cereal baits in addition to toxin-loaded invertebrates. As part of a wider study, we quantified visitation rates to brodifacoum bait stations by Shore Skinks Oligosoma smithi, and recorded the first observation of this species consuming toxic bait. Bait stations (n = 56) recorded up to 81.5% tracking incidence by Shore Skinks across one of two pest-controlled grids. Skinks were occasionally observed inside bait stations feeding on invertebrates. Of the 805 skinks caught in pitfall traps over the 6 month period, none showed clinical or behavioural signs of anticoagulant toxicosis. Further research into the acute toxicity and chronic sub-lethal impacts of pesticides on herpetofauna is required before potential impacts on these fauna can be dismissed.

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Gül, Nursel, Nuri Yiğit, Fulya Saygılı, Ebru Demirel, and Ceren Geniş. "Comparison of the effects of difenacoum and brodifacoum on the ultrastructure of rat liver cells." Archives of Industrial Hygiene and Toxicology 67, no. 3 (September 1, 2016): 204–9. http://dx.doi.org/10.1515/aiht-2016-67-2783.

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Abstract We used transmission electron microscopy to examine the cytotoxic effects of the second-generation anticoagulant rodenticides difenacoum and brodifacoum on rat liver. A single dose of difenacoum or brodifacoum was administered to rats by gastric gavage and liver samples were taken after 24 h, four days or seven days. In the livers of rats treated with difenacoum for 24 h, hepatocytes typically showed increased numbers of lysosomes, as well as enlargement of both the perinuclear space and the cisternae of the rough endoplasmic reticulum (RER), while sinusoids were irregularly shaped and contained Kupffer cells. Similar irregularities occurred in brodifacoum-treated rats at the same time point, but additionally increased numbers of vacuoles, damaged mitochondrial cristae, and clumping of chromatin were observed in hepatocytes, and hemolysed erythrocytes were noted in the sinusoids. Comparable findings were made in each group of rats after four days. After seven days of difenacoum treatment, hepatocytes suffered loss of cytoplasmic material and mitochondrial shrinkage, while RER cisternae became discontinuous. In contrast, exposure to brodifacoum for seven days caused the formation of numerous vacuoles and lipid droplets, disordered mitochondrial morphology, chromatin clumping and invagination of the nuclear envelope in hepatocytes. Sinusoids in the livers of rodenticide-treated rats contained an accumulation of dense material, lipid droplets, cells with pycnotic nuclei and hemolysed erythrocytes. Overall, our results show that brodifacoum causes more severe effects in liver cells than difenacoum. Thus our microscopic data along with additional biochemical assays point to a severe effect of rodenticide on vertebrates.

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Patočka, Jiří, Georg Petroianu, and Kamil Kuča. "TOXIC POTENTIAL OF SUPERWARFARIN: BRODIFACOUM." Military Medical Science Letters 82, no. 1 (March 8, 2013): 32–38. http://dx.doi.org/10.31482/mmsl.2013.003.

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Underwood, Elizabeth L., JoLeigh Sutton, Ira Keith Ellis, Brian Qualls, Jon Zamber, and Brian N. Walker. "Prolonged coagulopathy after brodifacoum exposure." American Journal of Health-System Pharmacy 71, no. 8 (April 15, 2014): 639–42. http://dx.doi.org/10.2146/ajhp130537.

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Morgan, Brent W., Christian Tomaszewski, and Iris Rotker. "Spontaneous hemoperitoneum from brodifacoum overdose." American Journal of Emergency Medicine 14, no. 7 (November 1996): 656–59. http://dx.doi.org/10.1016/s0735-6757(96)90082-0.

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Kruse, James A., and Richard W. Carlson. "Fatal rodenticide poisoning with brodifacoum." Annals of Emergency Medicine 21, no. 3 (March 1992): 331–36. http://dx.doi.org/10.1016/s0196-0644(05)80900-x.

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Olmos, Valentina, and Clara Magdalena López. "Brodifacoum Poisoning with Toxicokinetic Data." Clinical Toxicology 45, no. 5 (January 2007): 487–89. http://dx.doi.org/10.1080/15563650701354093.

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TECIMER, COSKUN, and LUNG T. YAM. "Surreptitious Superwarfarin Poisoning With Brodifacoum." Southern Medical Journal 90, no. 10 (October 1997): 1053–55. http://dx.doi.org/10.1097/00007611-199710000-00018.

