水库鲢鱼小鞘指环虫病鳃组织病理及其防治

在１９９１－１９９３年，笔者在清原县金家水库和后楼水库用敌敌畏进行了鲢小鞘指环虫病的防治试验，并对大水面防治鱼病的施药方法作了初步探索。试验结果表明，０．０８－０．２０ｐｐｍ的敌敌畏均能有效杀灭此虫。组织病理研究发现，病鱼鳃瓣缺损，粘液增多，鳃血管扩张充血，出血，呼吸上皮肿胀。上皮细胞增生，使鳃小片融合，鳃丝呈棍棒状；相邻几条鳃丝发生融合，形成一片上皮细胞板。病状严重时，鳃小片坏死、解体。     

斑点叉尾(鱼回)鳃结构的扫描电镜观察

应用扫描电镜对斑点叉尾鮰（Ictaluruspunctatus）鳃的表面微细结构进行了观察。结果表明,斑点叉尾鮰鳃的表面结构和微细结构与其他硬骨鱼类基本相似,鳃弓和鳃耙表面被具环形微嵴的扁平上皮细胞所覆盖,鳃弓表面细胞之间有孔洞;鳃耙基部较粗壮;中部鳃丝上皮细胞表面的微嵴两侧有细小的横突,有些微嵴出现融合或间断;端部和基部鳃丝上皮细胞表面的微嵴消失,形成密集颗粒状突起;鳃小片的高度和片间距较大。讨论了斑点叉尾鮰鳃的形态结构与其生理功能的关系。     

一例金鱼指环虫病、小瓜虫病和烂鳃病并发的诊治技术

１ 症状 金鱼无食欲，体消瘦，活动呆滞，体表无明显症状。翻开鳃盖，可见鳃盖内表皮有轻度充血，鳃丝末端浮肿、粘液增多，粘附有污物，鳃丝间偶有发现白点，呈淡红色。剖检时，除肠内无食物外，各内脏器官基本正常。镜检一个视野有４个小瓜虫或幼体，两个视野有３只指环虫，且鳃丝上皮细胞脱落，血管有血窦，严重时呈坏死性烂鳃。所检查的５尾金鱼４尾都是如此，另一尾病症较轻。因此，诊断为金鱼小瓜虫病、指环虫病和烂鳃病并发。２ 发生原因２．１ 进货时金鱼在产地就有虫卵和孢子，至水温、环境适宜时，虫、菌即大量繁殖，感染金鱼。２…     

加州鲈非细菌性疾病及其防治

１ 车轮虫病１．１ 病 因 由原虫类的多种车轮虫寄生于加州鲈体表及鳃部感染引起。１．２ 症状 病鱼体黑而瘦，食欲减退或不摄食，群游于池边。大量寄生时，鳃组织分泌大量粘液，鳃丝发白腐烂，严重时池边慢游最后死亡。１．３ 危害及流行情况 ４～５月份最为流行。对鱼苗、鱼种危害较大。该病传播速度快，感染率高，感染强度大，且易继发感染。１．４ 防治方法 １）生石灰彻底清塘，杀灭病原体；２）注意放养密度和保持水质清新；３）苗种入池前用３％食盐水浸洗３～５分钟；４）全池泼洒０．７ ｇ／ｍ３硫酸铜、硫酸亚铁合剂（５：２），…     

鲫鱼三代虫病及其鳃组织的病理研究

本文报道了鲫鱼感染三代虫后的症状及鳃组织的病理情况。症状主要是：患病鱼表现出极度的不安并在水中无规律地狂游，鳃丝缺损甚至末端缺失．病理组织切片研究表明：三代虫对鲫鱼鳃的危害主要是影响鳃组织的正常气体交换，严重时导致病鱼的窒息死亡．本研究结果可为养殖业预防三代虫病提供基础生物学资料。     

欧洲鳗短钩拟指环虫病及其鳃组织病理

报道了患短钩拟指环虫病欧洲鳗的症状、流行状况和鳃显微组织病理.游动和呼吸频率异常、鳃丝浮肿和鳃上粘液增多为该病的主要症状.该病尽管在冬季也有发生,但水温在26℃以上的春末、夏季和秋初是最易发病的流行季节,流行出现明显的季节性变化.患病欧洲鳗鳃的组织病理变化主要表现出5种类型,其一是鳃小片上皮细胞增生,使邻近的鳃小片相连;其二是鳃小片粘液细胞增生,同样使鳃小片连成一片,增生的粘液细胞经阿利新蓝(Alclan blue)和过碘酸雪夫氏(Periodic acid schiff)二者联合染色后呈蓝紫色的染色反应,属于Ⅳ型的粘液细胞;其三是鳃小片肿大,但单层扁平上皮细胞无肿大现象,上皮细胞层与毛细血管相分离,鳃小片上皮细胞坏死,上皮细胞层破裂,血细胞外溢,鳃小片上皮细胞坏死脱落后,失去鳃小片原有的结构;其四是鳃小片肿大同时伴随单层扁平上皮细胞肿大,进一步发展,鳃小片上皮细胞坏死脱落后,鳃小片同样失去原有的结构;其五是鳃小片毛细血管严重充血扩张,比原毛细血管扩张几倍到十几倍,形成充满红细胞的棒状到球状的动脉瘤.结果表明鳃上皮细胞增生、粘液细胞增生、鳃小片肿大、上皮细胞坏死脱落和严重充血成动脉瘤等病理变化都可导致患病欧洲鳗呼吸困难,轻者影响其生长,重者最终因呼吸衰竭而死亡.     

