Toxin Of The Month: Rat Bait

Rat bait is commonly used on many farms and consequently cattle can often be exposed to it. Learn more about the damage it causes and how it can be treated.

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Rodenticide Toxicity

Rat bait is commonly used on many farms and consequently cattle can often be exposed to it. Fortunately, poisoning is rarely reported, but it does happen.

It’s probably more common in farm dogs and cats than in livestock, and the mechanism of toxicity and the clinical signs are the same for all. Cats and dogs can suffer primary poisoning by consuming bait directly, or secondary poisoning from eating poisoned rats.

Normal Blood Clotting

When there is damage to a blood vessel, most commonly from an injury or wound, very small specialist cells in the blood called platelets are drawn to the site of the wound and stick to each other to effectively plug the damage and stop blood loss. This platelet plug is unstable, and so a series of chemical reactions between blood clotting factors need to occur in the blood and liver to result in the formation of a net-like substance called fibrin. Fibrin intertwines between platelets and stabilises the platelet plug over the wound. Once bleeding has stopped, the damaged blood vessel can then undergo repair and healing.

Vitamin K is vital to the blood clotting process as it activates the blood clotting factors in the liver, enabling fibrin to be produced. When Vitamin K has been used up, it is cleverly recycled again ready for future use.

How Does Rat Poison Work?

Rodenticides work by inhibiting a protein that allows the recycling of Vitamin K in animals. Without working Vitamin K, net-like fibrin cannot be produced to stabilise the blood clot.

First generation anticoagulant rodenticides such as warfarin and dicoumarol have a short half life and so are not present in the cow for long. To cause toxicity, the cow must ingest the poison multiple times. However second generation products such as brodifacoum and bromadiolone have a longer half life and so can be very toxic after a single dose.

What Do You See?

The cow’s reserves of Vitamin K will be used up before blood clotting is affected, so signs start to show a few days after the cow has ingested the poison.

In these cases, the platelet plug is still formed to try and stop any bleeding from injuries, however it’s unstable as no fibrin is present. The plug will successfully stop any bleeding from small blood vessels but will be dislodged from a larger blood vessel, causing heavy bleeding.

Haematomas (accumulations of blood outside blood vessels) can happen wherever a larger blood vessel is injured. These often present as external large masses, such as on the shoulder from a knock on a gatepost, however sometimes bleeding will be internal, either into joints or the body cavity. This is life threatening and is more readily confirmed on post mortem examination than in the live animal.

The live animal may also present with pale mucous membranes (oral/vulval/ocular) due to severe blood loss, an elevated heart and respiratory rate and may be in respiratory distress. Unfortunately, sudden death is the most common presentation.

Diagnosis

  • A blood sample from the affected animal will reveal prolonged clotting times and often low red blood cell count.
  • Post-mortem findings of haematomas, bleeding into joints and internal haemorrhage.
  • History of rodenticide exposure (although this can be difficult to prove).

Treatment

  1. Affected cattle must be given Vitamin K subcutaneously or intramuscularly twice daily for at least 5 days. Newer rodenticide products will require a longer duration of treatment.
  2. Affected cattle that have suffered severe blood loss should receive a blood transfusion from a healthy donor.

References

‘Bleeding Disorders in cattle’- In Practice, Charlotte Bell, Volume 33 Issue 3

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