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为进一步掌握上海地区养殖凡纳滨对虾(Litopenaeus vannamei)病原的流行趋势及特点,定期对上海主养区的凡纳滨对虾开展了8种流行病病原监测及分析工作。51份样品的分子检测和细菌分离鉴定结果显示,有4种病原检测出阳性,其中虹彩病毒1(DIV1)阳性检出率为29.41%,传染性皮下及造血组织坏死病毒(IHHNV)为3.92%,致急性肝胰腺坏死病副溶血弧菌(VpAHPND)为1.96%,副溶血弧菌(Vp)为19.61%;而白斑综合征病毒(WSSV)、桃拉综合征病毒(TSV)、偷死野田村病毒(CMNV)、虾肝肠胞虫(EHP)等4种病原未检出。408项病原检测结果中,4种病原的阳性总样本数量为28份,总体阳性率为6.86%。结果表明,上海地区养殖凡纳滨对虾的病原携带率处于较低水平,DIV1、副溶血弧菌(Vp)是携带的主要病原。在实际生产中应根据病原流行特点,从苗种选购、养殖过程管理、药物选用等方面进行综合防控,减少病害发生。 相似文献
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对虾急性肝胰腺坏死病(Acute hepatopancreatic necrosis disease,AHPND)是由致AHPND副溶血弧菌(AHPND-causing Vibrio parahaemolyticus,VpAHPND)携带的pVA1-like质粒所表达的PirA~(Vp)和PirB~(Vp)毒力蛋白对对虾肝胰腺的急性毒性所致。本研究用2.19×10~5 CFU/ml VpAHPND分离株20130629002S01对凡纳滨对虾(Litopenaeus vannamei)进行浸泡感染,于感染后2~9 d采集对虾的肝胰腺、鳃、肠道、肌肉组织,采用实时荧光定量PCR方法,检测各组织中的pir AVp拷贝数。结果显示,感染后凡纳滨对虾各组织均能检测到pirA~(Vp),其中,肝胰腺在感染后第4天达到峰值,为8.71×10~4 copies/mg,而鳃、肌肉、肠道分别在第3、4、5天达到峰值,分别为9.08×10~3、2.59×10~4、5.76×10~4 copies/mg。早期感染鳃组织中先出现Vp_(AHPND)的富集,在高死亡发生期,Vp_(AHPND)数量在肝胰腺和肠道出现高峰,在死亡数量逐渐下降的后期,各组织的Vp_(AHPND)均快速下降,肠道、肝胰腺和肌肉中的Vp_(AHPND)水平趋于接近。对虾肝胰腺组织病理切片显示,同一时间有临床症状的病虾和濒死对虾相比,濒死对虾表现出更严重的AHPND病理特征,且二者的组织病理特征均随着感染时间的延长变得更为严重,但检测到的Vp_(AHPND)数量呈下降趋势。研究表明,在Vp_(AHPND)感染过程中,组织中的pirA~(Vp)基因数量不能代表对虾的发病程度,发病程度及组织病理严重的AHPND样品中Vp_(AHPND)的数量不一定处于高水平状态。 相似文献
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急性肝胰腺坏死病(Acute Hepatopancreatic Necrosis Disease,AHPND)是由副溶血弧菌(Vibrio parahaemolyticus)引起的对虾病害,本研究从患AHPND的凡纳滨对虾样品中分离得到5株副溶血弧菌,采用致AHPND的副溶血弧菌(VPAHPND)的相关质粒的引物AP2进行PCR检测,表明这5株菌中均存在AHPND相关质粒.利用丝裂霉素C进行溶源性噬菌体筛选和噬菌体诱导发现,其中2株副溶血弧菌(20130629002S01和20130726001S01)可能存在溶源性噬菌体感染;从经0.5 μg/ml丝裂霉素C诱导的20130629002S01和20130726001S01中分别分离得到两种噬菌体phage1和phage2.透射电镜观测显示,phage1为有尾噬菌体,phage2为球形噬菌体.将上述5株副溶血弧菌进行卤虫无节幼体人工感染实验,结果显示,它们对卤虫无节幼体均有致病力,且各分离株的毒力表现出显著性差异;20130629002S01和20130726001S01两株带有溶源性噬菌体的副溶血弧菌的致病力显著低于无噬菌体的副溶血弧菌(20130721001S02).本研究结果表明,5株VPAHPND分离株都含有AHPND相关的质粒,表现出显著的毒力差异,可能携带不同的溶源噬菌体,也可能不携带溶源噬菌体,溶源噬菌体与副溶血弧菌各分离株的毒力并无必然相关性. 相似文献
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一例日本囊对虾暴发性死亡的病原分析 总被引：1，自引：0，他引：1
为了阐明山东省潍坊市一对虾养殖场发生日本囊对虾暴发性死亡的原因,采用分子生物学检测方法,对发病对虾进行了白斑综合征病毒(white spot syndrome virus,WSSV)、桃拉综合征病毒(Taura syndrome virus,TSV)、黄头病毒(yellow head virus,YHV)、传染性皮下及造血组织坏死病毒(infectious hypodermal and hematopoietic necrosis virus,IHHNV)、传染性肌肉坏死病毒(infectious myonecrosis virus,IMNV)、偷死野田村病毒(covert mortality nodavirus,CMNV)及急性肝胰腺坏死病(acute hepatopancreatic necrosis disease,AHPND)7种病原的检测,且对发病对虾进行了常规组织病理学观察。同时采用16S r DNA细菌鉴定方法及浸泡回接感染实验对分离自发病对虾体内的可疑病原菌进行了分子鉴定及毒力测试。结果显示,发病对虾样品核酸检测呈现WSSV强阳性,IHHNV和CMNV为弱阳性,其他4种病原为阴性。组织病理学观察发现,在对虾的胃、鳃等上皮组织中存在WSSV包涵体,头部肌肉纤维出现离散。对分离编号为2901、2902、2903的3株优势可疑病原菌鉴定结果显示,3株菌分别与印度格里蒙菌、交替单胞菌及溶藻弧菌相似,相似度分别为99%、99%及100%。攻毒结果显示,3株可疑病原菌的LC50分别为9.8×107、1.1×108与2.3×108 CFU/m L,各细菌毒力均较弱,非导致对虾出现暴发性死亡的病原。研究表明,导致本次日本囊对虾暴发性死亡的病因与混合感染病原WSSV、IHHNV、CMNV有关,其中WSSV感染是造成日本囊对虾暴发性死亡的主因,研究结果可为解析当前养殖日本囊对虾疾病暴发及其成因提供参考。 相似文献
