Prevalence of Anticoagulant Rodenticide Exposure in Red-tailed Hawks (Buteo jamaicensis) in New York State and Diagnostic Utility of Russell Viper Venom Test for Detecting Associated Coagulopathies

Anticoagulant rodenticides (ARs) continue to be used across the United States as a method for controlling unwanted rodent species. As a consequence, wild birds of prey are exposed to toxins by eating poisoned prey items. ARs prevent the hepatic recycling of vitamin K and thereby impede the post-translational processing of coagulation factors II, VII, IX, and X that is required for procoagulant complex assembly. Through this mechanism of action, ARs cause hemorrhage and death in their target species. Various studies have documented the persistence of these contaminants in birds of prey but few have attempted to use affordable and accessible diagnostic tests to diagnose exposure in free-ranging birds of prey. In our study free-ranging red-tailed hawks were found to be exposed to difethialone and brodifacoum. Eleven of sixteen (68%) livers tested for AR exposure were positive. Difethialone was found in 1/16 (6%) liver samples, and brodifacoum was detected in 15/16 (93%) liver samples. Difethialone was found at a concentration of 0.18 ppm and brodifacoum concentrations ranged from 0.003-0.234 ppm. Two out of 34 (6%) RTH assessed for blood rodenticide had brodifacoum in blood with measured concentrations of 0.003 and 0.006 ppm. The range of clotting times in the prothrombin time (PT) and Russell’s viper venom time assays for control RTH were 16.7 to 39.7 seconds and 11.5 to 91.8 seconds, respectively. No correlation was found between PT and RVVT in the control or free-range RTH, and there was no relationship found between the presence of liver anticoagulant residues and clotting times in the PT and RVVT.

Acute hemorrhage and death in calves following chlorophacinone exposure

Three calves were submitted to the Iowa State University Veterinary Diagnostic Laboratory for diagnostic evaluation following an abrupt increase in morbidity and mortality in a calf herd associated with epistaxis and widespread hemorrhage. Each of the submitted calves had moderate-to-severe hemorrhage within various tissues and body cavities, including the thymus, subcutaneous region of the neck, mediastinum, lungs, pericardial sac, heart, spleen, perirenal fat, urinary bladder, and skeletal muscle, including the diaphragm. An anticoagulant rodenticide screen was performed on the livers of each calf. Significant concentrations of chlorophacinone were detected at 4.2, 3.6, and 2.9 ppm in liver. Multiple piles and an open pail of white powdery material were present within the facility in which the calves were housed and were identified as the sources of chlorophacinone. Acute hemorrhage and death occurred in fourteen 1.5-mo-old, crossbred calves following ingestion of the vitamin K antagonist chlorophacinone.

Anticoagulant rodenticide ingestion: Who will develop coagulopathy?

Introduction: Development of coagulopathy after anticoagulant rodenticide ingestion varies among patients. This study aimed to identify factors that were associated with coagulopathy after anticoagulant rodenticide ingestion. Methods: This was a retrospective cohort study, conducted in the Hong Kong Poison Information Centre. All patients who reported rodenticide exposure and presented to the Accident and Emergency Department from 1 January 2010 to 31 December 2019 were recruited. Coagulopathy was defined as International Normalized Ratio of 1.3 or above. Results: One hundred sixty-nine patients were included in the final analysis. The median age was 44 years old. Forty-nine patients developed coagulopathy (International Normalized Ratio ⩾1.3). Univariate analysis (at p < 0.05) showed that age (p = 0.003), ingestion of first-generation anticoagulant rodenticide (p = 0.017), ingestion of more than one pack (p < 0.001), intentional ingestion (p = 0.002), hypoalbuminemia (p < 0.001), elevated alanine aminotransferase level (p = 0.041) and abnormal estimated glomerular filtration rate (p = 0.005) on presentation, and co-ingestion with paracetamol (p = 0.018) were associated with coagulopathy after anticoagulant rodenticide ingestion. Among these, ingestion of more than one pack (p < 0.001; odds ratio = 19.8; 95% confidence interval = 6.78–65.7), ingestion of first-generation anticoagulant rodenticide (p = 0.006; odds ratio = 5.2; 95% confidence interval = 1.96–15.2), hypoalbuminemia (p < 0.001; odds ratio = 22.4; 95% confidence interval = 6.17–99.0) and elevated alanine aminotransferase level on presentation (p = 0.039; odds ratio = 7.11; 95% confidence interval = 1.58–33.1) were statistically significant in the multivariate analysis. Conclusion: Ingestion of more than one pack and ingestion of first-generation anticoagulant rodenticides were significantly associated with the development of coagulopathy after anticoagulant rodenticide ingestion. Patients who developed hypoalbuminemia or elevated alanine aminotransferase level as a result of anticoagulant rodenticide ingestion were also significantly associated with the development of coagulopathy.

