Blue-Green Algae Poisoning in Animals
Summary: The growth of highly toxic blue-green algae
can occur in the waters of Indiana.
Poisoning by the neurotoxins causes rapid death with or
without signs of cholinesterase inhibition. Poisoning by
the hepatotoxins causes massive liver necrosis with severe
intrahepatic hemorrhage and death. Diagnosis is based on
history of exposure, clinical signs, blue-green algae in
the GI tract, and necropsy findings.
Introduction: Blue-green algae are not true algae,
but are cyanobacteria which grow in fresh water in temperate
areas world-wide, including Indiana.
Under the appropriate weather and water conditions, usually
in the late summer or fall after a drought, the blue-green
algae can form a rapidly growing "bloom". These
blooms can occur in farm ponds and larger bodies of water
forming a thick, often foul-smelling scum of brown, to green,
to blue-green algae. Winds can then blow the blue-green
algae to the shore and concentrate it wlierethe animals
have to drink it with the water. In many instances, the
algae will not be poisonous. However, sometimes, for unknown
reasons, the blue-green algae in these blooms form ncuroloxinsor
hepatotoxins which can prove deadly to animals drinking
the water.
Neurotoxins: Two neurotoxins can be produced
by blue-green algae: anatoxin-a oranatoxin-a(s). The neurotoxins
produced are extremely poisonous and can kill within a few
minutes. They are so toxic that the animals are sometimes
found dead next to the contaminated water. Animals poisoned
with anatoxin-a show a rapid onset of rigidity and muscle
tremors followed by paralysis, cyanosis, and death. Poisoning
with anatoxin-a(s) (s is for salivation) causes cholinesterase
inhibition similar to organophosphorous/ carbamate insecticides.
Therefore, the clinical signs are excessive salivation,
diarrhea, urination, and death. In lethal cases, the nicotinic
signs of tremors, incoordination, and paralysis may also
be present. Anatoxin-a(s) does not appear to cross the blood-brain
barrier so brain cholinesterase is not inhibited. Poisoning
with either anatoxin-a oranatoxin-a(s) does not result in
gross or microscopic lesions. Therefore, diagnosis is based
on a history of exposure to blue-green algae, clinical signs
and the possible presence of blue-green algae in the GI
tract (see below).
Hepatotoxins: Some species of blue-green algae produce
hepatotoxins: microcystin or nodularin. While extremely
toxic, these do not kill livestock as rapidly as the anatoxins.
Following ingestion of water containing a toxic amount of
these poisons, GI disturbances, characterized by vomiting
(depends on species), abdominal pain, and diarrhea (often
bloody) frequently occur. This is followed by weakness,
lack of responsiveness and death. In the liver, destruction
of hepatocytesoccurs soon after ingestion. Rapid necrosis
of the liver cells often results in severe hemorrhage into
the liver which can cause shock and death. If death due
to shock does not occur, then death results from liver failure
often within 24 hours. In animals which survive, secondary
(hepatogenous)photo-sensitization has been reported. On
post-mortem examination, the liver is often enlarged, swollen
and dark red. In some cases, there is significant edema
around the gall bladder. Histologically, there is massive
liver necrosis with severe intrahepatic hemorrhage.
Diagnosis: Toxicoses due to the neurotoxins or hepatotoxins
are diagnosed based on history of exposure to blue-green
algae in the water, clinical signs, the presence of blue-green
algae in the GI tract and in the cases of the hepatotoxins,
gross and histologic liver lesions. In addition to tissue
samples, a small amount of contents from the duodenum and
upper ileum should be collected and fixed in 10% neutral
buffered formalin (NBF) for identification of blue-green
algae. In cases of suspected blue-green algae poisoning,
the algae should be collected from the suspected source
soon after the incident. Great care should be taken to insure
safety of the collectors. A gallon of the blue-green algae
cells should be collected for toxin identification. Additionally,
a 5 ml sample of cells should be mixed with an equal volume
of 10% NBF to fix them for identification.
- by Scott Wallace, Class of 1997
- edited by Toxicology:
- Jennifer Harms, BS, Toxicology Technician,
- Christina Wilson, BS, Assistant Chemist,
- RobertEverson,PhD, Analytical Chemist
- Stephen Hooser,DVM, PhD, Toxicologist
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