FISHERY BULLETIN: VOL. 85, NO. 4 



ence of antibodies against the parasite, several 

 histological cross sections show worms in stages 

 of degeneration, and host destruction of larval 

 and adult cestodes has been shown in other 

 teleosts (Kennedy and Walker 1969; Smith 1973; 

 MacKenzie 1975). Examination of a small num- 

 ber of pyloric caeca, liver, spleen, lateral arteries, 

 and stomach vasculature of large yellowfm tuna 

 (>45 kg) showed >85% infection, suggesting 

 1) that the parasite may move out of the dorsal 

 aorta into other large arteries as yellowfin tuna 

 grow, 2) that the host response to the parasite 

 may be less vigorous in vessels other than the 

 dorsal aorta, and/or 3) that the parasite may pref- 

 erentially select other vessels in larger fish. 

 Baudin Laurencin (1971) found a decrease in 

 branchial artery infection of yellowfin tuna with 

 increasing body size, but no change in rates of 

 infection of abdominal vessels. 



The change in the rate of infection seen in Au- 

 gust and September 1985 in small yellowfin tuna 

 (Fig. 1) is, we believe, due to a large influx of 

 uninfected fish into the Hawaiian fishery. Al- 

 though we have no direct corroborating evidence, 

 such as increased catch per unit effort for this size 

 yellowfin tuna at that time. Tester and Naka- 

 mura (1957) have shown that there are repeated 

 influxes of small yellowfin tuna into areas near 

 the main Hawaiian Islands during late summer 

 and early fall. Furthermore, the dramatic differ- 

 ences seen in relative condition factors, relative 

 liver weights, and relative heart weights between 

 unparasitized fish caught during August- 

 September 1985, and the remaining unpara- 

 sitized fish, clearly imply that the former group 

 had a different history. 



We have no evidence nor are we hypothesizing 

 that these groups come from genetically isolated 

 subpopulations. We do believe, however, that the 

 two groups were separate most likely since hatch- 

 ing. We do not know the maximum lifespan of the 

 dorsal aorta parasite, but one yellowfin tuna 

 killed after 172 days in captivity at the Kewalo 

 Research Facility was parasitized. Since fish in 

 captivity are fed only frozen food and their tanks 

 are supplied with filtered seawater (Queenth and 

 Brill^), it is unlikely this fish became infected 

 after capture. Yellowfin tuna of the 1-3 kg size 

 range are about 270-360 days old (Uchiyama and 



SQueenth, M.K. K., and R.W. Brill. 1983. Operations and 

 procedures manual for visiting scientists at the Kewalo Re- 

 search Facility. Southwest Fish. Cent. Admin. Rep. H-83-7, 16 

 p. Natl. Mar. Fish. Serv., NOAA, Honolulu, HI. 



Struhsaker 1981) and therefore could have car- 

 ried the parasite most of their lives. 



The slow increase in prevalence from October 

 1985 through March 1986 remains to be ex- 

 plained, but could be due to emigration of the new 

 group of yellowfin tuna out of the Hawaiian fish- 

 ery or slowly increasing infection of the new 

 group. This latter explanation implies higher 

 prevalence of the parasite around islands which 

 could be due either to a greater number of final 

 (shark) or intermediate hosts around islands. 



Pathology 



The severe enarteritis associated with D. talis- 

 mani infection suggests that the parasite is recog- 

 nized by the fish's defense system as foreign ma- 

 terial in the dorsal aorta. Dead worms within the 

 inflammatory tissue imply that the parasite is 

 not well adapted for survival in this location. Pre- 

 sumably, D. talismani would elicit, and be at- 

 tacked by, a similar inflammatory response irre- 

 spective of its location within the vasculature. 

 This response was not observed in other vessels 

 and additional work is needed to clarify the site 

 specificity of the immune response. Our findings 

 also suggest that cellular elements are responsi- 

 ble for the destruction of the larval cestodes when 

 located in the dorsal aorta. 



Effect of the Infection of the 

 Dorsal Aorta on Natural Mortality 



We found no evidence to support our original 

 hypothesis that infected yellowfin tuna are activ- 

 ity limited and therefore less able to secure food. 

 When the data from the unparasitized fish caught 

 August-September 1985 are excluded, there are 

 no differences in relative condition factors, rela- 

 tive liver weights, or relative heart weights be- 

 tween parasitized and unparasitized fish. When 

 parasitized and unparasitized fish from the single 

 school caught 15 January 1985 are compared, no 

 significant differences in these parameters, mean 

 short-term (i.e., RNA/DNA ratios), or mean long- 

 term (i.e., relative otolith weights) growth are ev- 

 ident. 



Because parasite emboli appear to cause almost 

 complete occlusion of the anterior dorsal aorta 

 (the only blood vessel supplying the viscera and 

 swimming muscles), the lack of differences be- 

 tween infected and uninfected fish was not ex- 

 pected. Overstreet (1977), investigating the ef- 

 fects of plerocercoid infection on sciaenid fishes in 



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