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从某对虾育苗场2个育苗池中分别采集了发生摄食下降、活力降低及死亡率增高等症状的未知疾病的凡纳滨对虾(Litopenaeus vannamei)溞状幼体3期(Z3)和1期(Z1)的样品。用PCR检测白斑综合征病毒(WSSV)、传染性皮下及造血组织坏死病病毒(IHHNV)、急性肝胰腺坏死病副溶血弧菌(VpAHPND)、桃拉综合征病毒(TSV)、传染性肌坏死病毒(IMNV)、黄头病毒(YHV)、虾肝肠胞虫(EHP)、偷死野田村病毒(CMNV)和虾血细胞虹彩病毒(SHIV)等9种已知病原为阴性。组织病理学诊断观察到肝胰腺小管上皮细胞内存在不明褐色团块。使用2216E培养基对致病菌分离鉴定,得到2株溶藻弧菌(Vibrio alginolyticus),浸浴感染悉生卤虫(Artemia franciscana)幼体后的平均存活率分别为58%和83%。采用Illumina HiSeq高通量测序方法对这2个溞状幼体样品中细菌16S rRNA基因的2个高变区(V3~V4)进行总细菌菌群的测序,分析揭示了未知病因病虾中细菌菌群的多样性和相对丰度,门水平上2个样品的优势菌群均包括变形菌门(Proteobacteria)、拟杆菌门(Bacteroidetes)和厚壁菌门(Firmicutes),但相对丰度有显著差异;在属水平上相对丰度最高的均为弧菌属(Vibrio),在2个样品中的丰度分别为74.3%和60.5%,此外,Z1样品相对高丰度(21.9%)的属为黏着杆菌属(Tenacibaculum)。育苗管理信息及上述病例分析结果提示,该疾病可能是由于在过期存放的幼体饲料质量下降所致的营养障碍情况下,有一定致病性的溶藻弧菌条件性感染所引起的疾病。 相似文献
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近年来,虾肝肠胞虫(Enterocytozoon hepatopenaei, EHP)流行使我国养殖对虾遭受严重经济损失,现场快速检测是EHP防控的重要技术保证。本研究对本实验室研发的EHP现场快速检测试剂盒的分析特异性(ASp)、分析灵敏度(ASe)、诊断特异性(DSp)、诊断灵敏度(DSe)、重复性和稳定性6项性能参数开展了系统评估。ASp测试显示,该试剂盒与对虾白斑综合征病毒(WSSV)、偷死野田村病毒(CMNV)、虾血细胞虹彩病毒(SHIV)、致急性肝胰腺坏死病副溶血弧菌(VpAHPND)、传染性皮下及造血组织坏死病毒(IHHNV)等5种对虾常见病原及健康对虾无交叉反应;ASe测试显示,该试剂盒检测下限为101 copies/反应;以EHP TaqMan RT-qPCR方法为标准,比较了试剂盒对298份临床样品的测试结果,试剂盒的DSp为99.2%、DSe为91.7%;试剂盒对EHP阴性样品及强阳性样品的检测重复率为100%,弱阳性样品检测重复率为95.8%;试剂盒在–20℃和–40℃条件下分别可保存7个月和12个月以上。本研究表明,本实验室研制的EHP现场快速检测试剂盒具操作简便、快速、灵敏度高、特异性强、重复性好和稳定性强等优点,可满足对虾养殖现场对EHP的高灵敏度检测。 相似文献
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本研究从患急性肝胰腺坏死病(Acute hepatopancreatic necrosis disease,AHPND)的凡纳滨对虾(Litopenaeus vannamei)肝胰腺中分离到一株优势菌,编号为20160303005-1,通过16S rRNA和分子伴侣蛋白groEL基因序列分析,并结合生理生化特征,将该细菌鉴定为副溶血弧菌(Vibrio parahaemolyticus),其血清型为O1:KUT(K untypeable)。基因分析结果显示,该菌株携带可引起对虾AHPND的相关毒力蛋白基因pirA~(VP)和pirB~(VP),但不携带副溶血弧菌临床菌株毒力基因:耐热直接溶血毒素(Thenmostable direct hemolysin,tdh)和相对耐热直接溶血毒素(TDH-related hemolysin,trh)基因。菌株对凡纳滨对虾具有较强的致病性,浸泡感染的半数致死剂量(LD_(50))为7.96×10~3 CFU/ml。对虾急性感染后,6 h肝胰腺颜色变浅,肠胃变空;9 h肝胰腺呈浅白色,萎缩变小。9 h死亡数过半,24 h全部死亡。组织病理学分析显示,感染后对虾肝胰腺小管崩塌,上皮细胞严重脱落,呈现出典型的AHPND病理症状。药敏实验结果显示,该菌对庆大霉素、环丙沙星和头孢他啶等16种药物敏感,对阿莫西林、替卡西林和头孢噻吩等5种药物表现为耐药。上述研究可为该病原的流行病学及药物防控研究提供基本数据。 相似文献
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引起凡纳滨对虾急性肝胰腺坏死病的副溶血弧菌MLST新序列型 总被引：1，自引：1，他引：0
