Abstract

Starting in the fall of 2004, state agencies in Maryland were notified of morbidity and mortality events involving dogs, possible algal toxin water exposure, and ingestion of dark false mussels (Mytilopsis leucophaeata). Eight dogs presented at an emergency clinic with vomiting (some vomited mussels), diarrhea, depression, and acute liver failure and four dogs died (50%). In 2004–2005, clinic records from the dogs were compared for notable common parameters including age, species, sex, location, algal bloom proximity, vaccination history, clinical signs, chemistry profiles, CBCs, and medications. No common etiology was determined. Only one carcass was available for post mortem examination; histopathology results indicated a severely affected "end-stage" liver and a chronic condition. No algal toxins were detected in liver tissue. Four (50%) dogs were Labrador retrievers.

Again in the fall of 2014, dogs in the same county were reported with similar histories of mussel ingestion and liver failure. Records from 18 dogs that presented to the emergency clinic from October 29, 2014–January 15, 2015 were assessed as in 2004. No common cause for the illness was determined. Seven of 18 (39%) dogs were Labrador retrievers or Labrador mixes. A letter was distributed to area veterinarians urging them to contact authorities to report dogs with liver failure and known or suspected ingestion of mussels. During November 2015–January 2016, three dogs were reported in liver failure with a history of dark false mussel ingestion. One carcass from a Labrador retriever known to ingest mussels scraped from the bottom of a boat was made available for necropsy and toxicological examination. Implicated mussels were also examined. Notable findings on gross examination included dehydration, icterus, hemorrhage in the duodenum and colon and approximately 1 L of bloody fluid in the peritoneal cavity. Histopathologic examination revealed severe, diffuse, acute hepatic necrosis and moderate, multifocal, mural hemorrhage in the duodenum. The remaining viable hepatocytes were noted to variably contain some copper positive pigment; however, the copper did not resemble what is typically seen in canine copper storage disease. No algal toxins (anatoxin, microcystins, nodularin) were detected. Only pentobarbital (euthanasia solution) was detected on the GC/MS organic chemical screen. The complete mineral screen revealed a copper level in the liver of 144 ppm wet weight (normal 30–100; elevated 250–400; toxic > 400) and a copper level in the kidney of 62.8 ppm wet weight (normal 5–15; toxic > 20). The final diagnosis was acute copper toxicity, but the source of the copper is still unknown; antifouling paint is one possibility. Mussel analysis is pending and could potentially help determine the source.

Acknowledgements

The authors wish to thank the owners of affected dogs for allowing us to analyze diagnostic test results from affected animals, cooperating veterinarians in Anne Arundel County, Laine Songer, and staff at the University of Pennsylvania, and the MD Departments of Agriculture, Environment, Health and Mental Hygiene and Natural Resources.

* Presenting author

Literature Cited

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