Single Nucleotide Polymorphisms (SNPs) Within Vkorc1 in Rodent Populations in a Tropical City-state: Implications for Anticoagulant Rodenticide Use for Rodent Control

Anticoagulant rodenticides are commonly used in rodent control because they are economical and have great deployment versatility. However, rodents with Single Nucleotide Polymorphism (SNP) mutations within the Vkorc1 gene are resistant to the effects of anticoagulant rodenticide use and this influences the effectiveness of control strategies that rely on such rodenticides. This study examined the prevalence of rat SNP mutations in Singapore to inform the effectiveness of anticoagulant rodenticide use. A total of 130 rat tail samples, comprising 83 Rattus norvegicus (63.8%) and 47 Rattus rattus spp. (36.2%) were conveniently sampled from November 2016 to December 2019 from urban settings and sequenced at exon 3 of Vkorc1. Sequencing analysis revealed 4 synonymous and 1 non-synonymous mutations in Rattus rattus spp. samples. A novel synonymous mutation of L108L was identified and not previously reported in other studies. Non-synonymous SNPs were not detected in the notable codons of 120, 128 and 139 in Norway rats, where these regions are internationally recognised to be associated with resistance from prior studies. Our findings suggest that the prevalence of anticoagulant rodenticide resistance in Singapore is low. Continued monitoring of rodenticide resistance is important for informing rodent control strategies aimed at reducing rodent-borne disease transmission.

Anticoagulant rodenticide exposure and toxicosis in bald eagles (Haliaeetus leucocephalus) and golden eagles (Aquila chrysaetos) in the United States

Raptors, including eagles, are geographically widespread and sit atop the food chain, thereby serving an important role in maintaining ecosystem balance. After facing population declines associated with exposure to organochlorine insecticides such as dichlorodiphenyltrichloroethane (DDT), bald eagles (Haliaeetus leucocephalus) have recovered from the brink of extinction. However, both bald and golden eagles (Aquila chrysaetos) are exposed to a variety of other toxic compounds in the environment that could have population impacts. Few studies have focused on anticoagulant rodenticide (AR) exposure in eagles. Therefore, the purpose of this study was to determine the types of ARs that eagles are exposed to in the USA and better define the extent of toxicosis (i.e., fatal illness due to compound exposure). Diagnostic case records from bald and golden eagles submitted to the Southeastern Cooperative Wildlife Disease Study (University of Georgia) 2014 through 2018 were reviewed. Overall, 303 eagles were examined, and the livers from 116 bald eagles and 17 golden eagles were tested for ARs. The percentage of AR exposure (i.e., detectable levels but not associated with mortality) in eagles was high; ARs were detected in 109 (82%) eagles, including 96 (83%) bald eagles and 13 (77%) golden eagles. Anticoagulant rodenticide toxicosis was determined to be the cause of mortality in 12 (4%) of the 303 eagles examined, including 11 bald eagles and 1 golden eagle. Six different AR compounds were detected in these eagles, with brodifacoum and bromadiolone most frequently detected (81% and 25% of eagles tested, respectively). These results suggest that some ARs, most notably brodifacoum, are widespread in the environment and are commonly consumed by eagles. This highlights the need for research to understand the pathways of AR exposure in eagles, which may help inform policy and regulatory actions to mitigate AR exposure risk.