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The Biology of Sea Turtles, Vol. II
by chronic biotoxin exposure. Such may be the case in GTFP, where oncogenic
viruses and tumor-promoting toxins may be acting in concert (Landsberg, 1996), with
particular effects on immunosuppressed animals (Bossart et al., 2002). Eutrophication
may directly increase viral and bacterial loads as well, in addition to the increased
severity and frequency of algal blooms (Herbst and Klein, 1995).
In sea turtles, there appears to be an association between the distribution of toxic
dinoflagellates ( Prorocentrum spp.) and the occurrence of fibropapilloma disease
among Hawaiian green sea turtles (Landsberg et al., 1999). These benthic dinoflagellates are epiphytic on seagrasses and macroalgae, and would thus be consumed by
foraging green turtles. Prorocentrum are of particular interest because this group
produces the tumor-promoting toxin okadaic acid, also detected in the tissues of
Hawaiian green turtles ( C. mydas ) with GTFP (Landsberg et al., 1999).
More direct, toxic effects of red tide blooms of Gymnodinium have been suggested, although a direct link has yet to be demonstrated between brevetoxin and
large die-offs of turtles such as have recently occurred in Florida. Chronic brevetoxicosis has been suggested as the likely primary etiology for manatee deaths that
occurred in the same time frame (Bossart et al., 1998); simultaneous epizootics for
manatees, fish, and cormorants associated with Gymnodinium blooms have occurred
in the past (O’Shea et al., 1991). Sea turtle strandings in Florida increased significantly during four recent red tide blooms of the dinoflagellate Karenia brevis , with
live turtles displaying symptoms of neurological disorders (Redlow et al., 2002). In
nonsurviving animals associated with these blooms, liver brevetoxins were often as
high as or higher than those in manatees determined to have died of brevetoxin
poisoning. Patterns of bioaccumulation or species-specific susceptibility were also
detected: brevetoxins were highest in Kemp’s ridley turtles, intermediate in loggerhead tissue (only 1 animal), and lowest in greens (Redlow et al., 2002). Such dieoffs appear to primarily affect juvenile and subadult turtles that are residents of
nearshore waters; however, effects on breeding populations could be significant
should springtime HABs continue into the start of the nesting season.
A secondary but important effect of eutrophication is the general degradation
of the marine environment, which can seriously devalue its use as turtle habitat.
Even nontoxic algal blooms (brown tides) can result in the loss of seagrass beds at
nutrient-rich locations (Havens et al., 2001), as can increased levels of turbidity or
changes in salinity (Figure 6.2). Prolonged blooms can also add large amounts of
decaying matter to the water, causing hypoxic or anoxic conditions and furthering
the devastation (Epstein et al., 1998). Havens et al. (2001) reported that a dense lawn
of macroalgae on the bottom of one Virginia estuary reduced sediment–water nitrogen exchange when the algae were actively growing, but resulted in high nitrogen
release during algal senescence. Such significant impacts on invertebrates and seagrasses would be magnified up the food chain, potentially resulting in large areas
of ocean “desert,” which appear to be occurring with increasing frequency. In Hervey
Bay, Australia, for example, more than 1000 km 2 of seagrass beds have been lost,
resulting in significant mortality and migration of the dugong population and the
reduction of commercial prawn and fish catches (Brodie, 1999). The effects of such
large-scale eutrophication on resident sea turtle populations are completely unknown
because in-water population studies are lacking in affected areas.
1123 book.book Page 174 Monday, November 11, 2002 11:11 AM
The Biology of Sea Turtles, Vol. II
by chronic biotoxin exposure. Such may be the case in GTFP, where oncogenic
viruses and tumor-promoting toxins may be acting in concert (Landsberg, 1996), with
particular effects on immunosuppressed animals (Bossart et al., 2002). Eutrophication
may directly increase viral and bacterial loads as well, in addition to the increased
severity and frequency of algal blooms (Herbst and Klein, 1995).
In sea turtles, there appears to be an association between the distribution of toxic
dinoflagellates ( Prorocentrum spp.) and the occurrence of fibropapilloma disease
among Hawaiian green sea turtles (Landsberg et al., 1999). These benthic dinoflagellates are epiphytic on seagrasses and macroalgae, and would thus be consumed by
foraging green turtles. Prorocentrum are of particular interest because this group
produces the tumor-promoting toxin okadaic acid, also detected in the tissues of
Hawaiian green turtles ( C. mydas ) with GTFP (Landsberg et al., 1999).
More direct, toxic effects of red tide blooms of Gymnodinium have been suggested, although a direct link has yet to be demonstrated between brevetoxin and
large die-offs of turtles such as have recently occurred in Florida. Chronic brevetoxicosis has been suggested as the likely primary etiology for manatee deaths that
occurred in the same time frame (Bossart et al., 1998); simultaneous epizootics for
manatees, fish, and cormorants associated with Gymnodinium blooms have occurred
in the past (O’Shea et al., 1991). Sea turtle strandings in Florida increased significantly during four recent red tide blooms of the dinoflagellate Karenia brevis , with
live turtles displaying symptoms of neurological disorders (Redlow et al., 2002). In
nonsurviving animals associated with these blooms, liver brevetoxins were often as
high as or higher than those in manatees determined to have died of brevetoxin
poisoning. Patterns of bioaccumulation or species-specific susceptibility were also
detected: brevetoxins were highest in Kemp’s ridley turtles, intermediate in loggerhead tissue (only 1 animal), and lowest in greens (Redlow et al., 2002). Such dieoffs appear to primarily affect juvenile and subadult turtles that are residents of
nearshore waters; however, effects on breeding populations could be significant
should springtime HABs continue into the start of the nesting season.
A secondary but important effect of eutrophication is the general degradation
of the marine environment, which can seriously devalue its use as turtle habitat.
Even nontoxic algal blooms (brown tides) can result in the loss of seagrass beds at
nutrient-rich locations (Havens et al., 2001), as can increased levels of turbidity or
changes in salinity (Figure 6.2). Prolonged blooms can also add large amounts of
decaying matter to the water, causing hypoxic or anoxic conditions and furthering
the devastation (Epstein et al., 1998). Havens et al. (2001) reported that a dense lawn
of macroalgae on the bottom of one Virginia estuary reduced sediment–water nitrogen exchange when the algae were actively growing, but resulted in high nitrogen
release during algal senescence. Such significant impacts on invertebrates and seagrasses would be magnified up the food chain, potentially resulting in large areas
of ocean “desert,” which appear to be occurring with increasing frequency. In Hervey
Bay, Australia, for example, more than 1000 km 2 of seagrass beds have been lost,
resulting in significant mortality and migration of the dugong population and the
reduction of commercial prawn and fish catches (Brodie, 1999). The effects of such
large-scale eutrophication on resident sea turtle populations are completely unknown
because in-water population studies are lacking in affected areas.
1123 book.book Page 174 Monday, November 11, 2002 11:11 AM