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125.e2 Blue-Green Algae Toxicosis

Blue-Green Algae Toxicosis
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propel toxic algae to the shoreline, where
BASIC INFORMATION
carbamate insecticides, organochlorines
animals are exposed when they drink BGA- • Neurotoxic agents: organophosphate and
Definition contaminated water.
Syndrome characterized by a sudden onset of • Backyard fountains can also grow BGA, and Initial Database
neurologic signs or acute liver failure in dogs pets have been exposed during the cleaning • Hepatotoxic syndrome
as a result of ingestion of blue-green algae process (e.g., drinking out of bucket contain- ○ CBC: leukocytosis and thrombocytopenia
(BGA) toxins ing algae). ○ Serum biochemistry panel: significant
• Common toxin-producing genera of fresh increase in liver enzymes, glucose, and
Synonym and brackish water BGA include Microcystis, possibly creatine phosphokinase. Hypo-
Cyanobacteria toxicosis Anabaena, Oscillatoria, Aphanizomenon, glycemia is possible after hyperglycemia.
Nodularia, and Nostoc spp. ○ Serum bile acids: increase commonly
Epidemiology • Acute hepatotoxic syndrome occurs early
SPECIES, AGE, SEX ○ Most commonly described poisoning by ○ Coagulation profile: whole blood clotting
• Dogs: all breeds, ages, and both sexes BGA; caused by low-molecular-weight time may be normal initially; prothrombin
susceptible cyclic heptapeptides and pentapeptides time and activated thromboplastin times
• Cats: not reported known as microcystins and nodularins. increase twofold to fourfold.
Microcystin-LR (MCLR) is the most • Neurotoxic syndrome
RISK FACTORS toxic and the most frequently encoun- ○ Because of rapid effect of the toxins, no
BGA blooms are favored by stagnant water, tered of approximately 50 similar significant serum biochemical changes are
warm water temperatures, ample sunlight, and peptides. expected.
high nutrient levels from fertilizer, animal waste, ○ After ingestion, BGA toxins are preferen-
and sewage runoff. tially absorbed from the ileum. Advanced or Confirmatory Testing
○ Once inside hepatocytes, toxins inhibit • Postmortem (hepatotoxicosis): rounding of
GEOGRAPHY AND SEASONALITY protein phosphatases (PPs) types 1 and hepatocytes, disruption of hepatic cords, loss
Blooms occur mostly in summer or fall. 2A (PP1 and PP2A), causing hyperphos- of sinusoidal integrity, intrahepatic hemor-
phorylation of cytosolic and cytoskeletal rhage, and centrilobular necrosis
Clinical Presentation proteins, leading to cytoskeletal disrup- • Neurotoxic syndrome: acetylcholinesterase
DISEASE FORMS/SUBTYPES tion, damage, and necrosis. levels are decreased peripherally (blood) but
• Acute neurotoxic syndrome ○ Death is possibly due to massive intra- normal in brain and retina
• Subacute hepatotoxic syndrome hepatic hemorrhage, hypovolemia, shock, • Microscopic identification of toxigenic algae:
and liver failure. obtain large specimen (1-2 L) of the algae by
HISTORY, CHIEF COMPLAINT • Peracute neurotoxic syndrome; responsible straining the cells out of the water with cheese-
• History of swimming in or drinking water toxins cloth. Specimens can be sent for identification,
from a pond, lake, or river ○ Anatoxin-a: an alkaloid and potent purification, and quantification of algal toxins;
• Vomiting, diarrhea, weakness, and collapse postsynaptic depolarizing neuromuscular for mouse bioassay; or for ELISA.
(>6 hours after exposure): hepatotoxic blocking agent that affects nicotinic and
syndrome muscarinic acetylcholine receptors TREATMENT
• Salivation, vomiting, diarrhea, dyspnea, ○ Anatoxin-a(s): inhibits peripheral (but not
tremors, muscle fasciculations, ataxia, weak- central) cholinesterase irreversibly and Treatment Overview
ness, seizures, and death (>15 minutes after is the only known naturally occurring Early decontamination (induce emesis and give
exposure): neurotoxic syndrome organophosphorus cholinesterase inhibitor charcoal) of patients not showing clinical signs.
(similar to organophosphate pesticides) For overtly ill patients, treatment of muscarinic
PHYSICAL EXAM FINDINGS and central nervous system (CNS) signs, preven-
• Presence of algae on the muzzle or fur. Bluish DIAGNOSIS tion/treatment of liver damage, and supportive
green and slimy or may be dried if later care are cornerstones of therapy.
presentation Diagnostic Overview
• Hepatotoxic syndrome: see History, Chief A tentative diagnosis is based on history of Acute General Treatment
Complaint, above. Pale mucous membranes, exposure (drinking or swimming in a pond) • Decontamination of patient
poor capillary refill time, tachycardia or and rapid onset of clinical signs (vomiting, ○ Emesis: in asymptomatic animals
bradycardia, signs of abdominal pain, rapid shock, liver failure, or neurologic signs). Given ○ Activated charcoal 1-2 g/kg PO
weak pulse, hypothermia, and shock the potential speed and intensity of progression, ○ Cholestyramine 300 mg/kg PO q 4-6h
• Neurotoxic syndrome: see History, Chief treatment may be initiated on this basis. Toxi- for 3 days may be more effective than
Complaint above. cosis can be confirmed by purification and charcoal (can be obtained from a human
identification of toxins, but turnaround time pharmacy).
Etiology and Pathophysiology means these methods are not clinically useful ○ Noncompetitive bile acid transport inhibi-
• BGA are microscopic organisms that form for an affected patient (rather for preventative tors, rifampin, and bile salts such as
colonies visible to the naked eye, rely on purposes or medicolegal reasons). ELISA tests cholate and deoxycholate can inhibit
photosynthesis for energy, and have a cell and liquid chromatography tests are available uptake of microcystins. Their usefulness,
wall similar to gram-negative bacteria. for water testing. however, in clinical algal toxicoses has not
• Accumulations of large amounts of BGA in been determined.
lakes, ponds, or rivers are known as water- Differential Diagnosis • Control muscarinic and neurologic signs.
blooms. BGA blooms are light to dark green • Hepatotoxic agents: Amanita mushroom, sago ○ Atropine sulfate for muscarinic signs:
or sometimes reddish brown. Wind can palm, acetaminophen, iron, xylitol, arsenic 0.04-0.1 mg/kg IV prn

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