针对12株引起凡纳滨对虾急性肝胰腺坏死病(AHPND)的致病性副溶血弧菌,运用多位点测序技术,分析致病菌株的遗传特征。实验选择副溶血弧菌的7个管家基因dnaE、gyrB、recA、dtdS、pntA、pyrC及tnaA,对12株AHPND致病菌扩增测序。将核酸序列上传至PubMLST数据库进行比对后获得每株菌的序列型。收集其他地区AHPND致病性副溶血弧菌的多位点序列分型(MLST)数据,采用eBURSTV3及MEGA5.0软件进行遗传进化分析。结果显示,2014年中国广东分离的AHPND致病株属于一个新序列型ST1710(42、134、99、79、141、41、51),仅与库中ST415及ST975同源性较高。目前,急性肝胰腺坏死致病株的9种ST型可归为2个克隆组和5个单体。经系统发育树进一步分析可知新序列型ST1710与单体ST975遗传关系相近。本研究首次报道中国AHPND分离株的序列型,丰富了PubMLST数据库,并为其遗传进化研究奠定了理论基础。 相似文献
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根据偷死野田村病毒(CMNV)的保守基因序列,设计筛选出1对特异性引物CMN279,利用已公布的凡纳滨对虾白斑综合征病毒(WSSV)和传染性皮下及造血器官坏死病毒(IHHNV)特异性引物WSS235和IHHN356,建立了一种同时检测WSSV、IHHNV和CMNV的多重PCR检测方法。收集18种病原、健康对虾组织及WSSV、IHHNV、CMNV阳性病料,开展特异性测试,该方法可以特异性扩增出WSSV、IHHNV、CMNV基因片段,健康对虾肌肉组织、其他18种病原均未扩增出任何片段,特异性强。应用克隆方法制备目的基因质粒,应用连续稀释质粒方法开展灵敏度测试,测定该方法检测灵敏度分别为WSSV 9.74fg、IHHNV7.65fg、CMNV 10fg;与已报道的多重PCR检测灵敏度相比较,检测灵敏度提高10倍。应用本研究建立的多重PCR检测方法与实验室标准检验方法同时进行22个样品检验,多重PCR检验方法的检验结果与实验室标准方法检验结果符合率为100%。上述实验结果表明:本研究建立的多重PCR检验方法具有特异性强、灵敏度高、检验时间短、检验结果准确度高的特点,可用于WSSV、IHHNV和CMNV三种病原的快速检测诊断。 相似文献
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Sixteen candidate disease‐resistant parameters were selected through which to evaluate the acute hepatopancreatic necrosis disease (AHPND)‐resistant capability of Exopalaemon carinicauda after three generations of selection for AHPND‐causing strain of Vibrio parahaemolyticus (VPAHPND) resistance in our previous study. However, these parameters required further verification. In this study, another AHPND‐resistant E. carinicauda series was obtained through a short‐term selection procedure, consisting of three virulent challenge rounds of selection (about three‐week interval for each challenge) with VPAHPND infection. After this selection, the survival rate at 144 hr post infection (hpi) increased from 23.33% to 37.78% and the observed 48‐hr LD50 of VPAHPND to shrimp increased from 105.5 cfu/ml to 106.5 cfu/ml. Then, the immune response of this AHPND‐resistant E. carinicauda was studied using the 16 candidate AHPND‐resistant parameters selected for in our previous study. The improved VPAHPND clearance rate in hpi, increased total haemocyte counts, haemocyanin concentration, alkaline phosphatase activity and expressions of six immune‐related genes (Tollip and ALF in haemocytes and hepatopancreas; lysozyme, crustin and cathepsin B in hepatopancreas; and LGBP in haemocytes) at 24 hpi after the three‐round challenge selection suggest that these immune parameters may be reliable markers for the evaluation of the physiological status and potential AHPND‐resistant phenotypes in E. carinicauda. 相似文献