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BERRY, RICHARD G., JOHN A. MORRISON, JOHN W. WATTS, JOHN W. ANAGNOST, and JORGE J. GONZALEZ. "Surreptitious Superwarfarin Ingestion With Brodifacoum." Southern Medical Journal 93, no. 1 (January 2000): 74–75. http://dx.doi.org/10.1097/00007611-200001000-00016.

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BERRY, RICHARD G., JOHN A. MORRISON, JOHN W. WATTS, JOHN W. ANAGNOST, and JORGE J. GONZALEZ. "Surreptitious Superwarfarin Ingestion With Brodifacoum." Southern Medical Journal 93, no. 1 (January 2000): 74–75. http://dx.doi.org/10.1097/00007611-200093010-00017.

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SHEPHERD, GREENE, WENDY KLEIN-SCHWARTZ, and BRUCE D. ANDERSON. "Acute, unintentional pediatric brodifacoum ingestions." Pediatric Emergency Care 18, no. 3 (June 2002): 174–78. http://dx.doi.org/10.1097/00006565-200206000-00006.

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Booth, Karen. "Brodifacoum poisoning in a dog." New Zealand Veterinary Journal 37, no. 2 (June 1989): 74–75. http://dx.doi.org/10.1080/00480169.1989.35564.

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Grayson, J. L. "Brodifacoum poisoning in a dog." New Zealand Veterinary Journal 37, no. 4 (December 1989): 173. http://dx.doi.org/10.1080/00480169.1989.35598.

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Munday, J. S., and L. J. Thompson. "Brodifacoum Toxicosis in Two Neonatal Puppies." Veterinary Pathology 40, no. 2 (March 2003): 216–19. http://dx.doi.org/10.1354/vp.40-2-216.

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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.

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Littin, K. E., C. E. O'Connor, N. G. Gregory, D. J. Mellor, and C. T. Eason. "Behaviour, coagulopathy and pathology of brushtail possums (Trichosurus vulpecula) poisoned with brodifacoum." Wildlife Research 29, no. 3 (2002): 259. http://dx.doi.org/10.1071/wr01068.

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Brodifacoum is a second-generation anticoagulant rodenticide used widely for controlling brushtail possums (Trichosurus vulpecula) in New Zealand. We determined its toxic effects on possums to make inferences about the welfare of brodifacoum-poisoned possums. Caged possums were fed a lethal dose of brodifacoum in cereal baits then either bled and killed 4, 8, 12, 16 or 20 days later to establish the effects on blood-clotting, or observed for behavioural changes until death. Blood-clotting time was prolonged 8 days after possums first began ingesting brodifacoum and time to death was 20.7 ± 1.7 days (mean ± s.e.m.). Clinical signs of poisoning, including changed appearance, pale noses and external bleeding, appeared from 14 days after initial poisoning (7 days before death). Possums gradually became inactive and lethargic, typically crouching and lying in abnormal postures for 6 days before death. Feed intake reduced concurrently, resulting in significant loss of body weight of 5.9 ± 2.1%. All possums had widespread, usually severe, haemorrhaging. Internal haemorrhages first appeared in all possums 8 days after initial ingestion. These haemorrhages, and consequent blood loss, may cause distress, pain, weakness or sickness, and this is supported by evidence from humans and other animals. Reduced feed intake, inactivity, lethargy and the display of abnormal postures suggest that possums do experience distress for at least 6 days before death.

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Arepally, Gowthami M., and Thomas L. Ortel. "Bad weed: synthetic cannabinoid–associated coagulopathy." Blood 133, no. 9 (February 28, 2019): 902–5. http://dx.doi.org/10.1182/blood-2018-11-876839.

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Abstract Recent multistate outbreaks of coagulopathy caused by brodifacoum-tainted synthetic cannabinoids or “fake weed” highlight the public health impact of long-acting anticoagulant rodenticides (LAARs). Patients presenting with this syndrome have had recent exposure to synthetic cannabinoids, evidence of isolated vitamin K antagonism with or without bleeding, and detectable levels of brodifacoum and other LAARs in circulation. This article will provide information on synthetic cannabinoids, LAARs, and coagulopathic manifestations arising from use of adulterated synthetic cannabinoids and their management.

