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Abstract INTERPLAY BETWEEN DINOFLAGELLATE TOXINS, MEMBRANE STEROL COMPOSITION, AND PARASITISM BY AMOEBOPHRYA. Xuemei Bai1 and D. Wayne Coats2 Parasitic dinoflagellates of the genus Amoebophrya infect
many bloom-forming dinoflagellates, including several toxic species.
These parasites can spread rapidly through host populations and
have been linked to the decline of red tides. The fate of host toxins
during bloom decline caused by parasitism is unknown. Equally unresolved
is the performance of parasites in host strains that differ in toxin
content. The ichthyotoxic dinoflagellate Karlodinium veneficum
produces karlotoxins (KmTX) that permeabilize cell membranes, resulting
in cell death through osmotic lysis. Membrane sterol composition
appears to govern sensitivity KmTX, with a preponderance of 4?-methyl
sterols (gymnodinosterol) providing immunity to the toxin. Like
its host, Amoebophrya sp. ex K. veneficum possesses
gymnodinosterol and is presumed to be immune to KmTX. We examined
the effect of purified KmTX on several host-parasite systems, the
ability of Amoebophrya to infect non-toxic to highly toxic
K. veneficum, and toxin levels of parasitized K. veneficum
over the infection cycle. Addition of purified KmTX to culture medium
had no effect on survival or infectivity of Amoebophrya
ex K. veneficum, but caused mortality and reduced infection
of Amoebophrya from other host species. Parasite prevalence
was positively correlated with K. veneficum toxicity, suggesting
that Amoebophrya is more likely to control toxic blooms
than non-toxic blooms . KmTX ml-1 increased with growth
of K. veneficum in control cultures, but declined in infected
cultures as the parasite completed its life cycle. On a cellular
basis, toxin content of infected and uninfected cultures differed
little during the experiment, suggesting that the parasite does
not actively catabolise host toxin. Rather, infection appears to
promote degradation of toxins via death of host cells and subsequent
bacterial activity. Thus, this parasite may limit the occurrence
of toxic K. veneficum blooms in marine and estuarine environments,
while simultaneously functioning as a pathway for dissipation of
host toxin.
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