Here is a different type of rodenticide (mouse/rat poison): cholecalciferol. We know if it poisons mice and rats it is toxic to dogs and cats, since they are mammals, too. The question is how does it affect them?
What is the toxic principal/how does it poison? (Hint: Last week, we had a toxin that altered Vitamin K metabolism, this week is another poison that involves a vitamin.)
What signs might you see?
Is there a treatment?
How poisonous is cholecalciferol/what is the prognosis? Remember our scale of: Fair - treatable if caught in time; Poor - might not survive even with treatment; or Grave - likely to be fatal even with treatment. (Another hint, last week's anticoagulants had a Fair prognosis, this week is different.)
Be bold, be brave - jump in with your guesses. Partial credit is awarded for any attempt to answer, and please show all your work. Neatness counts!
ANSWERS:Cholecalciferol is Vitamin D3. Not only is it found in rodenticides like Rampage, Quintox and Rat-B-Gone, it is also found in multivitamins and some calcium supplements like Viactiv. While it is possible for a pet to be overdosed on Vitamin D3 by eating vitamin or mineral supplements, the risk is much greater from ingesting rodenticides containing cholecalciferol.
Vitamin D3 is a fat soluble vitamin. It is necessary to maintain the delicate balance of calcium and phosphorous in the body. Calcium is not only needed for strong bones, it is a major part of the electrical system of the heart muscle. Excessive intake of Vitamin D3 leads to abnormal calcium and phosphorous levels, irregular heart beats, and the mineralization of soft tissues. In other words, calcium is deposited in the soft tissues of the body, essentially “turning them into bone.” The GI tract, skeletal muscle, heart and blood vessels may be affected, but the kidneys are usually the primary problem.
Clinical signs are vomiting and diarrhea (sometimes bloody.) The bait pellets are blue, so blue vomitus is a key finding. Other signs, including increased water intake and urination, lethargy, and muscle weakness, may be seen in the first 48 hours after poisoning. High doses results in acute renal (kidney) failure. Death can occur in severely affected animals. Those which survive may have long-term consequences, including chronic renal failure and cardiac arrhythmias.
If an animal is observed eating this type of poison, immediate attention is mandatory. It must be treated immediately after ingestion by decontamination (induce vomiting, gastric lavage, administer cathartics and activated charcoal) and must be monitored for physical symptoms and any changes in blood calcium, phosphorous, and kidney levels. If there are no physical or biochemical changes in four days, the prognosis is good for recovery.
In animals with clinical signs or elevated calcium levels, treatment consists of IV saline solution, furosemide (a diuretic) and prednisone to increase excretion of calcium in the urine. Diets low is calcium and phosphorous and oral phoshate binders are also part of the treatment process, which may last 6 weeks or longer. Prognosis in these cases is poor, due to the potential for chronic, lifetime kidney and heart damage.
The toxic dose starts at 0.5mg/kg body weight. This is the equivalent of 6 grams (about ½ tablespoon) of the typical 0.075% concentration bait in a 20 pound dog. (Another source gave a much higher level, 12-20mg/kg, as the toxic dose.) Secondary poisoning, from eating a mouse or rat which died from cholecalciferol poisoning, has not been reported.
This is not a common poison, at least in my area. I had to go to 10 different stores to find one example of a Vitamin D3-based rodenticide. I have only seen one case of cholecalciferol toxicity in 21 years of practice.