• 한국수산과학회지
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• 제46권5호
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• pp.575-581
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• 2013

We examined the effect of starvation on the occurrence of tunic softness to determine the cause of mass mortality of cultured Halocynthia roretzi (Drasche) in the Tongyeong region, Korea. In terms of the survival rate of H. roretzi and the occurrence rate of tunic softness, H. roretzi starved for 35 days at water temperatures of 8, 12, and $15^{\circ}C{\pm}0.5^{\circ}C$ (room temperature of $15^{\circ}C{\pm}1^{\circ}C$) did not exhibit tunic softness at water temperatures of either $8^{\circ}C$ or $12^{\circ}C$. for morphological changes, although the tunic of H. roretzi was shrunken and became visibly smaller with a darkening color in all experimental groups, as compared to the state prior to starvation, its tunics bulbs continuously. The ratio of RNA/DNA concentrations and protein contents for each of the tunic sections were lower in the starved group. Our results indicate that tunic softness is not related to feeding deficiency, as no histopathological symptoms were apparent in the digestive gland or tunic of H. roretzi due to starvation.

• 한국어병학회지
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• 제34권1호
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• pp.63-70
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• 2021

As a part of research to elucidate the pathogenesis of so called Soft Tunic Syndrome(STS), that caused mass mortalities in the cultured sea squirts, Halocynthia roretzi, the epidemiological and pathological analysis were done to both clinically normal and diseased groups of the farms of Tongyoung and Geoje coastal areas in southeast sea from February to July, 2008. In the histological finding of the tunic, most of individuals showed tunic softness syndromes that included the disarrangement and destruction of tunic fiber with the simultaneous presence of flagellates-like cells, recently suspected as main agents of tunic softness syndromes. Simultaneously, the intensive degenerative changes of the skeletal muscle of diseased sea squirts were recognized. The changes were characterized with the hyalinization and condensation of muscle fibril and hemocytic infiltration in the muscle fibers. Those were thought to be a kind of typical Zenker's necrosis as in the skeletal muscle of higher vertebrates. Besides of the diseased sea squirts, Zenker's necrosis of skeletal muscles were seen in the normal ones. Epidemiological inquiry for diseased groups revealed that the higher incidences of tunic softness syndrome were recorded in the fast growing groups and in the sites presuming the organic pollution. And Higher malondialadehyde(MDA) and glutathione peroxidase(GPx) activity were detected in the groups showing STS. Those results suggested that Zenker's necrosis of body muscles was a kind of"nutritional myopathy" by oxidative stress. Conclusively, it was considered that Zenker's necrosis of body muscles gives an important clue for elucidating pathogenesis of STS of cultured squirts. And it seems that the necrosis were caused by the oxidative stress to body muscle during abnormal rapid growth of sea squirts.

• 한국어병학회지
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• 제22권3호
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• pp.229-237
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• 2009

The causative agent for the tunic softness syndrome of the cultured ascidian Halocynthia roretzi from Jan 1999 to Feb 2009 was identified using virus isolation and polymerase chain reaction (PCR). The pathogenicity of the isolated virus MABV UR-1 strain was determined by experimental infection trials. The cytopathic effects was observed in CHSE-214 cell line at a level 5.1% (4/78) in normal ascidian and 1.8% in abnormal ascidian showing tunic softness syndrome signs. MABV gene was detected in 16.8% (18/107) of normal and 13.1% (5/38) of abnormal organisms by PCR. The ratio of MABV isolation and gene detection was similar level in normal and soft tunic diseased ascidian. Based on the VP2/NS junction region sequences, eight strains of virus isolated from ascidian, were included in the same genogroup with MABV which is originally isolated in wide ranges of marine fish and shellfish species. The UR-1 strain caused 60% mortality (36.5% mortality in control group) by immersion infection and 37% mortality (same mortality in control group) in injection infection indicating no significant differences in infected and control groups. These results suggest that ascidian can act as reservoir of the MABV, and this virus is not directly related with the ascidian mortality.