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Ferencz, László, and Daniela Lucia Muntean. "Identification of new superwarfarin-type rodenticides by structural similarity. The docking of ligands on the vitamin K epoxide reductase enzyme’s active site." Acta Universitatis Sapientiae, Agriculture and Environment 7, no. 1 (December 1, 2015): 108–22. http://dx.doi.org/10.1515/ausae-2015-0010.

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Abstract The rodenticide brodifacoum is highly toxic to mammals and birds, and extremely toxic to fish. It is a highly cumulative poison due to its high lipophilicity and extremely slow elimination. For this reason, it may be interesting to find similar compounds in order to enlarge the spectrum of vitamin K epoxide reductase enzyme inhibitors used today in pest control. We used the Similar Compounds search type of the Chemical Structure Search of the PubChem Compound Database to locate records that are similar to the chemical structure of brodifacoum, using pre-specified similarity thresholds. Using the threshold ≥ than 95% for the similar structures criteria, we found 14 compounds (from over 30 million entries) that meet this criteria. Two of these compounds have a better binding affinity to vitamin K epoxide reductase enzyme than brodifacoum, but the binding energy of the other 12 substances is also high, having identical or lower lipophilicity; consequently, they will eliminate faster, possibly lacking a part of the adverse effects.

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Brown, Kerry P. "Impact of brodifacoum poisoning operations on South Island RobinsPetroica australis australisin a New ZealandNothofagusforest." Bird Conservation International 7, no. 4 (December 1997): 399–407. http://dx.doi.org/10.1017/s0959270900001726.

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SummarySouth Island RobinsPetroica australis australiswere monitored through two different brodifacoum (Talon 20 P, 20 ppm) control operations targeting stoatsMustela ermineaand ship ratsRattus rattusin aNothofagusforest. Repeated observations of banded and radio-tagged territorial adult Robins were used to monitor survival from 6 to 8 weeks after poisoning. Where poison was deployed in bait feeders, 96.7% (29/30) of marked Robins definitely survived, whilst where poison was freely broadcast, only 52.2% (12/23) of marked Robins definitely survived. At the non-treatment site 85.7% (18/21) of marked Robins definitely survived. This study demonstrates that individual Robins are at risk from poisoning from exposed brodifacoum on the forest floor and therefore, probably from aerial application of brodifacoum. Further research is required to determine whether the benefit to Robin populations from successful predator control outweighs the loss of some Robins from poisoning. Conservation managers must take a wide view of the ecological community impacts when controlling introduced mammalian predators.

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Crosbie, SF, FJ Laas, MER Godfrey, JM Williams, and DS Moore. "A Field Assessment of the Anticoagulant Brodifacoum Against Rabbits, Oryctolagus-Cuniculus." Wildlife Research 13, no. 2 (1986): 189. http://dx.doi.org/10.1071/wr9860189.

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The effectiveness of 100 p.p.m. brodifacoum for controlling an island population of rabbits was assessed and compared with that of 200 p.p.m. 1080 (sodium monofluoroacetate). Both compounds were applied in an apple-based, raspberry-flavoured jam bait after pre-feeding with the same non-toxic bait. Brodifacoum and 1080 both reduced rabbit populations by 85% on average, compared with an average 'natural' decline of 34% on untreated sites; these estimates of poisoning mortality may be considered conservative, however, because of post-poisoning migration onto poisoned sites.

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Feinstein, Douglas L., Kamil Gierzal, Asif Iqbal, Sergey Kalinin, Richard Ripper, Matthew Lindeblad, Alexander Zahkarov, et al. "The relative toxicity of brodifacoum enantiomers." Toxicology Letters 306 (May 2019): 61–65. http://dx.doi.org/10.1016/j.toxlet.2019.02.011.

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Godfrey, M. E. R., F. J. Laas, and C. G. Rammell. "Acute toxicity of brodifacoum to sheep." New Zealand Journal of Experimental Agriculture 13, no. 1 (January 1985): 23–25. http://dx.doi.org/10.1080/03015521.1985.10426055.

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Osterhoudt, Kevin C., and Fred M. Henretig. "Bias in pediatric brodifacoum exposure data." Pediatric Emergency Care 19, no. 1 (February 2003): 62. http://dx.doi.org/10.1097/00006565-200302000-00017.

