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Basics ⬇

Outline

BASICS

Overview!!navigator!!

  • Cantharidin is the toxic compound found in blister beetles (primarily Epicauta spp. but also Pyrota spp.)
  • Toxicosis results from ingestion of baled alfalfa hay, or other alfalfa feeds, containing dead blister beetles
  • Cantharidin is rapidly absorbed from the GI tract and is excreted unchanged in the urine
  • The vesicant properties of cantharidin cause irritation, vesicle formation, ulceration, or erosions throughout the GI tract and bladder
  • Colic and/or sudden death
  • Hypocalcemia, hypomagnesemia, renal failure, cardiac abnormalities
  • Large swarms of blister beetles concentrate in alfalfa fields from the southern USA

Signalment!!navigator!!

  • All ages affected
  • No genetic or sex predisposition

Signs!!navigator!!

  • Typically several horses are affected within minutes to hours after feeding
  • Severity depends on the amount of cantharidin ingested
  • High doses = sudden death within hours; lower doses = symptoms that last for days
  • Restlessness, irritability
  • Sweating, fever
  • Colic, pawing the ground
  • Muscle fasciculations
  • Diaphragmatic flutter
  • Anorexia, loose stools, oral lesions
  • Playing in water without drinking
  • Congested mucous membranes, increased capillary refill times
  • Tachycardia, tachypnea
  • Stranguria, hematuria
  • Aggressive behavior
  • Seizures before death

Causes and Risk Factors!!navigator!!

  • Feeding of baled alfalfa that has been crimped or alfalfa cubes/pellets increases risk
  • Large swarms of beetles within fields among mature alfalfa or flowering plants
  • Malicious poisoning has occurred

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Colic from a variety of other causes
  • Ionophore toxicosis
  • History of feeding alfalfa or alfalfa products, hypocalcemia with or without concurrent hypomagnesemia, and discovery of beetles in hay or GI contents

CBC/Biochemistry/Urinalysis!!navigator!!

  • Hypocalcemia
  • Hypomagnesemia
  • Hyposthenuria with possible hematuria
  • Hyperproteinemia and increased packed cell volume due to dehydration
  • Leukocytosis may be observed in cases of bacterial infection-compromised GI epithelium

Other Laboratory Tests!!navigator!!

N/A

Imaging!!navigator!!

N/A

Other Diagnostic Procedures!!navigator!!

  • Analysis of urine or intestinal contents by HPLC or GC-MS
  • Any level of cantharidin detected is considered clinically significant
  • Urine (500 mL) is the specimen of choice for cantharidin analysis
  • Intestinal contents (500 mL) can also be tested
  • Analysis for cantharidin should be done early on since it is rapidly excreted through the urine unchanged
  • Liver, kidney, and serum can be used but are not the specimens of choice

Pathologic Findings!!navigator!!

  • Large doses can result in sudden death without gross lesions
  • Gross lesions may include ulceration of the oral mucosa and lips but are most common in the terminal esophagus, stomach, and the intestines, which may consist of areas of ulceration or erosion that may (or may not) be hemorrhagic
  • Hyperemic areas of the mucosal lining of the entire GI tract and urinary bladder have been noted
  • White streaks on the heart may be seen grossly
  • Microscopic lesions include acantholysis of the mucosa of the GI tract, epithelium of the urinary tract, and endothelium of vessels. Myocarditis, renal tubular nephrosis, and degenerative changes in the kidneys and GI tract can also be seen

Treatment ⬆ ⬇

TREATMENT

  • Cantharidin toxicosis is an emergency and requires in-hospital treatment
  • Focus treatment on enhancing fecal and urinary elimination of cantharidin, correcting dehydration, managing serum calcium and magnesium abnormalities, and controlling pain
  • Intensive supportive treatment may be required for 3–10 days, depending on the severity of illness
  • Initiate fluid therapy to adequately rehydrate the horse, decrease serum cantharidin levels, and aid in toxin excretion via the kidneys
  • Monitor serum calcium frequently
  • Stall rest for 5–10 days