• 한국어병학회지
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• 제24권3호
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• pp.197-204
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• 2011

멍게 물렁증 원인규명의 일환으로 2011년 3월에 경남 통영에서 채집된 물렁증 멍게와 건강한 멍게를 대상으로 병리학적 검사를 실시한 결과 물렁증 멍게의 경우 체액량, 비만도 및 피막지수가 현저히 감소하였다. 물렁증 멍게의 피막 imprint 관찰과 배양 시 2개의 편모를 가진 원생동물이 확인되었으며, 물렁증 멍게에 대한 이들 편모충의 감염률은 97.5%인 반면 건강한 멍게에서는 검출되지 않아 본 편모충은 물렁증 멍게에서 특이적으로 검출되는 것으로 조사되었다. 조직학적 검사결과 물렁증 멍게에서 피막섬 유질다발의 붕괴 현상이 관찰되었으며, 편모충으로 추정되는 원생동물들이 다수 관찰되었다. 통영산 물렁증 멍게에서 확인된 편모충은 일본에서 검출된 그것과 매우 유사한 형태적 특징을 갖고 있으며, 향후 공격실험 등 물렁증 유발과 편모충과의 연관성에 대한 추가 연구가 요망된다.

• 환경생물
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• 제31권3호
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• pp.204-212
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• 2013

본 연구는 멍게 대량폐사의 주요 현상으로 나타나고 있는 물렁증 발생의 원인을 찾기 위하여 저산소의 영향에 의한 물렁증 발생, 생존률, 대사율 및 병리조직학적 변화를 분석하였다. 용존산소의 감소에 따른 멍게의 생존률은 용존산소 농도 $2mg\;L^{-1}$에서 노출 4일째 모두 폐사하였으며, $3mg\;L^{-1}$에서는 노출 5일째 50%를 나타내어 5days-$LC_{50}$은 $3.55mg\;L^{-1}$ (1.86~$4.96mg\;L^{-1}$)로 나타났다. 그러나 저산소에 노출된 기간 동안 물렁증 발생은 관찰되지 않았다. 산소소비율은 대조구와 비교하여 용존산소 농도 $5mg\;L^{-1}$ 이하에서 유의하게 감소하여 저산소에 노출되면 일정기간 호흡률을 조절하는 것으로 추정된다. 저산소에 의한 멍게의 새낭, 소화선 및 피낭의 병리조직학적인 변화는 각 기관을 구성하고 있는 상피 세포층의 괴사, 혈구세포의 침윤, 세포핵 응축 및 변형 등이 관찰되었다. 형태적인 변화는 피낭이 쪼글어들어 부피가 작아지고 내부 기관은 탈색되고 아가미와 간췌장의 괴사가 관찰되었다.

• 한국어병학회지
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• 제23권3호
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• pp.313-322
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• 2010

Edible tunicate Halocynthia roretzi, one of the most commercially important aquatic organisms in Korea, has been killed by tunic softness syndrome since last decade. The intracellular protistan parasite observed by the transmission electron microscope in hemocytes of the tunicate was considered to be the causative agent of the mass mortality. The goal of the present work is to examine the characteristic features of the parasite by identifying the 18S rDNA sequences of the parasite. The experiments conducted include amplification of presumptive 18S rDNA from diseased tunicate tissues with UNonMet-PCR and sequencing the product. A preliminary phylogenetic analysis was performed on the presumptive parasite rDNA. A digoxigenin labeled DNA probe was designed on the basis of the sequences of rDNA. Dig-ISH assay was conducted to diagnose the protistan parasite. A PCR using UNonMet-PCR primer generated 595 bp SSU rDNA fragment. Subsequently, PCRs with primer pair expended this sequence to 1542 bp. This is the first partial sequences of SSU rDNA gene to be published on the protistan parasite that has presumed causing the mass mortality of tunicate. Since the Dig-ISH technique demonstrated the presence of infection in hemocytes on the all host tissues, the fragment was confirmed to be the intracellular protistan parasite SSU rDNA. A phylogenetic analysis suggested that the protistan parasite may be a unique eukaryote that is closely related to Apicomplexa.