318
Marine Mammal Physiology: Requisites for Ocean Living
suggesting that the evolution of the synthesis system was not exclusively driven toward
toxin production (Cusick and Sayler 2013; Hackett et al. 2013). Indeed, the main site of the
saxitoxin toxicity in mammals (sodium channels) had not evolved when genes associated
with saxitoxin production (sxt cluster) appeared in cyanobacteria (Murray et al. 2011).
14.3.1 Cetaceans
Large whales and other cetaceans are exposed to toxins present in HABs in areas where
their temporal and spatial ranges overlap. Evidence of PSTs and DA in fecal samples of
North Atlantic right whales (Eubalaena glacialis) suggests that individuals are exposed to
these algal toxins on a regular basis (70%–80% contained traces of PST, 25%–30% contained traces of DA, and 22% of the fecal samples collected showed exposure to both DA
and PST, Doucette et al. 2012). Interestingly, while PST is often recognized accumulating
in shellfish, the fact that it can accumulate in the tissues of highly motile fish such as
cod raises some interesting ecologic considerations. For instance, during the fall of 1987,
14 humpback whales (Megaptera novaengliae) died in Cape Cod from apparent saxitoxin
poisoning (Geraci et al. 1989). While plankton and shellfish in the immediate vicinity
did not contain traceable concentrations of saxitoxin, stomach content analysis of the
whales found a high prevalence of mackerel, which spawn in the waters of the Gulf
of St. Lawrence. The concentrations of STX in mackerel liver were 154 μg/100 g tissue,
which is nearly double the threshold for human consumption of mussels of 80 μg/100 g
mussel (Geraci et al. 1989). It is tempting to view HABs as limited by the spatial and temporal lifespan of the toxin-producing algae, however, when considering the lifespan and
motility of fish consumers able to accumulate the toxin, the overall scope of the effects
of HABs increases dramatically.
14.3.2 Pinnipeds
Saxitoxin has been implicated in the mortality of a number of Hawaiin monk seals (Monachus
schauinslandi) due to the presence of the toxin in seal tissues (mean 12.55 ± 10.09 μg
dcSTX per 100 g tissue, n = 7) and prey species, as well as pulmonary trauma consistent
with drowning due to paralysis (Hernández et al. 1998). However, the authors conclude
that, as with most cases of algal toxin poisoning, without reference concentrations, it is
difficult to establish the etiology of mortality. There is some speculation that ciguatoxin,
a toxin present in reef fish, has contributed to the decline of Hawaiian monk seal populations, although currently this remains rather speculative (Van Dolah et al. 2003). Recent
work has shown detectable levels of ciguatoxin activity in blood samples from Hawaiian
monk seals (0.43–5.49 pg/ml P-CTX-1 equivalent), affirming prior speculation that individuals were indeed exposed to the toxin and transfer to marine mammals is possible
(Bottein et al. 2011).
Although the impact of biotoxins on Hawaiin monk seals is concerning due to their
conservation status, the power of these poisons to influence pinniped health on a population scale is perhaps better demonstrated in the dense and closely monitored colonies
of California sea lions (Zalophus californianus) and harbor seals (Phoca vitulina) along the
California coastline. In 1998, a UME of California sea lions was convincingly linked
through multiple lines of evidence to domoic acid—a neurotoxin produced by diatoms
of the Pseudo-nitzschia genus (Scholin et al. 2000). Mammalian exposure is due primarily to dietary consumption of contaminated prey species (Lefebvre and Robertson 2010),
which in the case of California sea lions appears to be largely attributed to the filter
Marine Mammal Physiology: Requisites for Ocean Living
suggesting that the evolution of the synthesis system was not exclusively driven toward
toxin production (Cusick and Sayler 2013; Hackett et al. 2013). Indeed, the main site of the
saxitoxin toxicity in mammals (sodium channels) had not evolved when genes associated
with saxitoxin production (sxt cluster) appeared in cyanobacteria (Murray et al. 2011).
14.3.1 Cetaceans
Large whales and other cetaceans are exposed to toxins present in HABs in areas where
their temporal and spatial ranges overlap. Evidence of PSTs and DA in fecal samples of
North Atlantic right whales (Eubalaena glacialis) suggests that individuals are exposed to
these algal toxins on a regular basis (70%–80% contained traces of PST, 25%–30% contained traces of DA, and 22% of the fecal samples collected showed exposure to both DA
and PST, Doucette et al. 2012). Interestingly, while PST is often recognized accumulating
in shellfish, the fact that it can accumulate in the tissues of highly motile fish such as
cod raises some interesting ecologic considerations. For instance, during the fall of 1987,
14 humpback whales (Megaptera novaengliae) died in Cape Cod from apparent saxitoxin
poisoning (Geraci et al. 1989). While plankton and shellfish in the immediate vicinity
did not contain traceable concentrations of saxitoxin, stomach content analysis of the
whales found a high prevalence of mackerel, which spawn in the waters of the Gulf
of St. Lawrence. The concentrations of STX in mackerel liver were 154 μg/100 g tissue,
which is nearly double the threshold for human consumption of mussels of 80 μg/100 g
mussel (Geraci et al. 1989). It is tempting to view HABs as limited by the spatial and temporal lifespan of the toxin-producing algae, however, when considering the lifespan and
motility of fish consumers able to accumulate the toxin, the overall scope of the effects
of HABs increases dramatically.
14.3.2 Pinnipeds
Saxitoxin has been implicated in the mortality of a number of Hawaiin monk seals (Monachus
schauinslandi) due to the presence of the toxin in seal tissues (mean 12.55 ± 10.09 μg
dcSTX per 100 g tissue, n = 7) and prey species, as well as pulmonary trauma consistent
with drowning due to paralysis (Hernández et al. 1998). However, the authors conclude
that, as with most cases of algal toxin poisoning, without reference concentrations, it is
difficult to establish the etiology of mortality. There is some speculation that ciguatoxin,
a toxin present in reef fish, has contributed to the decline of Hawaiian monk seal populations, although currently this remains rather speculative (Van Dolah et al. 2003). Recent
work has shown detectable levels of ciguatoxin activity in blood samples from Hawaiian
monk seals (0.43–5.49 pg/ml P-CTX-1 equivalent), affirming prior speculation that individuals were indeed exposed to the toxin and transfer to marine mammals is possible
(Bottein et al. 2011).
Although the impact of biotoxins on Hawaiin monk seals is concerning due to their
conservation status, the power of these poisons to influence pinniped health on a population scale is perhaps better demonstrated in the dense and closely monitored colonies
of California sea lions (Zalophus californianus) and harbor seals (Phoca vitulina) along the
California coastline. In 1998, a UME of California sea lions was convincingly linked
through multiple lines of evidence to domoic acid—a neurotoxin produced by diatoms
of the Pseudo-nitzschia genus (Scholin et al. 2000). Mammalian exposure is due primarily to dietary consumption of contaminated prey species (Lefebvre and Robertson 2010),
which in the case of California sea lions appears to be largely attributed to the filter