The Korean Journal of Malacology (한국패류학회지)

The Malacological Society of Korea (한국패류학회)
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Dissemination of Perkinsus olseni is affected by the viability of Ruditapes philippinarum

급성 폐사 바지락 (Ruditapes philippinarum) 으로부터 Perkinsus olseni의 확산 기작

  • Nam, Ki-Woong (Department of Aquatic Life Medicine, College of Ocean Science and Technology, Kunsan National University) ;
  • Jeung, Hee-Do (Tidal Flat Research Institute, National Fisheries Research Institute) ;
  • Song, Jae-Hee (Tidal Flat Research Institute, National Fisheries Research Institute) ;
  • Choi, Kwang-Sik (Jeju National University) ;
  • Park, Kyung-Il (Department of Aquatic Life Medicine, College of Ocean Science and Technology, Kunsan National University)
  • 남기웅 (군산대학교 해양과학대학 해양생명응용과학부 수산생명의학전공) ;
  • 정희도 (국립수산과학원 갯벌연구소) ;
  • 송재희 (국립수산과학원 갯벌연구소) ;
  • 최광식 (제주대학교 해양과학대학 해양의생명과학부 해양생명과학전공) ;
  • 박경일 (군산대학교 해양과학대학 해양생명응용과학부 수산생명의학전공)
  • Received : 2015.11.13
  • Accepted : 2015.12.30
  • Published : 2015.12.30
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Abstract

This study was conducted in order to elucidate the dissemination mechanism of P. olseni using field and laboratory experiments. For this purpose, we quantified the level of P. olseni infection in buried (healthy) and surfaced (gapped) R. philippinarum from a clam bed on Wi-do Island on the west coast of Korea. In addition, the levels of internal and released P. olseni cells from artificially infected (and later dead) R. philippinarum were monitored for 8 days using the RFTM-2 M NaOH lysis method. Our results indicate that P. olseni cells in buried R. philippinarum was $2,655,625{\pm}1,536,936cells/clam$; the level in gapped R. philippinarum was considerably lower, $28,203{\pm}24,889cells/clam$ (p < 0.05). In the laboratory experiment, the P. olseni cells remained in the host tissue 2 days after death was approximately 50% lower than the level of infection measured in living clams. The level dropped to 20% 4 days after death and to 1.5% 6 days after death; eight days after death, P. olseni cells were undetectable since the R. philippinarum flesh had completely decomposed. The level of released cells on the day of death was only 0.05% of the internal level in live R. philippinarum; however, the level increased to 2.3% 5 days after death then gradually decreased and no released cells were detected 8 days after death. Therefore, our laboratory experiment suggest that the low level of P. olseni infection observed in gapped R. philippinarum at Wi-do Island could be caused by lysis of the most of P. olseni cells during the decomposition of dead R. philippinarum tissues. Until the end of decomposition of R. philippinarum, 6.68% of the total amount of P. olseni was released within 8 days. Our study showed that the amount of P. olseni cells from dead host is a considerably higher level than naturally released from healthy R. philippinarum, suggesting that death of the host plays an important role in the dissemination of P. olseni.

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References

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