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Anuphap Prachumwat Suparat Taengchaiyaphum Natthinee Mungkongwongsiri Diva J. Aldama‐Cano Timothy W. Flegel Kallaya Sritunyalucksana 《Journal of the World Aquaculture Society》2019,50(1):5-17
Outbreaks of acute hepatopancreatic necrosis disease (AHPND) have caused great economic losses to many shrimp‐producing countries in Asia since its first appearance in 2009. The causative agent was reported in 2013 as specific isolates of Vibrio parahaemolyticus (VPAHPND) that were later found to harbor a plasmid (pVA) encoding the Pir‐like binary toxin genes Pir vpA and Pir vpB. VPAHPND isolates colonize the shrimp stomach and release the binary toxins that cause massive sloughing of tubule epithelial cells followed by shrimp mortality. More recent information indicates that pVA plasmid and variants occur in many V. parahaemolyticus serotypes and also in other Vibrio species such as Vibrio campbellii, Vibrio harveyi, and Vibrio owensii. Information on such genomic and proteomic studies of different VPAHPND isolates from different countries are reviewed. A cohort study carried out in Thailand in 2014 indicated that AHPND outbreaks account for only a portion of the disease outbreaks reported by shrimp farmers as outbreaks of early mortality syndrome (EMS). It is recommended that a regional research network and surveillance program for newly emerging or re‐emerging pathogens be established to speed up the process of diagnosis and the implementation of coordinated control measures and to avoid a repeat of the EMS/AHPND scenario. 相似文献
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为了阐明引起急性肝胰腺坏死病(acute hepatopancreatic necrosis disease, AHPND)副溶血性弧菌的接合型质粒在对虾养殖环境中的遗传多样性,实验从中国5个沿海省份的虾场收集了100个底泥样品,以质粒上编码接合转移蛋白的保守基因为目标,利用PCR法检测相关质粒的存在情况,并对质粒进行测序。结果显示,100个样品中有39个样品含有质粒的接合转移蛋白片段。从100个底泥样品中分离出15株副溶血性弧菌,其中13株含有1～2个质粒。质粒序列测序结果显示,这些质粒可分为8种类型/谱型,其中7种不携带pirAB,但均含有编码接合转移的基因簇。根据分离副溶血性弧菌携带质粒的8种谱型,分别选择8株副溶血性弧菌进行凡纳滨对虾攻毒实验,发现这些菌株对凡纳滨对虾的毒性有显著差异,实验虾死亡率为15%～100%。只有pirAB阳性菌株会对实验虾产生AHPND症状,死亡率为100%。对质粒组成进行分析表明,质粒之间遗传物质交换频繁,大部分质粒的遗传组成都来自一个183 kb的超大质粒pVP2HP。综上,本实验通过探究对虾养殖场底泥中结合性质粒的多样性,增强了人们对副溶血性弧菌... 相似文献