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Riley, Sarah B., Matthew Sochat, Karen Moser, Kara L. Lynch, Rosanna Tochtrop, T. Scott Isbell, and Anthony Scalzo. "Case of brodifacoum-contaminated synthetic cannabinoid." Clinical Toxicology 57, no. 2 (August 27, 2018): 143–44. http://dx.doi.org/10.1080/15563650.2018.1502444.

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Hromada, R., I. Miňo, Ľ. Korytár, E. Holotová, M. Ondrašovič, T. Pošiváková, P. Korim, and L. Takáč. "Potential Health Risk to Humans Related to Accumulation of Brodifacoum and Bromadiolone in the Wheat Grown on Rodenticide Contaminated Soil." Folia Veterinaria 63, no. 3 (September 1, 2019): 18–26. http://dx.doi.org/10.2478/fv-2019-0023.

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Abstract The aim of this study was to determine in a model experiment the potential residues of bromadiolone and brodifacoum in the wheat grown on soil treated with these rodenticides and to compare them with the respective acceptable daily intake (ADI) in order to obtain information lacking in the scientific literature. The study focused on the level of residues of chronic rodenticides Broder G, with the active ingredient brodifacoum, and DERATION G, with the active ingredient bromadiolone, in wheat (Triticum spp.). The preparations were used in the form of granular bait. In the wheat grown on the soil treated with 100 g.m−2 of the preparation BRODER G, the brodifacoum residues ranged from 0.012 to 0.0218 mg.kg−1, while the treatment of soil with 500 g.m−2 resulted in residues ranging between 0.0344 and 0.0436 mg.kg−1. When using the preparation DE-RATION G, bromadiolone residues ranged between 0.012 and 0.018 mg.kg−1 after the treatment of soil with 100 g.m−2 and between 0.030 and 0.0428 mg.kg−1 after the treatment with 500 g.m−2. We observed that the acceptable daily intake was exceeded significantly in all of the cases and the residual levels depended on the rodenticide dose. In the case of brodifacoum, the ADI was exceeded more than 700-fold at a dose of 100 g.m−2 and more than 1400-fold at a dose of 500 g.m−2 of soil. With bromadio-lone, the ADI was exceeded 150-fold at a dose of 100 g.m−2 and more than 350-fold at a dose of 500 g.m−2. This indicates the risk to consumers from such crops.

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Djedovic, S., M. Vuksa, M. M. Petrovic, J. Bojkovski, I. Pavlovic, G. Jokic, and B. Stojnic. "Control of brown rat (Rattus norvegicus) on a dairy farm in Serbia." Biotehnologija u stocarstvu 28, no. 3 (2012): 623–33. http://dx.doi.org/10.2298/bah1203623d.

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Rattus norvegicus is a synanthropic species living almost exclusively around facilities for keeping domestic animals. This three-year research focused on options for reducing economic damage caused by this rodent species in stables for heavy milking cows by testing preparations with active substances of various origin. It involved an environmentally friendly product based on sodium selenite 0.1%, a cholecalciferol-based natural product 0.75%, as well as anticoagulant rodenticides containing the active substances bromadiolone 0.005% and brodifacoum 0.005%. These preparations were formulated as granules, plate bait or grain bait. The environmentally friendly sodium selenite product achieved 76.2% efficacy in the first year of research, 70% in the second, and 67.5% in the third. The synthetic products based on bromadiolone and brodifacoum demonstrated high efficacy in all of the three experimental years and in all three formulations. The cholecalciferol rodenticide had 71.4% efficacy in the first year, 68% in the second, and 67.7% in the third. The data show that the environmentally safe product had a lower efficacy due to high rodent abundance and inadequate epidemiological conditions existing on the farm of heavy milking cows, while the bromadiolone and brodifacoum-based products achieved high efficacy.

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Weitzel, JN, JA Sadowski, BC Furie, R. Moroose, H. Kim, ME Mount, MJ Murphy, and B. Furie. "Surreptitious ingestion of a long-acting vitamin K antagonist/rodenticide, brodifacoum: clinical and metabolic studies of three cases." Blood 76, no. 12 (December 15, 1990): 2555–59. http://dx.doi.org/10.1182/blood.v76.12.2555.2555.

