Ete is an extract derived from the marine tunicate Ecteinascidia turbinata. This extract was used to modulate the resistance of the American eel, Anguilla rostrata, to infection by the pathogenic bacterium, Aeromonas hydrophila. Ete injected intraperitoneally (i.p.) was found to dramatically reduce mortality in eels challenged with a lethal dose of bacteria. This protective effect was observed only when the Ete was administered after the bacterial challenge (+ 2 days). Ete given i.p. before (-6, -4 or -2 days) or on the same day as the bacteria did not protect and, in fact, suppressed resistance in some instances. Limited studies with the intravenous (i.v.) route of injection of Ete indicated that when Ete was given two days after lethal bacterial challenge there was also protection. Ete given i.v. on the same day as bacteria appeared to suppress resistance. It is quite interesting that when eels were given a sublethal challenge of bacteria, followed by Ete  i.v. on day +2, these eels showed a significant increase in resistance to lethal challenge (5 days after first challenge) when compared to eels receiving a sublethal dose of bacteria alone and followed by a lethal challenge.

The actual mechanism of enhancement of resistance is unknown. Our results suggest that the production of antibody is not the major factor, and it appears that potentiation of phagocytic functions may be critical to the increased resistance mediated by Ete. This was deduced from the findings that the treatment regimen which ensured the best protection against death from A. hydrophila (Ete administered i.p. 2 days after infection) was associated with opposite effects on phagocytic elements and antibody production, promoting the former and inhibiting the latter. The i.p. route (in contrast with the i.v. route) also stimulated granulocytis.

(This work was supported by a grant from the South Carolina Sea Grant Consortium.)