A 3-year-old Cairn Terrier dog that had been in contact with sea water containing cyanobacteria (blue-green algae) was euthanized because of acute hepatic failure and anuria after a 5-day illness. Histologic findings included lytic and hemorrhagic centrilobular hepatocellular necrosis and renal tubular necrosis. The cyanotoxin nodularin was detected in liver and kidney by highperformance liquid chromatography-mass spectrometry. Nodularin is a potent hepatotoxin produced by the algal species Nodularia spumigena. The intensity of algal blooms has increased during the past decades in the Baltic Sea region, thus increasing the risk for intoxications in domestic and wild animals. The authors describe the pathologic findings of cyanobacterial toxicosis in a dog with direct identification of the toxin from organ samples.Keywords cyanobacterium, dog, hepatic necrosis, kidney, liquid chromatography-mass spectrometry, liver, nodularin, renal tubular necrosis Hepatic necrosis due to toxins produced by blue-green algae (cyanobacteria) is a well-known cause for acute hepatic failure and death in wild and domestic animals. Although at least 40 species of cyanobacteria, with worldwide distribution, can synthesize a range of hepatotoxins, neurotoxins, and dermatotoxins, the threat of cyanotoxin-contaminated water is often ignored.
3,24Blooming of blue-green algae, especially the toxigenic species Nodularia spumigena, occurs annually in the Baltic Sea region, presenting a threat for animals exposed to contaminated water. Previously, the identification of blue-green algal toxin was laborious, requiring water samples and the use of experimental animals; 5,6,10,16,25,26 algal toxins have not been analyzed routinely from animal tissues in diagnostic cases. In this report, blue-green algal toxicosis was confirmed by direct toxin analysis from organ samples.
Case HistoryA 3-year-old female Cairn Terrier weighing 9.6 kg was exposed to sea water containing blue-green algae in the Finnish southwest coastal region of the Baltic Sea. The exact route of exposure is uncertain; the dog was not seen swimming in the sea but may have consumed algal scum or drunk contaminated water. Subsequently, the dog became acutely lethargic with vomiting and inappetence. Initially, it was treated supportively with antiemetics and fluid therapy. Three days after the onset of clinical signs, the dog was admitted to the university hospital because of further clinical deterioration.Upon physical examination, the dog was lethargic, dehydrated, and icteric. Abnormal hematologic findings included mild nonregenerative anemia (packed cell volume, 32%; reference range, 38%-57%; mean corpuscular volume and hemoglobin within reference ranges) with normal leukocyte count (14.0 Â 10 9 /liter; reference range, 5.4-17.4 Â 10 9 /liter). Serum biochemistry profile abnormalities included elevated alanine aminotransferase (6211 U/liter; reference range, 18-77 U/liter), alkaline phosphatase (392 U/liter; reference range, 33-215 U/liter), total bilirubin (272.5 mmol/liter...