Introduction

• Cause: ingestion of cyanobacterial species known to produce toxins under certain conditions.
• Seasonal heavy growths between June and December.
• Signs: toxicity → wide range clinical signs including neurotoxicosis, hepatotoxicosis, nephrotoxicosis or a combination if more than one cyanobacterial species involved.
• Diagnosis: history, clinical signs, identification of algae.
• Treatment: fluid therapy, emetics, activated charcoal.
• Prognosis: poor - animals can recover → treatment worthwhile.

Pathogenesis

Etiology

• Exposure to toxins in water courses.
• 'Algal blooms' occur on warm sunny days of late spring/summer .
• High levels of nitrogenous compounds in water.
• A high percentage of cyanobacteria produce toxins (hepatotoxins, cytotoxins, neurotoxins).
• The relative concentration of each of the above varies with different species of cyanobacteria.
• Blooms often have many constituent species and although there is usually a dominant type, there may be several toxins causing toxicosis.

Predisposing factors

• Dogs which have a liking for water, eg gun dogs. Retrievers are particularly at risk.
• Whilst some animals show aversion to algal blooms, dogs show a preference for cyanobacteria infested water even when given a clean water alternative.

Pathophysiology

• Cyanobacteria often, but not always, have a blue-green color (can also be red, brown and black).  
• It is believed that cyanobacterial toxicoses are associated with scums accumulating along leeward shores through wind and water movement → degeneration of the algae → release of intracellular toxins into the surrounding environment.
• Dogs ingest this toxin while drinking, swimming or grooming → signs of alpha cyanobacterial species.
• Toxic effects vary depending on:
  • Cyanobacterial species.
  • Stage of decomposition.
  • Ingested dose.

• The principal documental syndromes are:
  • Acute hepatotoxicosis: caused by cyclic peptides → rounding and dissociation of hepatocytes → necrosis. Death results from hypovolemic shock Shock with hyperkalemia Hyperkalemia and/or hypoglycemia Hypoglycemia in protracted cases.
  • Nephrotoxicosis: tubular necrosis nephrosis has been reported in addition to hepatic changes.
  • Peracute neurotoxicoses: caused by depolarizing agent anatoxin-a (bicyclic secondary amine) → nicotinic receptors → respiratory paralysis → death. Death due to respiratory failure is also caused by anatoxin-a(s) (unstable cholinesterase inhibitor).
  • Gastrointestinal upset: often accompanies above syndromes and may be primary presenting sign. This might be due, in part, to the action of cyanobacterial liposaccharide endotoxins.
  • Some further toxins are cytotoxic.
  • Hepatotoxins suspected of → neoplasia (similar in action to okadeic acid).

Timecourse

• Neurotoxicosis: sudden death or severe distress/convulsions within 15 minutes of ingestion.
• Hepatotoxicosis: slower, less dramatic onset.
• Course of disease: hours - several days.

Diagnosis

Treatment

Prevention

Outcomes