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Abstract 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.

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Weitzel, JN, JA Sadowski, BC Furie, R. Moroose, H. Kim, ME Mount, MJ Murphy, and B. Furie. "Surreptitious ingestion of a long-acting vitamin K antagonist/rodenticide, brodifacoum: clinical and metabolic studies of three cases." Blood 76, no. 12 (December 15, 1990): 2555–59. http://dx.doi.org/10.1182/blood.v76.12.2555.bloodjournal76122555.

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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.

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Cuthbert, R. J., P. Visser, H. Louw, and P. G. Ryan. "Palatability and efficacy of rodent baits for eradicating house mice (Mus musculus) from Gough Island, Tristan da Cunha." Wildlife Research 38, no. 3 (2011): 196. http://dx.doi.org/10.1071/wr11016.

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Context Introduced house mice (Mus musculus) are a serious predator of seabird chicks at Gough Island, resulting in declining populations of several threatened species. This has prompted the preparation of plans to eradicate mice from Gough and other islands. However, relatively little is known about the palatability and efficacy of rodent baits for house mice, as most studies have focussed on rats (Rattus spp.). Aims The study’s aim was to test the palatability of non-toxic forms of two commercially available rodent pellet bait formulations (Pestoff® 20R and Final®) and a new pellet bait formulated specifically for mouse control (Pestoff® 20M) to house mice on Gough Island. We also tested the efficacy of toxic Pestoff 20R and Final pellets containing 20 and 25 ppm of the anticoagulant toxin brodifacoum. Methods Five trials with 50 mice housed in individual cages and kept at ambient temperature and light cycles, were undertaken during the year. Palatability of bait pellets was measured over five days and compared with a non-toxic control food (standard ‘rodent pellets’ sourced from a pet food supplier). Toxic bait trials were run for 25 days with bait administered at 1, 2 and 10 g for a 24-h period and at 20 g per day for 72 h. Key results All three baits were highly palatable; however, mice showed the greatest preference for Pestoff 20M and 20R, consuming a larger mass of bait. Estimated oral LD50 values of brodifacoum for Gough mice were 0.44 mg kg–1 and the average time to death following exposure was 5.5 days (range 0–16 days). Two mice (~1% of those tested) survived after apparently ingesting doses of brodifacoum estimated to be 5 and 10 times the oral LD50 values, potentially indicating a lower susceptibility to brodifacoum in some individuals, although subsequent exposure at higher doses resulted in mortality. Conclusions The results of this study confirmed that house mice on Gough Island find bait pellets highly palatable and that brodifacoum is an effective toxin with LD50 values and time to death within the same range (0.4 to 0.52 mg kg–1 and 5.2 days) as other studies, indicating no major difference in the susceptibility of Gough mice to this poison. Implications We recommend that bait manufacturers produce formulations designed to be attractive to mice and consider the use of higher concentrations of brodifacoum to increase the likelihood of all mice obtaining a toxic dose when small quantities of bait are consumed, although higher toxin concentrations must be balanced against the increased risks to non-target species. Eradication operations targeting mice should undertake more than one bait drop to ensure any individuals surviving the initial drop have access to sufficient toxic bait to cause mortality upon second or subsequent exposure.

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Dong, Xinfeng, Shuxuan Liang, and Hanwen Sun. "Determination of seven anticoagulant rodenticides in human serum by ultra-performance liquid chromatography-mass spectrometry." Analytical Methods 7, no. 5 (2015): 1884–89. http://dx.doi.org/10.1039/c4ay02536a.

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Anticoagulant rodenticide residues (warfarin, coumatetralyl, diphacinone, chlorophacinone, brodifacoum, bromadiolone, and flocoumafen) in human serum were determined by sensitive high-performance liquid chromatography-mass spectrometry.

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Oliveri, Cecilia V., James R. Stubbs, Tatyana Chernova, Gary Ellis Carnahan, Tara N. Evans, Andrew Gammill, and Jonathan Siegel. "Short-Term Use of Phenobarbital in the Treatment of “Superwarfarin” Poisoning." Blood 104, no. 11 (November 16, 2004): 4024. http://dx.doi.org/10.1182/blood.v104.11.4024.4024.