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

  • Administer AC (1–4 g/kg as an aqueous slurry) via nasogastric tube, then mineral oil (2–4 L) 2–3 h later to prevent occupation of adsorptive sites on the AC
  • Repeated doses of mineral oil recommended
  • Adult horses may receive 500 mL of a commercial calcium-containing fluid (not exceeding 23 g of calcium compound per 100 mL) if administered slowly. Dilute commercial calcium preparations in isotonic fluids to decrease the chance of adverse cardiac responses and to allow more rapid administration. Dilute calcium in a ratio of 1:4 with saline or dextrose if frequent administration is required to control synchronous diaphragmatic flutter or muscle fasciculations
  • Hypomagnesemia may require addition of magnesium as well as calcium to the isotonic fluids
  • Prednisolone sodium succinate (50–100 mg as an initial dose) may be administered IV over 1 min for severe shock
  • Consider sucralfate (1 g per 45 kg PO every 6–8 h) in horses exhibiting clinical signs of gastritis—water playing
  • Commonly prescribed analgesics (e.g. flunixin meglumine) may not provide adequate pain relief. Therefore, administer α2-adrenergic agonists (e.g. detomidine 20–40 μg/kg IV or butorphanol tartrate 0.02–0.1 mg/kg IV every 3–4 h, not to exceed 48 h). Detomidine at 40 μg/kg dose should provide analgesia for 45–75 min
  • Xylazine (1.1 mg/kg IV) is also an α2-adrenergic agonist and may be substituted for detomidine for analgesia
  • Use broad-spectrum antibiotic therapy if septic complications from GI mucosal ulceration are likely

Contraindications/Possible Interactions!!navigator!!

  • Do not include calcium in fluids containing sodium bicarbonate because of possible precipitation of calcium
  • Aminoglycoside antibiotics are potentially nephrotoxic and should be avoided
  • Nonsteroidal anti-inflammatory drugs should be used with caution because of potential GI and renal complications
  • Diuretics—furosemide
  • Acepromazine maleate—may potentiate shock
  • Do not administer detomidine concurrently with potentiated sulfonamides (e.g. trimethoprim–sulfa combinations) because fatal dysrhythmias can result
  • Use caution with corticosteroids—they are reported to cause laminitis

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

Monitor hydration status, electrolytes, and response to analgesics.

Prevention/Avoidance!!navigator!!

  • Do not feed contaminated alfalfa
  • Owners should inspect hay for beetles when feeding. Inspection can be aided by feeding small individual flakes instead of large bales. This may not be possible for hay cubes
  • Cut hay before the bloom stage so plants do not attract adult blister beetles. First cutting and late cuttings are often safer because they are before and after peak beetle activity, respectively
  • Avoid driving equipment over and crushing standing or cut hay

Possible Complications!!navigator!!

  • Complications are unusual, but laminitis has been reported
  • Any time the heart is damaged, there could be the possibility of sudden death

Expected Course and Prognosis!!navigator!!

  • Prognosis ranges from poor to excellent and depends on the amount of cantharidin ingested, early recognition of intoxication, and aggressiveness of therapy
  • A more favorable prognosis may be given if the animal survives for 2–3 days after toxin exposure

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Pregnancy/Fertility/Breeding!!navigator!!

Use corticosteroids with caution in pregnant mares.

Synonyms!!navigator!!

  • Blister beetle poisoning
  • Equine cantharidiasis

Abbreviations!!navigator!!

  • AC = activated charcoal
  • GC-MS = gas chromatography mass spectrometry
  • GI = gastrointestinal
  • HPLC = high-pressure liquid chromatography

Suggested Reading ⬆ ⬇

Gwaltney-Brant SH, Dunayer EK, Youssef HY. Terrestrial zootoxins. In: Gupta RC, ed. Veterinary Toxicology: Basic and Clinical Principles. San Diego, CA: Elsevier, 2012:969–992.

Stair EL, Plumlee KH. Insects. In: Plumlee KH, ed. Clinical Veterinary Toxicology. St. Louis, MO: Mosby, 2004:101–103.

Author(s) ⬆

Author: Scott L. Radke

Consulting Editors: Wilson K. Rumbeiha and Steve Ensley

Acknowledgment: The editors acknowledge the prior contribution of Sandra E. Morgan.