Investigation of a Microcystis aeruginosa cyanobacterial freshwater harmful algal bloom associated with acute microcystin toxicosis in a dog

dc.citation.doi10.1177/1040638712445768en_US
dc.citation.epage687en_US
dc.citation.issue4en_US
dc.citation.jtitleJournal of Veterinary Diagnostic Investigationen_US
dc.citation.spage679en_US
dc.citation.volume24en_US
dc.contributor.authorvan der Merwe, Deon
dc.contributor.authorSebbag, Lionel
dc.contributor.authorNietfeld, Jerome C.
dc.contributor.authorAubel, Mark T.
dc.contributor.authorFoss, Amanda
dc.contributor.authorCarney, Edward
dc.contributor.authoreiddmerween_US
dc.contributor.authoreidjcnietfeen_US
dc.date.accessioned2012-09-26T16:48:34Z
dc.date.available2012-09-26T16:48:34Z
dc.date.issued2012-05-17
dc.date.published2012en_US
dc.description.abstractMicrocystin poisoning was diagnosed in a dog exposed to a Microcystis aeruginosa dominated freshwater harmful algal bloom at Milford Lake, Kansas, which occurred during the summer of 2011. Lake water microcystin concentrations were determined at intervals during the summer, using competitive enzyme-linked immunosorbent assays, and indicated extremely high, localized microcystin concentrations of up to 126,000 ng/ml. Multiple extraction and analysis techniques were utilized in the determination of free and total microcystins in vomitus and liver samples from the poisoned dog. Vomitus and liver contained microcystins, as determined by enzyme-linked immunosorbent assays, and the presence of microcystin LR was confirmed in vomitus and liver samples using liquid chromatography coupled with tandem mass spectrometry. Major toxic effects in a dog presented for treatment on the day following exposure included fulminant liver failure and coagulopathy. The patient deteriorated rapidly in spite of aggressive treatment, and was euthanized. Postmortem lesions included diffuse, acute, massive hepatic necrosis and hemorrhage, and acute necrosis of the renal tubular epithelium. A diagnosis of microcystin poisoning was based on the demonstration of M. aeruginosa and microcystin-LR in the lake water, as well as in vomitus produced early in the course of the poisoning, the presence of microcystin-LR in liver tissue, and on a typical clinical course.en_US
dc.identifier.urihttp://hdl.handle.net/2097/14760
dc.relation.urihttp://doi.org/10.1177/1040638712445768en_US
dc.subjectMicrocystis aeruginosaen_US
dc.subjectMicrocystinen_US
dc.subjectLiver failureen_US
dc.subjectRenal failureen_US
dc.titleInvestigation of a Microcystis aeruginosa cyanobacterial freshwater harmful algal bloom associated with acute microcystin toxicosis in a dogen_US
dc.typeArticle (author version)en_US

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Figure 1. Liver in which there is acute, diffuse necrosis and hemorrhage with almost complete loss of hepatocytes. Hematoxylin and eosin stain. Bar = 100 μm.
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Figure 2. Photomicrograph of kidney with multiple groups of acutely necrotic tubules in which the epithelium is brightly eosinophilic and individual cells have lost their nuclei or the nuclei are karyorrhectic (arrows). Note that adjacent to necrotic tubules are tubules with intact epithelium with viable appearing nuclei and that glomeruli are normal and that erythrocytes are still intact and individualized. H&E stain, bar = 100 μm.
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Figure 3. Photomicrograph of kidney with acutely necrotic tubules in the upper one third of the photograph. Note the intact, vacuolated proximal convoluted tubular epithelium (arrows) and the intact distal convoluted tubule (arrowhead) that contains a group of sloughed, necrotic epithelial cells. H&E stain, bar = 25 μm.
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Figure 4. Spherical Microcystis aeruginosa colonies forming roughly circular mats of closely packed individual organisms in vomitus from a dog that ingested lake water during an algal bloom. Unstained. Bar = 100 μm.

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