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Abstract Background: “Superwarfarin” was developed in the 1970s as an anticoagulant rodenticide. The half-life of the “superwarfarin”, brodifacoum, is four times longer than warfarin. Patients with significant brodifacoum ingestions have often required long-term treatment with vitamin K1 (e.g., 6 months), occasionally with adjunctive phenobarbital therapy. Case: A 52-year-old male was admitted to the hospital after being found unconscious at home. He was pale and tachycardic at presentation with an oozing laceration on his right leg and bright red blood per rectum. Two liters of maroon fluid were recovered via nasogastric lavage. Admission laboratory values included: PT > 300 seconds, aPTT > 300 seconds, hemoglobin 2.8 g/dL, hematocrit 8.8%, and platelet count 400,000 per μL. Metabolic acidosis with an increased anion gap was present. A drug screen (Toxi-Lab®) was negative. Alcohol, salicylate, and acetaminophen assays yielded negative results. The following day, the patient admitted ingesting with a total of 170 grams of brodifacoum with suicidal intent. Subcutaneous vitamin K1 (10 mg QID), octreotide acetate (50 mg PO), and pantoprazole sodium (40 mg PO) were administered. He improved clinically, but his PT (range: 22.4–47.4 seconds), INR (range: 2.1–5.5), and aPTT (range: 40–70 seconds) remained abnormal. On hospital day 5 his vitamin K1 dose was increased to 25 mg QID and oral phenobarbital (30 mg TID) was started. A total of thirty-eight units of plasma and 8 red cell units were transfused during the admission. He was transferred to an inpatient psychiatric facility on day 8, and he was discharged from that facility after 5 days. Vitamin K1 and phenobarbital were discontinued at this time. Three and one-half months later, the patient was asymptomatic. His laboratory values included: PT 13.2 seconds, INR 1.1, aPTT 25 seconds, hemoglobin 14.3 g/dL, and hematocrit 42%. A serum brodifacoum level yielded negative results. Conclusion: Superwarfarin has been noted to be an increasingly common cause of poisoning in the past 20 years, especially in intentional ingestions. Many cases have been successfully treated with long-term vitamin K1 — with adjunctive phenobarbital given to some patients. The rationale for using phenobarbital in this setting is that it increases warfarin metabolism by inducing cytochrome P450 isozymes known to be major catabolic enzymes for warfarin (CYP2C9/19) in the liver. We report the successful treatment of significant brodifacoum toxicity with a short course of vitamin K1 (13 days) in combination with phenobarbital (6 days). Figure Figure

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Wallace, S., C. Worsnop, P. Paull, and M. L. Mashford. "Covert self poisoning with brodifacoum, a ‘superwarfarin’." Australian and New Zealand Journal of Medicine 20, no. 5 (October 1990): 713–15. http://dx.doi.org/10.1111/j.1445-5994.1990.tb00405.x.

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Hedhiri, Salma, Ines Belwaaer, and Dorra Ben Salah. "Intoxication by brodifacoum: Three cases in Tunisia." Toxicology Letters 180 (October 2008): S167. http://dx.doi.org/10.1016/j.toxlet.2008.06.264.

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Chen, Mei-lan, Guang-feng Zhu, Li-xin Zhou, Jian-qing Min, Xiao-hong Chen, and Mi-cong Jin. "Analysis of trace bromadiolone and brodifacoum in environmental water samples by ionic liquid ultrasound-assisted dispersive liquid–liquid microextraction and LC-MS/MS." Anal. Methods 6, no. 15 (2014): 5879–85. http://dx.doi.org/10.1039/c3ay42317d.

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An ionic liquid-based ultrasonic-assisted dispersive liquid–liquid microextraction (IL-USA-DLLME) method was proposed for highly effective extraction of trace bromadiolone and brodifacoum in environmental water samples.

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Brown, K. P., N. Alterio, and H. Moller. "Secondary poisoning of stoats (Mustela erminea) at low mouse (Mus musculus) abundance in a New Zealand Nothofagus forest." Wildlife Research 25, no. 4 (1998): 419. http://dx.doi.org/10.1071/wr97069.