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为评估不同SNP标记密度对凡纳滨对虾AHPND抗性基因组预测准确性的影响，本实验对26个全同胞家系进行Vp AHPND侵染，收集686尾个体的存活时间数据，对其中242尾个体利用液相芯片“黄海芯1号”(55.0 K SNP)进行基因分型，基于A、G和H亲缘关系矩阵估计Vp AHPND侵染后存活时间的遗传参数；采用随机和等距抽取方式，基于55.0K SNP构建了8个低密度SNP面板(40.0、30.0、20.0、10.0、5.0、1.0、0.5和0.1 K)，利用GBLUP和ssGBLUP等方法预测Vp AHPND侵染后存活时间的基因组育种值，利用交叉验证方法计算其预测准确性，并与BLUP方法进行对比分析。遗传参数估计结果显示，Vp AHPND侵染后存活时间表现为高遗传力水平，估计值为0.68～0.79。在55.0 K SNP密度下，针对242尾基因分型个体数据集(G242)，利用BLUP、GBLUP和ssGBLUP方法获得的预测准确性分别为0.424、0.450和0.452,GBLUP和ssGBLUP比BLUP分别提升了6.13%和6.60%；针对686尾表型测定个体数据集(P686)... 相似文献
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Mohamed E. Megahed 《Journal Of Applied Aquaculture》2019,31(1):17-33
Acute hepatopancreatic necrosis disease (AHPND) has caused losses to shrimp farmers worldwide owing to Vibrio parahaemolyticus (VPAHPND). Selective breeding for disease resistance of shrimp was used as an alternative strategy for disease control. Five subsamples of shrimp from 20 full-sib families were subjected to a cohabitation challenge test. Juveniles of P. semisulcatus (mean weight 2.5 ± 0.17 g) were tested for survival after challenge with VPAHPND. Mortality in the challenge test was recorded daily, and the experiment was terminated after 96 days when the mortality ceased. Moderate heritabilities were estimated in resistance to VPAHPND based on a linear model (LM) and threshold model (TM). This indicates that disease resistance is a heritable trait, and a challenge test may serve as a basis for selection for resistance to VPAHPND in P. semisulcatus. However, further investigation is needed to confirm and quantify the additive genetic variation for resistance to VPAHPND in P. semisulcatus. 相似文献
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Monchai Pumkaew Suparat Taengchaiyaphum Sorawit Powtongsook Wiboonluk Pungrasmi Kallaya Sritunyalucksana 《Journal of the World Aquaculture Society》2019,50(4):878-886
Acute hepatopancreatic necrosis disease (AHPND) causes massive mortality in shrimp ponds within the first month poststocking. The causative agent is a specific strain of Vibrio parahaemolyticus (VPAHPND) that has acquired the capability to produce virulent binary toxins called ToxA and ToxB. This study aims to test the effect of the addition of an autoinducer‐2‐containing cell‐free supernatant (CFS) from the mutant Vibrio harveyi (VH) on growth and toxin production of VPAHPND. The relative AI‐2‐like activity in CFS was detected by luminescence assay. The effect of CFS (5 and 9%) on growth and toxin production of VPAHPND was evaluated. Compared to the control culture (without CFS‐VH addition), the addition of either 5 or 9% CFS‐VH affected the growth at the initial stage of VPAHPND. Similar growth profiles of VPAHPND were found with