Biological Opinions - Bureau of Reclamation

2011). Such high concentrations do not persist farther downstream in J.C. Boyle Reservoir;
however, chlorophyll-a concentrations increase again in the two largest reservoirs (i.e., Copco 1
and Iron Gate) in the Klamath Hydroelectric Reach. Seasonal algal blooms and elevated
chlorophyll-a concentrations have been observed in the Klamath Hydroelectric Reach
historically, including a USEPA survey in Iron Gate Reservoir in 1975 that documented algal
blooms in March, July, and October, including diatoms and blue-green algae). More
contemporary data indicates that chlorophyll-a levels in Copco 1 and Iron Gate Reservoirs can
be 2 to 10 times greater than those documented in the mainstem river, although not as high as
those found in the Keno Impoundment/Lake Ewauna (NCRWQCB 2010).
Some cyanobacteria species produce cyanotoxins (e.g., cyclic peptide toxins, such as
microcystin, that act on the liver; alkaloid toxins such as anatoxin-a and saxitoxin, that act on the
nervous system), which can cause irritation, sickness, or, in extreme cases, death to exposed
organisms, including humans (World Health Organization 1999). Species capable of producing
microcystin include Microcystis aeruginosa, while species in the genus Anabaena and AFA can
produce anatoxin-a and saxitoxin, but assays of AFA in UKL indicate that the strain in this lake
do not produce these toxins (Carmichael et al. 2000).
Algal toxins represent a potentially serious threat to suckers in UKL (VanderKooi et al. 2010,
Eldridge et al. 2012), especially microcystin, a liver toxin produced by the cyanobacterium M.
aeruginosa. Microcystin likely enters suckers through the gut as they consume midge larvae
containing the toxin (VanderKooi et al. 2010, Rosen et al. 2011, Eldridge et al. 2012).
Microcystins are actively taken up by the liver in fish where they disrupt normal cellular activity
by inhibiting protein phosphatases, and can ultimately result in widespread cellular death, loss of
liver structure, and mortality (Malbrouck and Kestemont 2006, California Environmental
Protection Agency (CEPA 2009). Due to the limited capacity of fish to detoxify microcystins,
they easily succumb to the toxic effects of elevated microcystin concentrations (Malbrouck and
Kestemont 2006, CEPA 2009). Additional sublethal effects of microcystins include reduced
growth rates and osmoregulation, modified behavior, reduction in immune system and cardiac
function, and histopathological effects in other organs (e.g., intestine, kidneys, heart, spleen, or
gills; Malbrouck and Kestemont 2006, CEPA 2009). Because microcystin is relatively stable,
persisting in situ for months (CEPA 2009), it potentially could accumulate in fish tissues and
have continued adverse effects through the winter (Malbrouck and Kestemont 2006).
Microcystin can also bioaccumulate in aquatic biota (Malbrouck and Kestemont 2006).
Age-0 suckers could be at a greater risk of harm than adult suckers by microcystin because
young life stages of fish are known to be generally more sensitive to toxic compounds
(Malbrouck and Kestemont 2006). Additionally, the mobility of juvenile suckers is limited
compared to adults, and juveniles are often found in shallow areas where wind-blown
cyanobacteria can accumulate, thus exposing them to microcystin.
Microcystin was first reported in UKL in 1996, when an investigation showed significant
microcystin levels in the lake (Gilroy et al. 2000). In 2007 and 2008 microcystin concentrations
reached levels peaked at 17 µg/L, which is greater than the World Health Organization limit for
drinking water (1 µg/L) and above the Oregon Department of Public Health guidelines for
issuing public health advisories (VanderKooi et al. 2010, Eldridge et al. 2012). In 2007,
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