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Two different brodifacoum (Talon 20 P™) poisoning regimes effectively killed 100% of resident radio-tagged stoats (Mustela erminea) by secondary poisoning in a New Zealand Nothofagus forest when mice (Mus musculus) were scarce. Resident possums (Trichosurus vulpecula) and ship rats (Rattus rattus) were also killed. The relative importance of different prey species as sources of poison for stoats has not been clearly identified but availability of poisoned prey will determine the efficacy of secondary poisoning in years of low prey abundance. Tracking tunnels did not accurately measure the decline in the stoat population and were probably influenced by immigrant stoats that were kill-trapped and contained high levels of poison. This study corroborates the findings of several other similar studies that secondary poisoning using brodifacoum effectively kills stoats.

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Andreev, Sergey V., Evgeny S. Belyaev, and Anatoly A. Ischenko. "NEW UNIVERSAL METHOD FOR DETERMINATION OF ANTICOAGULANTS IN RODENTICIDES." IZVESTIYA VYSSHIKH UCHEBNYKH ZAVEDENIY KHIMIYA KHIMICHESKAYA TEKHNOLOGIYA 62, no. 1 (December 30, 2018): 85–90. http://dx.doi.org/10.6060/ivkkt.20196201.5719.

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Solid paraffin briquettes are one of the most modern types of rodenticide baits, because they protect it from the environmental exposure and do not reduce palatability of rodents. This paper proposes a simple universal method for the determination of brodifacoum, bromadiolone and difenacoum in solid briquettes, which are a mixture of paraffin, poison and filler, which can be used as grain, flour and the like. The difficulty in the analysis of baits containing paraffin, is to get rid of it. For this, we propose to use hexane-acetonitrile extraction in the system. Paraffin dissolves in hexane, while brodifacoum, bromadiolone and difenacoum do not. The resulting two-phase system was separated using a separatory funnel and the bottom fraction was collected. If any fillers were present in the sample, they were filtered until the mixture was separated, the residue was washed with acetonitrile. Before introducing the sample into the chromatograph, it was filtered twice with PTFE filters with a porosity of 0.45 µm. The best separation was achieved using a Thermo Acclaim® Surfactant column using acetonitrile and 0.1 M aqueous ammonium acetate solution (pH 5.4) as the mobile phase in a gradient elution mode. All three poisons were detected at a wavelength of 264 nm. This method has a sensitivity of 0.028 mg. The linearity range is from 0.00067 to 0.01%. The recovery rate for bromadiolone is 94%, for brodifacoum, 98%, and for difenacoum, 90%.

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Moss, Zane N., Cheryl E. O'Connor, and Graham J. Hickling. "Implications of prefeeding for the development of bait aversions in brushtail possums (Trichosurus vulpecula)." Wildlife Research 25, no. 2 (1998): 133. http://dx.doi.org/10.1071/wr97018.

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Development of aversions, or learned ‘bait-shyness’, in frequently poisoned possum (Trichosurus vulpecula) populations is becoming increasingly detrimental to the efficacy of pest-control operations in New Zealand. This experiment aimed to identify the effects of prefeeding, a common management procedure, on the subsequent development of aversions in possums. Wild possums (n = 96) were captured and acclimatised, then allocated to one of three treatments groups that for seven days received either (i) no prefeed, (ii) plain RS5 cereal baits, or (iii) green-dyed and cinnamon-lured RS5 cereal baits. The possums were then offered a standard green-dyed and cinnamon-lured RS5 bait that contained a sublethal dose (0.4 mg kg-1) of the toxin sodium monofluoroacetate (1080). The possums were tested for development of an aversion towards a toxic RS5 1080 bait, a prefeed bait, and a prefeed bait containing an alternative toxin, brodifacoum. Most (96%) of the non-prefed possums became averse to the 1080 bait after two exposures, compared with only 55% and 9% of the two prefed groups. Similarly, 90% and 92% of the non-prefed possums were averse to prefeed and brodifacoum baits, respectively, compared with 8% and 14% of the prefed possums. This suggests that pest managers can reduce the risk of ‘bait shyness’ by prefeeding. A further advantage of prefeeding is that if poison shyness develops, use of an alternative toxin such as brodifacoum in the original bait base may still be successful.

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Wang, Yuchen, Viktoriya Kotik, Germin Fahim, Sayee Alagusundaramoorthy, Sherif Ali Eltawansy, Scott Mathis, and Julie Saleh. "Treatment of brodifacoum overdose with prothrombin complex concentrate." American Journal of Health-System Pharmacy 73, no. 1 (January 1, 2016): e14-e17. http://dx.doi.org/10.2146/ajhp150233.

