Hazardous algal blooms: Pets (and people) beware! (Proceedings) - Veterinary Healthcare
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Hazardous algal blooms: Pets (and people) beware! (Proceedings)


CVC IN SAN DIEGO PROCEEDINGS


Cyanobacterial Toxins

Cyanobacteria is another name for blue-green algae. Not all algae produce toxins. Cyanobacteria intoxication is most commonly associated with ingestion of water with excessive growth of Anabaena spp., Aphanizomenon spp., Oscillatoria spp., which produce the neurotoxins anatoxin-α and anatoxin-α(s); Microcystis spp., which produces the hepatotoxin microcystin; or Nodularia spp., which produces the hepatotoxin nodularin. Cyanobacteria ingested with water can be rapidly broken down in the gastrointestinal tract. In the acidic environment of the stomach, the bacteria are lysed with the resulting release of toxins. Free toxins can be rapidly absorbed from the small intestine. The microcystins are transported to the liver and enter this organ using a bile acid transporter.

The hepatotoxic microcystins and nodularin alter the cytoskeleton of liver cells. Microcystins bind covalently to and inhibit the function of the protein phosphatases, which regulate the phosphorylation and dephosphorylation of regulatory intracellular proteins. In vitro, microcystins act on intermediate filaments (vimentin or cytokeratin), microtubules, and microfilaments causing altered structural integrity of these cytoskeletal elements. Microcystins have also induced apoptosis in a variety of mammalian cells in vitro. Microcystins cause immediate blebbing of the cell membranes, shrinkage of cells, organelle redistribution, chromatin condensation, DNA fragmentation, and DNA ladder formation.

The neurotoxin anatoxin-α, most commonly produced by Anabaena flos-aquae, is a bicyclic secondary amine that causes depolarization of nicotinic membranes. The depolarization of neuronal nicotinic membranes is rapid and persistent and can lead to respiratory paralysis. The neurotoxin anatoxin-α(s) inhibits acetylcholinesterase in the peripheral nervous system. This toxin does not appear to cross the blood-brain barrier.

Risks associated with intoxication are dependent on the occurrence of certain environmental factors that promote algal growth. These factors include warm weather, increased nutrients in a body of water, and wind. A rapid increase in the growth of an algae "bloom" is more commonly noted in warm weather during the late summer and early fall. Rapid algal growth is enhanced by increased nitrogen and phosphorus in the water, which may be more prevalent in ponds that receive runoff from fertilized fields. Increased wind activity concentrates the cyanobacteria along the shoreline of the pond or lake, thereby increasing the risk of exposure.

Ingestion of water that contains cyanobacteria or their associated toxins can result in acute death with few clinical signs. Within 1 to 4 hours, animals that ingest microcystin or nodularin can present with a myriad of clinical signs that generally relate to damage of the liver such as lethargy, vomiting, diarrhea, gastrointestinal atony, weakness, and pale mucous membranes. Death often occurs within 24 hours, but may be delayed several days. Animals that ingest anatoxin-α can present acutely with muscle tremors, rigidity, lethargy, respiratory distress, and convulsions. Death from respiratory paralysis can occur within 30 minutes from the onset of clinical signs. Following ingestion of anatoxin-α(s), animals may present with signs consistent with inhibition of cholinesterase such as increased salivation, urination, lacrimation, and defecation as well as tremors, dyspnea, and convulsions. Death from respiratory arrest can occur within 1 hour.

Animals intoxicated with microcystin-producing cyanobacteria have elevated serum concentrations of hepatic enzymes. anatoxin-α(s) depresses the blood cholinesterase activity, but not the brain cholinesterase activity because it does not cross the blood-brain barrier.

Microcystin intoxication results in an enlarged liver that is congested and dark in color (hemorrhagic). Hepatic enlargement is thought to be a result of intrahepatic hemorrhage. Histologic examination of the liver reveals a centrilobular to midzonal necrosis and hemorrhage. Gross and microscopic lesions are typically not noted following intoxication with the anatoxins or saxitoxin.

A diagnosis of blue-green algal intoxication relies on the history, compatible antemortem and postmortem findings and detection of an algal toxin. A water sample should be carefully taken from the area of greatest concentration of algae. Examination of fresh or formalin-preserved samples using light microscopy identifies the toxin-producing cyanobacteria. A sample of the water might be used in a mouse bioassay or analyzed by mass spectrometry. It is also important to identify a toxin in a biological sample; presently analysis of a GI sample is the best way to confirm ingestion.

None of the cyanobacteria have antidotes. Therefore, therapy is directed toward symptomatic and supportive therapy. Decontamination of dogs includes induction of emesis if vomiting has not already occurred, administration of activated charcoal and a cathartic, and bathing if algae remain on the haircoat. Unfortunately, the rapid onset of clinical signs following toxin ingestion often precludes effective decontamination. Animals that present with signs associated with the hepatotoxic algae should be aggressively treated with fluids, corticosteroids, and other elements of shock therapy. Use of hepatoprotectants such as N-acetycysteine, silymarin or SAMe might be considered although their efficacy is unproven. Animals that present with signs associated with the neurotoxic algae require respiratory support and seizure control as needed. Additionally, animals with anatoxin-α(s) toxicosis may be treated with atropine to reverse muscarinic signs. Animals that exhibit clinical signs of intoxication have a poor to grave prognosis, depending on the amount of toxin consumed.

The key control measure is to limit or eliminate animal exposure to water containing the algae. The use of copper sulfate as an algaecide in ponds with a cyanobacterial bloom may be beneficial. After treatment with copper sulfate, animals must be removed from the water source for a period of 3 to 7 days to allow for the degradation of the cyanobacterial toxins. Many recreational bodies of water are monitored for the presence of blue-green algae and their associated toxins. If a health risk is identified, public notices or warnings are often displayed.


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