the addition of CFS‐VH at both concentrations. Western blot analysis suggests that the addition of CFS‐VH affected the production of both toxins. ToxA could be detected at the early hour post‐CFS‐VH inoculation, whereas the high amount of ToxB was detected when 5% CFS‐VH was added. However, interfering with the AI‐2 function with furanone, the AI‐2 antagonist resulted in a slight delay in the production of both toxins. Results from this study will help to design a novel strategy to control AHPND in shrimp culture. 相似文献
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Characterization of Vibrio parahaemolyticus causing acute hepatopancreatic necrosis disease in southern Thailand 
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下载免费PDF全文 J Kongrueng M Yingkajorn S Bunpa N Sermwittayawong K Singkhamanan V Vuddhakul 《Journal of fish diseases》2015,38(11):957-966
Vibrio parahaemolyticus was isolated from shrimp of five farms located in the Pattani and Songkhla provinces of southern Thailand. Using a PCR method targeted to the unique DNA sequences derived from the plasmid (AP2 primers) and the toxin gene (AP3 primers) of V. parahaemolyticus that caused acute hepatopancreatic necrosis disease (AHPND), a total of 33 of 108 isolates were positive. In contrast, all 63 and 66 isolates of clinical and environmental V. parahaemolyticus, respectively, obtained previously from 2008 to 2014 from the same area were negative. This implied that these strains were likely to be the cause of the outbreak of AHPND in this area. Intestinal samples proved to be a better source for the isolation of V. parahaemolyticus AHPND than the hepatopancreas. All isolates were investigated for haemolytic activity, virulence genes, serotypes, genotypes and antibiotic susceptibility. All the AHPND isolates had a unique O antigen, but small variations of the K antigens were detected from different farms. In addition, the DNA profiles of V. parahaemolyticus AHPND isolates were similar, but distinct from those clinical and environmental isolates. It is postulated that the causative agent of AHPND might have originated from one clone and then slightly different serotypes subsequently developed. 相似文献
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过氧化氢酶(catalase, CAT)是抗氧化酶体系的主要成员,在维持机体氧化还原平衡、抵御病原感染过程中具有重要作用。为研究CAT基因在软体动物应答病原胁迫过程中的作用,实验采用RACE技术通过克隆和序列拼接获得了缢蛏CAT基因的全长cDNA序列,并命名为ScCAT。ScCAT基因全长为2 840 bp,编码508个氨基酸。序列分析显示,Sc CAT蛋白含有1个CAT核心结构域(25～410),1个保守的酶活性位点(61FNRERIPERVVHAKGAGA78)和1个亚铁血红素结合位点(351RLFSYPDTH359)。多序列比对和系统进化树分析结果显示,Sc CAT属于CAT基因家族,且与无脊椎动物文蛤的亲缘关系最近。组织分布显示,ScCAT在所有检测的组织中均能表达,其中在肝胰腺中表达量最高,鳃中次之,血细胞中的表达量最低,分别为闭壳肌的85.67倍、50.09倍和0.76倍。在副溶血弧菌胁迫下,ScCAT在缢蛏肝胰腺中的表达明显上升,且在12 h达到最高值,为对照组的3.56倍;酶活性测定结果显示,副溶血弧菌胁迫显著诱导缢蛏肝胰腺和鳃组织中的CAT活性。为进一步探讨Sc CA... 相似文献
