cholecalciferol and Cat-Diseases

This article focuses on the 3 most commonly used rodenticide types: anticoagulants, bromethalin, and cholecalciferol. It is important to verify the active ingredient in any rodenticide exposure. Many owners use the term D-con to refer to any rodenticide regardless of the brand or type of rodenticide. The Environmental Protection Agency released their final ruling on rodenticide risk mitigation measures in 2008 and all products sold had to be compliant by June 2011, changing to consumer products containing either first-generation anticoagulants or nonanticoagulants, including bromethalin and cholecalciferol. These regulations have caused an increase in the number of bromethalin and cholecalciferol cases.

Topics: Aniline Compounds; Animals; Anticoagulants; Antidotes; Cat Diseases; Cats; Cholecalciferol; Dog Diseases; Dogs; Rodenticides; Vitamin K

The primary source of exposure to cholecalciferol in dogs and cats is ingestion of rodenticide baits with vitamin D3 as the active ingredient. Other sources of this toxin are human medications and rarely, contaminated pet food. Although the reported lethal dose 50% for cholecalciferol is 88 mg/kg, deaths have been seen with an individual exposure of 2 mc g/kg in dogs. Clinical signs are induced by profound hypercalcemia affecting multiple body systems. Clinical presentations may include anorexia, depression, muscle weakness, vomiting, polyuria, polydipsia, dehydration, abdominal pain, hematemesis, melena, and bradycardia. Tissue mineralization may develop if calcium × phosphorous product is greater than 60. Serum testing for hypercalcemia, hyperphosphatemia, and decreased serum parathyroid hormone are confirmatory. Initial treatment relies upon decontamination with emesis induction followed by administration of pulse-dose activated charcoal designed to interfere with the extensive enterohepatic recirculation of toxin. Medical management is designed to decrease serum calcium levels by use of intravenous fluid diuresis with administration of furosemide and prednisolone. Biphosphate pamidronate is used to inhibit calcium release from the bone. Phosphate binders aid in decreasing phosphate availability to interact with calcium. The prognosis is better if treatment is instituted early before development of hypercalcemia and hyperphosphatemia enables tissue mineralization to progress.

Topics: Animals; Cat Diseases; Cats; Cholecalciferol; Dog Diseases; Dogs; Hypercalcemia; Pets; Poisoning; Rodenticides

This article focuses on the 3 most commonly used rodenticide types: anticoagulants, bromethalin, and cholecalciferol. It is important to verify the active ingredient in any rodenticide exposure. Many animal owners may use the term “D-con” to refer to any rodenticide regardless of the actual brand name or type of rodenticide. The EPA released their final ruling on rodenticide risk mitigation measures in 2008 and all the products on the market had to be compliant by June 2011, changing to consumer products containing either first-generation anticoagulants or nonanticoagulants including bromethalin and cholecalciferol. These regulations are likely to cause an increase in the number of bromethalin and cholecalciferol cases.

Topics: Aniline Compounds; Animals; Anticoagulants; Cat Diseases; Cats; Cholecalciferol; Dog Diseases; Dogs; Rodenticides

Rodenticides are second only to insecticides in the prevalence of pesticide exposure. Hundreds of rodenticide products currently exist, yet only a handful of them are involved in most toxicoses of companion animals. The most commonly reported toxicoses in the United States are those caused by anticoagulant rodenticides, bromethalin, cholecalciferol, strychnine, and zinc phosphide. The pathophysiologic findings, diagnosis, and treatment of each of these five rodenticides are discussed.

Topics: Aniline Compounds; Animals; Cat Diseases; Cats; Cholecalciferol; Dog Diseases; Dogs; Drug-Related Side Effects and Adverse Reactions; Phosphines; Rodenticides; Strychnine; Zinc Compounds

Topics: Animals; Bone Resorption; Calcitonin; Calcium; Cat Diseases; Cats; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dog Diseases; Dogs; Female; Hyperparathyroidism; Hyperparathyroidism, Secondary; Hypoparathyroidism; Kidney; Liver; Male; Parathyroid Diseases; Parathyroid Glands; Parathyroid Hormone; Parathyroid Neoplasms; Pregnancy; Tetany

Two siblings, a 6-month-old sexually intact male weighing 2.5 kg (cat 1) and a sexually intact female (cat 2) British Shorthair cat weighing 2.3 kg, were examined because of a 3-week history of polyuria, lethargy and laboured breathing. One year previously, another sibling (cat 3) had been presented because of similar, yet more severe, clinical signs at the age of 5 months. Physical examination revealed lethargy, dehydration and polypnoea with slightly increased inspiratory effort. Diagnostic investigation revealed severe hypercalcaemia (cats 1-3), renal azotaemia (cats 1 and 3) and a radiologically generalised miliary interstitial pattern of the lungs (cats 1-3) attributable to hypervitaminosis D caused by ingestion of commercial cat food. Cat 3 was euthanased. Cats 1 and 2 were treated with isotonic saline solution (180 ml/kg IV daily), sucralfate (30 mg/kg PO q12h), terbutaline (only cat 1: 0.1 mg/kg SC q4h), furosemide (1.5 mg/kg IV q8h) and tapering doses of prednisolone. Cat 2 was normal on day 14. Cat 1 had stable renal disease and was followed up to day 672. The radiological generalised military interstitial pattern of the lungs had improved markedly. Excessive cholecalciferol-containing commercially available cat food poses a great hazard to cats. Supportive treatment may result in long-term survival and improvement of radiological pulmonary abnormalities.

