317
Chapter fourteen: Toxicology and poisons
(responsible for some red tides along with Karenia brevis) can be aerosolized by cell lysis
via wave/wind action and has been known to cause respiratory problems in humans and
other mammalian models (Franz and LeClaire 1989; Kirkpatrick et al. 2004). The saxitoxins have been identified as the toxins associated with paralytic shellfish poisoning (PSP)
which has been linked to episodic mass poisonings of humans, marine mammals, and
birds (Van Dolah et al. 2003).
While the co-evolution of chemical warfare between predator and prey has undoubtedly been occurring for millennia, it is perhaps surprising that cetaceans (and pinnipeds)
do not display more resistance to marine biotoxins. Historically, diagnostic methods
have limited the ability to identify or detectably measure algal biotoxins, and thus the
etiology of mass-strandings and die-offs was uncertain. However, with increasingly
sensitive and precise assays, there is now good evidence to suggest that algal biotoxins
are at least partially responsible for previously unexplained unusual mortality events
(UMEs) (Scholin et al. 2000; Van Dolah et al. 2003). The unique nature of HABs, including non-species-specific mortality, has led some to speculate about evidence for massstrandings in fossilized remains from the late Miocene epoch (approximately 7 Mya)
(Pyenson et al. 2014). At a site in the Atacama desert of Chile, Pyenson et al. (2014) found
four layers of multi-species assemblages stratified in the sedimentary substrate, including species of Balaenopteridae, Phocidae, and an aquatic sloth (Thalassocnus natans). The
unique orientation (supine) and proximity of the remains led the authors to conclude
that the individuals died rapidly at sea and were promptly washed ashore (spatial focusing) by the unique structure and currents of the supratidal flat (Pyenson et al. 2014).
While pathology of 6–9 Myr old fossils is undoubtedly filled with uncertainty, it is worth
noting that HABs have likely contributed to the evolution of marine mammals and have
even been hypothesized to have played a role in Phanerozoic mass extinctions (Castle
and Rodgers 2009).
Marine mammal mortality events have been associated with other marine biotoxins
such as domoic acid (Scholin et al. 2000) and brevetoxin (Flewelling et al. 2005). The task of
attributing mass-strandings and die-offs to marine biotoxins is often complicated by other
factors such as viruses, bacteria, and other pathogens as well as nutrition and immunologic
status of the individuals and populations. Rather than being pesky confounding variables,
however, these factors likely contribute to the overall health picture of the animal, and the
balance of two or more factors may well tip the scales from health to outright disease. With
respect to some mortality events documented in the USA, there is very strong diagnostic
evidence that some HAB-related mortality events for certain species are now considered
endemic (e.g., California sea lions and domoic acid, manatees and brevetoxin; F. Gulland,
pers. comm.).
Since most marine mammal species are not directly consuming the toxin-producing
organisms, it is important to consider the trophic transfer and biotransformation of biotoxins. For instance, Bricelj et al. (2005) found that genetic mutations in the sodium channel pore region of wild softshell clams (Mya arenaria) decreased affinity of the receptors to
PSTs (saxitoxin and tetrodotoxin). These resistant clams were able to tolerate much higher
concentrations of STX than their sensitive wild-type counterparts, which is presumably
favorable for the clams but rather unpropitious for the species which consume them.
Saxitoxin is a fascinating chemical, not only because it is a Schedule I Chemical Warfare
Agent but because it is produced by two kingdoms of life (cyanobacteria and dinoflagellates; Cusick and Sayler 2013). The two synthesis pathways appear to have evolved
independently, albeit based on conserved ancestral proteins (Hackett et al. 2013). Several
species of dinoflagellates that do not produce saxitoxin share homologs to toxic species,
Chapter fourteen: Toxicology and poisons
(responsible for some red tides along with Karenia brevis) can be aerosolized by cell lysis
via wave/wind action and has been known to cause respiratory problems in humans and
other mammalian models (Franz and LeClaire 1989; Kirkpatrick et al. 2004). The saxitoxins have been identified as the toxins associated with paralytic shellfish poisoning (PSP)
which has been linked to episodic mass poisonings of humans, marine mammals, and
birds (Van Dolah et al. 2003).
While the co-evolution of chemical warfare between predator and prey has undoubtedly been occurring for millennia, it is perhaps surprising that cetaceans (and pinnipeds)
do not display more resistance to marine biotoxins. Historically, diagnostic methods
have limited the ability to identify or detectably measure algal biotoxins, and thus the
etiology of mass-strandings and die-offs was uncertain. However, with increasingly
sensitive and precise assays, there is now good evidence to suggest that algal biotoxins
are at least partially responsible for previously unexplained unusual mortality events
(UMEs) (Scholin et al. 2000; Van Dolah et al. 2003). The unique nature of HABs, including non-species-specific mortality, has led some to speculate about evidence for massstrandings in fossilized remains from the late Miocene epoch (approximately 7 Mya)
(Pyenson et al. 2014). At a site in the Atacama desert of Chile, Pyenson et al. (2014) found
four layers of multi-species assemblages stratified in the sedimentary substrate, including species of Balaenopteridae, Phocidae, and an aquatic sloth (Thalassocnus natans). The
unique orientation (supine) and proximity of the remains led the authors to conclude
that the individuals died rapidly at sea and were promptly washed ashore (spatial focusing) by the unique structure and currents of the supratidal flat (Pyenson et al. 2014).
While pathology of 6–9 Myr old fossils is undoubtedly filled with uncertainty, it is worth
noting that HABs have likely contributed to the evolution of marine mammals and have
even been hypothesized to have played a role in Phanerozoic mass extinctions (Castle
and Rodgers 2009).
Marine mammal mortality events have been associated with other marine biotoxins
such as domoic acid (Scholin et al. 2000) and brevetoxin (Flewelling et al. 2005). The task of
attributing mass-strandings and die-offs to marine biotoxins is often complicated by other
factors such as viruses, bacteria, and other pathogens as well as nutrition and immunologic
status of the individuals and populations. Rather than being pesky confounding variables,
however, these factors likely contribute to the overall health picture of the animal, and the
balance of two or more factors may well tip the scales from health to outright disease. With
respect to some mortality events documented in the USA, there is very strong diagnostic
evidence that some HAB-related mortality events for certain species are now considered
endemic (e.g., California sea lions and domoic acid, manatees and brevetoxin; F. Gulland,
pers. comm.).
Since most marine mammal species are not directly consuming the toxin-producing
organisms, it is important to consider the trophic transfer and biotransformation of biotoxins. For instance, Bricelj et al. (2005) found that genetic mutations in the sodium channel pore region of wild softshell clams (Mya arenaria) decreased affinity of the receptors to
PSTs (saxitoxin and tetrodotoxin). These resistant clams were able to tolerate much higher
concentrations of STX than their sensitive wild-type counterparts, which is presumably
favorable for the clams but rather unpropitious for the species which consume them.
Saxitoxin is a fascinating chemical, not only because it is a Schedule I Chemical Warfare
Agent but because it is produced by two kingdoms of life (cyanobacteria and dinoflagellates; Cusick and Sayler 2013). The two synthesis pathways appear to have evolved
independently, albeit based on conserved ancestral proteins (Hackett et al. 2013). Several
species of dinoflagellates that do not produce saxitoxin share homologs to toxic species,