Page 813 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

772 SECTION | XI Bacterial and Cyanobacterial Toxins

VetBooks.ir MISCELLANEOUS FRESHWATER Australia, New Zealand, and Asia (Hawkins et al., 1997;
Saker and Griffiths, 2001; Fastner et al., 2003), but it
CYANOBACTERIAL TOXINS
should be considered a potential worldwide problem.
Although microcystin and anatoxin poisonings comprise
the majority of cases reported in animals, other cyanotoxins Cylindrospermopsin and deoxycylindrospermopsin have
been produced by C. raciborskii (Ohtani et al., 1992), and
are of concern. Dermatotoxic cyanobacterial toxins have 7-epicylindrospermopsin has been produced by
been reported to cause “swimmers’ itch” in Hawaii Aphanizomenon ovalisporum (Banker et al., 1997). After
(Serdula et al., 1982) and have recently been associated oral exposure, the LD 50 of cylindrospermopsin obtained
with dermatitis in a dog (Puschner et al., 2017). with culture extracts of C. raciborskii ranged from 4.4 to
In the documented case a dog developed severe pruritis, 6.9 mg/kg in equivalent cylindropsermopsin (Seawright
urticarial, and malaise after swimming in a freshwater et al., 1999; Shaw et al., 2000).
lake in California. Phycological and toxicological Nodularins are cyclic pentapeptides that lead to severe
evaluation revealed the presence of Anabaena/Trichormus hepatotoxicosis in the same way as microcystins (Harding
sp. and Lyngbya sp. and debromoaplysiatoxin. et al., 1995; Ufelmann and Schrenk, 2015). In addition,
Debromoaplysiatoxin can be produced in the marine and nodularin is a more potent tumor promoter than microcys-
freshwater environment and is a known dermatotoxin tin (Sueoka et al., 1997; IARC, 2006; Ufelmann and
(Kaneshima et al., 1983). In addition, debromoaplysiatoxin Schrenk, 2015). The only cyanobacterium species known
exposure may occur along with exposure to other cyanotox- to produce nodularin is Nodularia spumigena. This cyano-
ins and result in a complex clinical presentation. Saxitoxins bacterium can form extensive blooms in the Baltic Sea
and derived forms belong to the group of paralytic shellfish and in brackish waters in the summer (Francis, 1878;
poisoning (PSP) toxins and have been produced by a num- Sivonen et al., 1989). The risk of nodularin intoxication is
ber of freshwater cyanobacteria, including A. flos-aquae, twofold because toxin exposure can occur not only
Cylindrospermopsis raciborskii, Anabaena circinalis, through recreational or drinking water but also via con-
Lyngbya wollei, Planktothrix sp., and Aphanizomenon grac- tamination of seafood (Van Buynder et al., 2001). In cases
ile (Carmichael et al., 1997; Kaas and Henriksen, 2000; of acute hepatotoxicity, exposure to microcystins as well
Molica et al., 2005; Ballot et al., 2010). All saxitoxin ana- as nodularins must be considered.
logs have high toxicity in mammals by blocking voltage- β-N-methylamino-l-alanine (BMAA), a neurotoxic
gated sodium channels, leading to respiratory arrest, neuro- amino acid found globally is thought to be produced by all
muscular weakness, and cardiovascular shock. Massive fish cyanobacterial taxa and has been implicated in avian vacu-
mortalities have been linked to saxitoxins produced by both olar myelinopathy (Bidigare et al., 2009). BMAA can
freshwater cyanobacteria and marine dinoflagellates bioaccumulate in food chains such as fish and seafood and
(Pearson et al., 2010; Moustaka-Gouni et al., 2017). is of considerable human health concern because of its
Whereas intoxications of birds and cats have been associ- ability to destroy motor neurons in the brain, leading to
ated with ingestion of PSP contaminated fish and clams neurodegenerative diseases likes Parkinson’s disease,
(Landsberg, 2002), there is only one confirmed report of Alzheimer’s, and ALS, commonly referred to as the human
PSP toxin-associated mammalian mortality from exposure amyotrophic lateral sclerosis parkinsonism dementia
to contaminated freshwater (Negri et al., 1995). Fourteen complex of Guam (Guam ALS-PD) and lathyrism (Bradley
sheep showed signs of trembling, recumbency, and death in and Mash, 2009). Birds with avian vacuolar myelinopathy
Australia after exposure to toxic concentrations of PSPs develop ataxia, tilting, weakness, and death, and they have
produced by A. circinalis. Because PSP toxins are produced characteristic postmortem lesions of bilateral symmetrical
by several species of freshwater cyanobacteria, terrestrial vacuolation of the white matter of the brain and spinal cord
animals and humans are at risk of being exposed to these (Thomas et al., 1998). Monitoring of water for BMAA is a
toxins. Thus, it is important to reliably evaluate animals critical tool to assess nutrient reduction and to develop
with neurologic signs after access to freshwater for possible control strategies.
PSP exposure because the risk certainly exists.
Another cyanotoxin, the alkaloid cylindrospermopsin,
has caused deaths in cattle (Saker et al., 1999) and severe CONCLUDING REMARKS
gastrointestinal disease in humans. Cylindrospermopsin is AND FUTURE DIRECTIONS
a potent inhibitor of protein synthesis and can lead to var-
ious degrees of injury to the liver, kidneys, adrenal gland, The frequency and extent of harmful cyanobacterial
intestine, lung, thymus, and heart (Griffiths and Saker, blooms appears to increase with the addition of nutrients
2003). Furthermore, this cyanotoxin is of particular con- to surface freshwater ecosystems throughout the world.
cern because of its mutagenic and possibly carcinogenic As demonstrated in Table 57.1, numerous cyanobacterial
activities. Cylindrospermopsin has been found in Europe, species have the potential to produce a number of toxins