Topics: Animal Feed; Animals; Cat Diseases; Cats; Cholecalciferol; Female; Male; Vitamins

It has been suggested that tooth resorption (TR) in cats is associated with vitamin D3 status. The purpose of this study was to evaluate any correlation between serum 25-OH-D concentrations and the prevalence of TR. The healthy adult domestic cats (n=64) of this study had been fed similar premium dry-expanded foods throughout their lives. Serum 25-OH-D was measured, and cats received a single, complete periodontal examination, with periodontal probing of each tooth and exploration of the tooth surface using a dental explorer A complete set of 10 dental radiographs was taken for each cat. There were 168 TRs diagnosed in 40 of 64 cats (85 were Type 1 TR and 83 were Type 2). The mean serum 25-OH-D concentration was 187.7 +/- 87.3 nmol/L. The mean serum 25-OH-D in cats with one or more TR was 164.2 +/- 78.8 nmol/L, compared with 226.8 +/- 88.2 nmol/L for those without TR (p = 0.14). The mean serum 25-OH-D in the 13 cats with >5 TR was 131.2 +/- 49.5 nmol/L, which was significantly less than in cats with no TR (p < 0.05). There was no relationship between TR type and serum 25-OH-D. There was no effect of age or sex on serum 25-OH-D. On the contrary, variations in serum 25-OH-D were observed according to the studied breeds. There was no relationship between TR type and serum 25-OH-D. TR prevalence was greater in cats with lower serum 25-OH-D concentrations. In conclusion, the hypothesis that higher serum 25-OH-D concentrations are associated with a higher prevalence of TR is not supported by this study.

Topics: Animal Feed; Animals; Cat Diseases; Cats; Cholecalciferol; Diet; Female; France; Male; Prevalence; Regression Analysis; Tooth Resorption; Vitamin D

A 4-month-old 2.5-kg sexually intact female domestic shorthair cat was referred to the teaching hospital because of suspected cholecalciferol intoxication after ingestion of a cholecalciferol-containing rodenticide. At referral, the cat was hypercalcemic, hyperkalemic, and acidotic. Despite management of hypercalcemia and preservation of renal function with physiologic saline solution, furosemide, dopamine, and calcitonin, the cat died, apparently as a result of extensive pulmonary mineralization.

Topics: Animals; Calcinosis; Cat Diseases; Cats; Cholecalciferol; Female; Kidney; Lung; Lung Diseases; Rodenticides

Topics: Animals; Cat Diseases; Cats; Cholecalciferol; Male; Rodenticides

Topics: Animals; Cat Diseases; Cats; Cholecalciferol; Dog Diseases; Dogs; Poisoning; Rodenticides

Hypercalcemia (12.0 to 18.3 mg/dl) was detected in 3 cats that had eaten a rodenticide that contained cholecalciferol. Clinical signs included lethargy, anorexia, vomiting, and polydipsia. Treatment with furosemide and fluids administered IV resulted in normalization of the serum calcium concentration and in remission of the clinical signs in 2 cats. One cat with a serum calcium concentration of 18.3 mg/dl did not have clinical signs, was not treated, and was reportedly normal 9 months after initial examination. We attributed the uniformly favorable outcome of exposure to the rodenticide in these cats to the small quantity of the toxin ingested.

Topics: Animals; Cat Diseases; Cats; Cholecalciferol; Hypercalcemia; Male; Rodenticides

Calcium and phosphate metabolism as well as those substances which are essential in regulating this metabolism (parathyroid hormone, thyrocalcitonin and cholecalciferol) are briefly discussed. Of three known forms of bone disease (nutritional secondary hyperparathyroidism, rickets and hypervitaminosis A), the clinical symptoms, radiological changes, (histo)pathological findings, therapeutic procedures as well as the aetiological, pathogenic and pathophysiological features will be reviewed.

Topics: Animal Nutritional Physiological Phenomena; Animals; Birds; Bone and Bones; Bone Diseases; Calcitonin; Cat Diseases; Cats; Cholecalciferol; Dog Diseases; Dogs; Hyperparathyroidism, Secondary; Minerals; Osteoporosis; Parathyroid Hormone; Rickets; Vitamin A