19.
Acute hepatopancreatic necrosis disease (AHPND) of shrimps is an important disease, first appeared in China in 2009. Since then, AHPND has caused serious drops in shrimp production (up to 20 % worldwide). Although AHPND [originally termed as acute hepatopancreatic necrosis syndrome (AHPNS)] first appeared in 2009, it was not until 2013 that a laboratory infection model was devised and the causative agent identified as certain strains of Vibrio parahaemolyticus. AHPND has caused mortality from 40 to 100 % which usually occurs early (within approximately 35 days) after stocking shrimp fry in shrimp ponds; therefore, it was initially referred to as early mortality syndrome (EMS). Confusingly, other pathogens and environmental factors also cause EMS and are often attributed to AHPND by shrimp farmers. Frequently, farmers do not send samples for confirmatory tests requiring detection of the unique histopathology at the acute stage of disease (massive sloughing of hepatopancreatic epithelial cells without any accompanying signs of a pathogen). The gross signs presumptive of AHPND (lethargy, slow growth, empty stomach and midgut, and a pale to white, atrophied hepatopancreas) are insufficient for confirmatory diagnosis. Recently, molecular detection of AHPND bacteria using PCR has been developed, which has sped up diagnosis and increased research on the causative agent, alternative detection methods, and possible therapies. We hope that this review of research progress on AHPND will serve as a useful introduction for researchers who are currently unfamiliar with AHPND, but have backgrounds in bacterial virulence, detection, and epidemiology, and may be encouraged to participate in the research effort to reduce AHPND’s impact on shrimp cultivation. 相似文献
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盐度胁迫对三疣梭子蟹鳃Na+/K+-ATPase酶活的影响 总被引：2，自引：2，他引：0
通过钼蓝法测定三疣梭子蟹在3组实验盐度的胁迫过程中第2对和第6对鳃Na+/K+-ATPase酶活的变化,比较了3组实验盐度胁迫1 d时,鳃Na+/K+-ATPase的酶活大小。结果表明,在盐度胁迫初期,3组实验盐度下第2对和第6对鳃Na+/K+-ATPase的酶活下降;之后,各组实验盐度下第2对和第6对鳃Na+/K+-ATPase的酶活开始随胁迫时间增长而上升;最后,各组实验盐度下第2和第6对鳃Na+/K+-ATPase的酶活下降并趋于稳定。另外,胁迫1 d时,各组实验盐度下三疣梭子蟹前5对鳃Na+/K+-ATPase的酶活显著低于后3对鳃Na+/K+-ATPase的酶活。三疣梭子蟹对盐度变化的调节可分为被动应激期(酶活力下降)、主动调节期(酶活力逐渐上升)和适应期(酶活力稳定);三疣梭子蟹后3对鳃是离子转运、渗透压调节的主要部位。 相似文献