Karenia mikimotoi

And in a public ‘information card’ produced by the State of Texas Commission for
Environmental Quality - http://www.tceq.state.tx.us/files/gi-378.pdf_4146980.pdf
the same information is reiterated:
“P. parvum produces toxins that can affect gill-breathing organisms including
fishes and freshwater molluscs. The most visible result of a fish kill caused by
golden alga is dead and dying fishes of all species and sizes. Aquatic insects
do not appear to be affected and may be alive during a toxic event. Large
numbers of birds (including pelicans, cormorants, gulls, herons, and vultures)
may be present and actively feeding on the dead and dying fishes.
The Texas Department of State Health Services has stated that golden alga is not
known to cause human health problems, but people should not pick up dead or dying
fishes for consumption.
• Mammals and birds have been observed eating dead fishes and drinking
water within areas experiencing toxic golden alga blooms; no immediate
harmful effects have been recorded. Complications, secondary infections or
other effects may occur. Be careful of spines and bones from dead fishes
on the shoreline. Puncture wounds can get infected.
• Swimming near dead fishes is not recommended since bacteria levels
associated with decomposition may be high.”
Moustaka-Gouni et al. (2004) reported the coincidence of a Prymnesium parvum bloom
and the mass kill of birds and fish in Lake Koronia, Greece, in 2004. The bird kill was
later reported by the World Organization for Animal Health (OIE) to be due to avian
botulism - see ftp://ftp.oie.int/SAM/2004/FAUNE_A.pdf .
3.8 Fibrocapsa japonica
Harmful blooms of F. japonica causing extensive kills of farmed fish have occurred in
various parts of the world (Smayda, 2006 - Figure 9), mainly in temperate regions (see
de Boer et al., 2005). It was originally described in Japanese waters in 1973 and was
first observed in European coastal waters in 1991, including those of France and the
Netherlands, and two years later in the German Bight (Smayda, 2006 and refs.
therein). F. japonica has become well established in the North Sea and was reported
to have reached a population maximum of 2.4 million cells.L -1 during 1997 in the
German Bight (Rademaker et al., 1998).
As with other raphidophytes, the specific mechanisms of toxicity remain to be
elucidated. Khan et al. (1996a) isolated five neurotoxic components from a European
isolate of F. japonica, designated FjTx-I, FjTx-II, FjTx-IIIa, FjTx-IIIb and FjTx-IV, which
were tentatively identified as brevetoxin compounds, PbTx-1, PbTx-2, PbTx-9, PbTx-3
and oxidized PbTx-2 on the basis of TLC and HPLC analysis. Brevetoxins have also
been identified in an American strain of F. japonica by means of an ELISA technique
(Bridgers et al., 2004).
Using various sophisticated analytical techniques, including LC-MS, GC-MS and NMR,
Fu et al., (2004) elucidated the molecular structures of the three main haemolytic
compounds (Fj1, Fj2 and Fj3) isolated from a European strain of F. japonica. They
were identified as polyunsaturated fatty acids (PUFA): 6,9,12,15-octadecatetraenoic
acid (C18:4n-3, OTA), 5,8,11,14,17-eicosapentaenoic acid (C20:5n-3, EPA) and
5,8,11,14-eicosatetraenoic acid (C20:4n-6 = arachidonic acid, AA). Pure commercial
samples of EPA and AA were found to show the same spectroscopic and
chromatographic characteristics as Fj2 and Fj3 and had a similar strong haemolytic
effect. It was postulated that, when F. japonica cells accumulate in fish gills during
blooms, these PUFA could be the cause of ichthyotoxicity.
22 A Literature review of the potential health effects of marine microalgae and macroalgae