Presumptive monensin toxicosis in a 6-month-old dog

Felipe Reggeti, Matthew Kornya

Animal Health Laboratory, University of Guelph, Guelph, ON (Reggeti); Ontario Veterinary College, Clinical Studies, University of Guelph (Kornya).

AHL Newsletter 2024;28(2):32.

A 6-month-old intact male bloodhound presented to the Ontario Veterinary College (OVC) with a 2-3 day history of progressive ataxia, hind limb weakness, lethargy and red-brown discolored urine.

The CBC showed an inflammatory leukogram, as indicated by mild neutrophilic leukocytosis with a regenerative left shift and evidence of neutrophil toxicity, consisting of cytoplasmic basophilia and identification of Döhle bodies (Table 1). The biochemistry profile showed a markedly elevated activity of the enzymes creatine kinase (CK) and alanine-amino transferase (ALT), as well as a moderate hyperphosphatemia (Table 1). These findings were consistent with severe myopathy. Although ALT is relatively “liver specific” in dogs, and elevated activity in this case might have resulted from concomitant liver damage, the enzyme is also present in striated skeletal and cardiac muscle, and the elevated serum activity could have also resulted from severe muscle damage.

Table 1. CBC and biochemistry significant abnormalities.

Table 1. CBC and biochemistry significant abnormalities.

Urine was collected via cystocentesis. The urinalysis revealed a concentrated red urine that was highly positive for “protein” and “blood” on the reactive strip, with only rare erythrocytes noted on the sediment (Table 2). These findings ruled out hematuria. Since the animal was not anemic and there were no signs of hemolysis, the red discoloration of the urine and positive result for “blood” were interpreted as myoglobinuria, consistent with other laboratory findings supporting myopathy (rhabdomyolysis).

Table 2. Urinalysis

Table 2. Urinalysis

Supportive care was provided, including sedation, anxiolytics and IV fluids. The patient improved clinically, did not develop signs of cardiac disease and was discharged after a few days in the hospital. This dog lived on a farm and was seen consuming calf feed medicated with monensin. Based on this observation, clinical presentation and laboratory findings, a clinical diagnosis of monensin toxicosis was made.

Monensin is an ionophore antibiotic used as a feed additive in approved livestock species (poultry and cattle) due to anti-coccidial properties and enhancement of feed efficiency (Canada); and to reduce the incidence of ketosis in peri-parturient dairy cattle (Europe). However, incorrect dosing or exposure of non-target species (e.g., dogs and horses) may result in toxicosis and mortality. Although cases of monensin toxicosis in dogs are relatively uncommon, it is important to be aware of its potential toxicity and to take the necessary precautions to minimize the risk of exposure. A few reports in the UK raised concerns for increased frequency of cases in dogs leading to updated warnings on the safety of these products and the suggested “Guidelines for treatment of monensin toxicosis in dogs”.  AHL

References

1. Bates N, Edwards N. Monensin toxicity in dogs. Vet Rec 2016;178(25):638-9.

2. Hutchings F. Risk of monensin toxicity for dogs. VetRec 2022;190(1):39.

3. Anon. Guidelines for treatment of monensin toxicosis in dogs. SafetyCall International. www.myelanco.co.uk/pub/monensin-toxicityin-dogs