Salachan Paul Vinu, Jaroenlak Pattana, Thitamadee Siripong, Itsathitphaisarn Ornchuma, Sritunyalucksana Kallaya
Shrimp-pathogen interaction (SPI) laboratory, National Center for Genetic Engineering and Biotechnology (BIOTEC), National Science and Technology Development Agency (NSTDA), Yothi office, Bangkok, 10400, Thailand.
Center of Excellence for Shrimp Molecular Biology and Biotechnology, Faculty of Science, Mahidol University, Rama VI Rd., Bangkok, 10400, Thailand.
BMC Vet Res. 2017 Jan 5;13(1):9. doi: 10.1186/s12917-016-0923-1.
Enterocytozoon hepatopenaei (EHP) causes hepatopancreatic microsporidiosis (HPM) in shrimp. It is probably endemic in Australasia and was first characterized and named from the giant or black tiger shrimp Penaeus monodon from Thailand in 2009. Later, it was also found to infect exotic Penaeus vannamei imported for cultivation in Asia. HPM is not normally associated with shrimp mortality, but information from shrimp farmers indicates that it is associated with significant growth retardation that is not clearly noticeable until 2-3 months of cultivation. In order to study modes of HPM transmission and to test possible control measures, a laboratory challenge model was needed that would mimic the mode of infection in shrimp ponds.
We describe successful transmission in a cohabitation model with natural E. hepatopenaei (EHP)-infected shrimp in closed, perforated plastic containers placed in aquaria together with free-swimming, uninfected shrimp. After a period of 14 days all the free-swimming shrimp tested positive by PCR (approximately 60% with heavy infections evident by 1-step PCR positive test results) and gave positive histological and in situ hybridization results for E. hepatopenaei (EHP) in the hepatopancreas.
A laboratory cohabitation model for studying E. hepatopenaei (EHP) has been developed and used to confirm that E. hepatopenaei (EHP) can be directly transmitted horizontally among shrimp via water. The model will facilitate studies on methods to prevent the E. hepatopenaei (EHP) transmission.
肝肠胞虫（EHP）可导致对虾发生肝胰腺微孢子虫病（HPM）。它可能在澳大拉西亚地区呈地方性流行，2009年首次从泰国的斑节对虾（也称巨型或黑虎虾）中得以鉴定并命名。后来，还发现它可感染亚洲地区引进养殖的凡纳滨对虾。HPM通常与对虾死亡无关，但来自虾农的信息表明，它与显著的生长迟缓有关，这种生长迟缓在养殖2 - 3个月后才会明显显现。为了研究HPM的传播方式并测试可能的防控措施，需要一个能模拟对虾池塘感染模式的实验室攻毒模型。
我们描述了在一个同居模型中成功实现的传播，该模型是将自然感染肝肠胞虫（EHP）的对虾与未感染的自由游动对虾一起放置在水族箱中封闭的、有孔的塑料容器内。14天后，所有自由游动的对虾经聚合酶链反应（PCR）检测呈阳性（约60%的对虾感染严重，一步PCR阳性检测结果明显），并且在肝胰腺中对肝肠胞虫（EHP）的组织学和原位杂交检测结果也呈阳性。
已开发出一种用于研究肝肠胞虫（EHP）的实验室同居模型，并用于证实肝肠胞虫（EHP）可通过水在对虾之间直接水平传播。该模型将有助于开展预防肝肠胞虫（EHP）传播方法的研究。
