Page 812 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Cyanobacterial (Blue-Green Algae) Toxins Chapter | 57 771

VetBooks.ir dog deaths in New Zealand (Wood et al., 2007). In Treatment
addition to being a nicotinic agonist, homoanatoxin-a
There is no specific antidote for anatoxin-a. Because of
can increase the release of acetylcholine (ACh)
from peripheral cholinergic nerves through opening of the rapid onset of clinical signs, emesis is not likely to be
21 useful. Although no studies have evaluated the efficacy of
endogenous voltage-dependent neuronal L-type Ca
specific decontamination procedures, administration of
channels (Aas et al., 1996).
activated charcoal has been recommended. In addition,
Anatoxin-a(s) is different from anatoxin-a and
artificial respiration may be of benefit along with general
homoanatoxin-a. This neurotoxin has a unique chemical
supportive care. Specific measures to control seizures
structure and is a naturally occurring irreversible acetyl-
include benzodiazepines, phenobarbital, or pentobarbital.
cholinesterase (AChE) inhibitor. The increased concentra-
If given, they may cause CNS and respiratory depression,
tions of ACh in the synapse lead to persistent stimulation,
and careful monitoring of the animal is necessary. In any
followed by a neuronal muscular block (Cook et al.,
seizuring animal, control of body temperature is an
1990). The mechanism of toxic action is similar to that of
important part of the symptomatic care.
organophosphorus and carbamate insecticides, as well as
Treatment of animals poisoned with anatoxin-a(s) is
some chemical warfare nerve agents (Patocka et al.,
primarily symptomatic and supportive. Decontamination
2011). However, one of the main differences is that ana-
procedures can be considered but have not been
toxin-a(s) acts only in the periphery, whereas the insecti-
evaluated. It has been shown that 2-PAM is not able to
cides inhibit AChE in the brain and retina (Cook et al.,
reactivate the inhibited AChE and is therefore not recom-
1989). Animals poisoned with anatoxin-a(s) show a rapid
mended (Hyde and Carmichael, 1991). Atropine should
onset of excessive salivation (“s” stands for salivation),
be given at a test dose to determine its efficacy in animals
lacrimation, diarrhea, and urination. Clinical signs of nic-
with life-threatening clinical signs. After the test dose,
otinic receptor overstimulation including tremors, incoor-
atropine can be given repeatedly until cessation of saliva-
dination, convulsions, recumbency, and respiratory arrest
tion. It is important to carefully monitor the animal for
are most commonly observed in cases with a lethal out-
anticholinergic effects and to reduce or discontinue atro-
come. Animals often die within 30 min of exposure.
pine if adverse effects develop.
Animals that die from anatoxin-a, homoanatoxin-a, or
As with other cyanobacteria toxins, toxicity is strain
anatoxin-a(s) toxicosis do not show specific gross or
specific, and identification of the cyanobacteria alone can-
microscopic lesions. Anatoxin-a(s) poisoning has been
not predict the toxicity level. Therefore, detection of
reported in pigs, birds, dogs, and calves in the United
anatoxin-a in biological specimens is confirmatory, but
States and Europe (Mahmood et al., 1988; Cook et al.,
these tests are not routinely available (James et al., 1998;
1989; Onodera et al., 1997). Because of the lack of spe-
Puschner et al., 2010). Anatoxin-a was confirmed in stom-
cific detection methods for anatoxin-a(s), the natural
ach content, liver, urine, and bile of dogs (Gugger et al.,
occurrence of this neurotoxin has not been fully
2005; Puschner et al., 2010). In suspect cases, environ-
evaluated.
mental and biological samples should be saved for toxico-
logical and phylogenetic analysis.
Diagnosis of anatoxin-a(s) toxicosis is aided by the
Toxicity determination of blood AChE activity. However, organo-
In mice, the i.p. LD 50 of anatoxin-a is 200 μg/kg (Stevens phosphorus and carbamate insecticides can also inhibit
and Krieger, 1991), whereas the i.v. LD 50 is estimated to AChE, and additional diagnostic workup is needed to
be less than 100 μg/kg. The oral toxicity of anatoxin-a is establish a firm diagnosis. This includes the determination
of brain AChE postmortem (unchanged in cases of ana-
much higher, with an oral LD 50 in mice reported to be
toxin-a(s) poisoning), screening of gastrointestinal con-
greater than 5 mg/kg. Several studies have shown that
tents for insecticides, examination of stomach contents
there are significant species differences with regard to
(possible identification of cyanobacteria), and a careful
anatoxin-a toxicity. Whereas an anatoxin-a containing
evaluation of the environment (access to freshwater and
Aphanizomenon flos-aquae bloom was toxic to sheep after
access to insecticides). Detection methods for anatoxin-a
i.p. administration, oral administration failed to induce
(s) are rare. A biosensor method has been developed that
toxicity (Runnegar et al., 1988). In contrast, calves devel-
allows the quantitation of anatoxin-a(s) in environmental
oped toxicity after oral administration of an anatoxin-a
samples (Devic et al., 2002). New analytical methods for
containing A. flos-aquae bloom (Carmichael et al., 1977).
anatoxin-a(s) are necessary to better document the distri-
The i.p. LD 50 of homoanatoxin-a in mice is 250 μg/kg
bution of this neurotoxin in freshwater worldwide.
(Skulberg et al., 1992). Anatoxin-a(s) is much more toxic
than anatoxin-a or homoanatoxin-a, with an i.p. LD 50 in Phylogenetic analysis of 16 S rRNA gene sequences will
mice of 20 μg/kg (Briand et al., 2003). help in the species identification.