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Tahir, Mohammad, Muhammad F. Khan, and Kamal Tourbaf. "Impending Compartment Syndrome and Hemothorax After Brodifacoum Ingestion." Southern Medical Journal 101, no. 12 (December 2008): 1277. http://dx.doi.org/10.1097/smj.0b013e3181887566.

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Helmuth, Robin A., Donald W. McCloskey, David J. Doedens, and Dean A. Hawley. "Hematology: Fatal Ingestion of a Brodifacoum-Containing Rodenticide." Laboratory Medicine 20, no. 1 (January 1, 1989): 25–27. http://dx.doi.org/10.1093/labmed/20.1.25.

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STANZIALE, STEPHEN F., J. CATHRYN CHRISTOPHER, and ROBERT B. FISHER. "Brodifacoum Rodenticide Ingestion in a Patient With Shigellosis." Southern Medical Journal 90, no. 8 (August 1997): 833–35. http://dx.doi.org/10.1097/00007611-199708000-00013.

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Chandra, Abhinav B., Nanda K. Methuku, and Yiwu Huang. "Prolonged Coagulopathy Secondary to Superwarfarin Brodifacoum Rodenticide Ingestion." Blood 116, no. 21 (November 19, 2010): 4425. http://dx.doi.org/10.1182/blood.v116.21.4425.4425.

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Abstract Abstract 4425 Case description– A 47 year old man presented to emergency room due to back pain, hematuria and persistent gum bleed for more than one week after dental procedure. He had also noted easy bruisability for the last two months. He was found to have elevated PT and PTT. On admission, his PT was >120 sec with INR > 9.9 and his PTT > 100 sec. The abnormal PT and PTT were completed corrected by the addition of normal plasma on mixing study. Factor assay showed factor II level 19%, factor VII 1.5%, factor IX 7.4%, factor × 15%, factor V 87%, factor VIII 140%, factor XI 96%, and factor XII 49%. Since he had no other medical conditions and no history of hepatic dysfunction that would cause his coagulopathy, superwarfarin toxicity was suspected. Blood toxicology screen was positive for superwarfarin compound brodifacoum. He received few units of FFP and was given a loading dose of 50 mg phytonadione (vitamin K) followed by 20 mg three times daily. His PT and INR normalized and gum bleeding and hematuria resolved. The patient was discharged from hospital. Patient denied any intentional ingestion of rat poison, any suicidal ideation or any conflicts within family. He was exposed to rodenticide at his workplace. During outpatient follow up, patient was again found to have elevated PT/INR and on questioning informed that he was taking Chinese herbal medications provided by his friends to facilitate excretion of the rat poison. Patient was advised to stop taking any alternative therapies. His phytonadione was increased to 240 mg/day for more than two months which have normalized his coagulopathy. Discussion– Human toxicity from ingestion of older rodenticides that contain warfarin is uncommon because these products contain less warfarin and the drug is rapidly metabolized. Newer derivates of warfarin (superwarfarins) brodifacoum, difethialone and difenicoum have been developed to overcome warfarin resistance. These compounds are more toxic to humans than warfarin because of their more avid binding to hepatic microsomes and longer duration of action. Brodifacoum and difenicoum are far more potent and have a much longer half-life than warfarin. The half-life of brodifacoum has been described as long as 30 days. Superwarfarins produce their anticoagulation effect by inhibiting the conversion of vitamin K1 2,3 epoxide to vitamin K1. This reaction is coupled to the carboxylation reaction required to produce the active form of prothrombin and the other vitamin K dependent clotting factors. There is increase in the vitamin K epoxide to vitamin K ratio and severely decreased activity of vitamin K dependent clotting factors. The duration of coagulation disturbance can be from few weeks to as long as few months. As illustrated by our patient, the treatment of superwarfarin posioning requires large doses of phytonadione, ranging from 50 – 800 mg/day administered for several months. Our patient has required daily 240 mg of phytonadione over two months to normalize his coagulopathy. Disclosures: No relevant conflicts of interest to declare.

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Journal articles on the topic 'Brodifacoum'

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