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Poisoned Bobcat
updated: Jan 23, 2013, 12:00 PM

By Julia J. Di Sieno

On Sunday night our rescue hotline received another call for help. A jogger found this female bobcat shaking under an oak tree in Santa Ynez. While on scene our team witnessed many squirrel bait traps littered on nearly each land parcel. Despite our heroic efforts, treating our suffering bobcat she died early this morning.

This is our third bobcat, as well as many hawks that died from the same general area in Santa Ynez. Our findings have been reported to proper authorities.

PLEASE educate your neighbors and friends!


Trade Names: Ialon, Havoc, D-Con mice and rat traps Mechanism of Action: second-generation anticoagulant. Absorbed through the gut and inhibits the vitamin K-dependent steps in the synthesis of multiple clotting factors. Death usually occurs through gastric hemorrhage. Metabolism: brodifacoum is retained in the tissues at high rates, sometimes remaining in organ systems during the entire lifetime of an exposed animal. In a study that measured the retention of radioactive brodifacoum in the livers of single-dosed rats, 34% of the single dose is found in the liver after 13 weeks, and 11% of the dose remained in the liver for 104 weeks, approaching the normal lifespan of a rat (U.S. EPA MRID 42007502). Very highly toxic to mammals and birds.

Brodifacoum is extremely dangerous to birds through secondary exposure, especially raptors feeding on poisoned rats and mice. Hundreds of avian and other wildlife mortalities have been reported across North America.

Brodifacoum is absorbed through the gut and works by preventing the normal clotting of blood, leading to fatal hemorrhage. It is highly effective at small doses - usually a rodent ingests a fatal dose after a single feeding and will die within 4-5 days. The greatest risk to wildlife from brodifacoum is secondary poisoning. Rodents continue to eat poisoned bait so at the time of death the amount of brodifacoum present in their bodies is many times the amount required to kill them. Non-target wildlife such as predators and scavengers may then consume rodents that have ingested large doses of brodifacoum. It can take as little as one poisoned rodent, or a predator may accumulate enough brodifacoum after consuming several poisoned prey items, to induce life-threatening or fatal effects. A single dose of brodifacoum can depress blood clotting for months in some animals, including birds. Stress or slight wounds incurred in the fi eld, such as small scratches that normally occur when a raptorial bird captures its prey, are often suffi cient to cause a fatal hemorrhage. Raptor species maintain hunting territories that may include areas near agricultural or other industrial and urban buildings where rodent control is ongoing. Local avian predators may consume rodents living in and around these structures. However, the death of such a predator will most likely occur some distance away from treated sites, making it diffi cult to observe patterns of mortality attributable to any one cause. Furthermore, birds that have been exposed to lethal levels of brodifacoum may be more likely to die from other causes such as accidents or predation. Most mortality undoubtedly goes undiscovered. For these reasons, the true impact on birds of many pesticies, including brodifacoum is obscured.

More on Pesticides:

1) Widely used pesticides are not particularly specific for the "target" organism. Such pesticides can cause unintended and unwanted effects to "non-target" resources. Species can be exposed to pesticides by many routes, with the simplest form being direct contact or ingestion.

2) Animals can ingest pesticides indirectly through contaminated foods such as leafy material, seeds, and prey (including insects and other animals), or by water contamination through precipitation and irrigation (puddles, drinking water, bathing water or breeding).

3) Aquatic organisms can be exposed to pesticides entering water bodies through runoff and groundwater infi ltration. Measurable amounts of pesticides have been detected in rainwater.

4) Indirect effects of pesticides can also have signifi cant implications to animal species. For example, herbicide drift can harm plants and consequently damage the habitat upon which an animal species depends. A given pesticide can be relatively non-toxic to an animal species, but may be lethal to its prey or food plants. Similarly, an insecticide can indirectly harm an endangered plant that may depend upon a specifi c insect pollinator.

5) Wildlife, for example, are more susceptible to pesticide effects during nesting, nursing of young or during times of low food availability.

6) Primary exposure includes eating, drinking, preening of feathers, skin contact or breathing of vapors.

7) Secondary exposure occurs from scavenging on contaminated food, such as exposed carcasses, or feeding upon insects. If pesticide levels are high enough, wildlife often die suddenly.

8) Not as readily observed in wildlife are the sublethal, or non-fatal, consequences of ingesting pesticides. Behavior changes, weight loss, impaired or unsuccessful reproduction, high offspring mortality or deformed embryos are results of sublethal exposure to pesticides. Affected wildlife become easy prey for predators, while many lose their ability to adapt to environmental changes.

9) Pesticides can reduce insects that may be important food sources for young birds and fi sh, and habitat is similarly reduced when vegetation is destroyed -- a critical factor for small wildlife populations already stressed by insufficient habitat.


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