斑点叉尾鮰主要疾病与防治（下）

3.寄生虫性疾病 （1）小瓜虫病（Ichthyophthiriasis） 病原：小瓜虫病是由多子小瓜虫引起的，是斑点叉尾鮰一种危害较大的原虫性寄生虫病。由于病鱼体表粘液增多，游动异常，常见鱼体与固体物摩擦，继而在体表、鳍条和鳃上出现大量小白点，故小瓜虫病又称白点病（White spot disease）。     

洪湖碘泡虫在发病和隐性感染异育银鲫组织器官中的分布

为探究洪湖碘泡虫在被感染异育银鲫不同组织器官中的分布及不同感染阶段的差异，实验采用显微镜镜检、PCR检测及组织病理切片相结合手段，对发病及隐性感染异育银鲫的肌肉、伪鳃、鳃、头肾等11个组织器官进行了广泛检测分析。显微镜镜检发现，在发病鱼的咽、伪鳃和鳃能观察到孢囊或成熟孢子；在隐性感染异育银鲫的咽上壁与副蝶骨间结缔组织、伪鳃及其血管周边观察到大量棕黄色结节，并含有洪湖碘泡虫的成熟孢子。不同组织器官DNA样品PCR检测发现，在发病鱼除肌肉外的其他10个组织器官中均检测到洪湖碘泡虫存在，其中伪鳃检出率最高(100%)；隐性感染异育银鲫在咽上壁组织、伪鳃、头肾、体肾、脾脏及卵巢中检出洪湖碘泡虫，伪鳃检出率也为最高(26.7%)。组织病理切片显示，发病鱼咽上壁内分布着大量蜂巢状孢囊及成熟孢子，伪鳃被严重侵占和破坏；残存伪鳃鳃丝周边能观察到增殖和发育阶段的孢子生成细胞。综上所述，本研究首次报道了洪湖碘泡虫在发病和隐性感染异育银鲫不同组织器官中的分布差异，发现伪鳃可能是洪湖碘泡虫寄生和发育成熟的重要器官。结果为洪湖碘泡虫病的准确检验检疫和进一步开展致病机制研究奠定基础。     

苏氏Mang鲶鳃超微结构观察

对苏氏Mang鲶鳃结构进行扫描和透射电镜观察。Mang鲶鳃丝末端膨大呈杓状结构，每一鳃丝两侧具有许多呈褶状的鳃小片，相邻两鳃丝上的鳃小片紧密镶嵌排列。鳃弓和鳃耙表面分布众多味蕾。鳃丝呼吸面上皮细胞薄，高度血管化，形成呼吸面隆起，非呼吸面由微脊细胞彼此相连，间缝具分泌细胞开口。鳃小片由单层或数层外上皮细胞和由基膜相隔的柱状细胞及其围在血管腔的凸缘构成，氯细胞多分布在鳃小片基部，并有开口通外，还探讨了Mang鲶鳃丝和鳃小片特殊的结构与功能。     

香鱼寄生虫病及其防治

一、车轮虫病１．症状车轮虫寄生部位因鱼体大小而异，一般在苗种阶段时寄生在体表，规格大时则大多寄生在鳃上。镜检患病鱼体表和鳃便可确诊。鱼体少量寄生时不显症状，严重侵染皮肤、鳍、鳃时，车轮虫用它的齿轮环磨损香鱼体表皮细胞和鳃丝、鳍条的上皮细胞，刺激鱼体产生大量粘液，病鱼不摄食，成群沿塘边狂游，在水中跳跃，严重感染时能够使鳃丝和体表上皮细胞破坏、脱落，导致细菌侵入，造成鱼类大批死亡。２．流行与危害全国各地一年四季都有发生、水质混浊且有机质多的池塘较易发生，适宜繁殖温度２０～２８℃，４～７月份较流行。鳗…     

鲫圆形碘泡虫病组织病理学研究

采用常规石蜡切片、苏木精-伊红染色的方法,研究了鲫（ Carassius auratus auratus ）自然感染圆形碘泡虫（Myxobolus rotundus）后的组织病理变化。结果表明,感染圆形碘泡虫后,在鲫的头部、鳃和体表能形成大小不一的圆形或椭圆形乳白色孢囊,其孢囊为典型的3层结构：外层的结缔组织、双层质膜的外质以及各个发育阶段的孢子或营养体组成的内质。病理切片可见鱼体各组织器官均有不同程度的病变,主要表现为鳃丝粘连、肿胀增生;肝脏发生以肝血窦为中心的透明、空泡变性;肾小管内皮脱落,肾小球萎缩;肠道粘膜层脱落,肌层细胞肿胀病变;脾脏的含铁血黄素增多等异常现象。     

Hepatic microsporidiosis of juvenile grey mullet, Chelon labrosus (Risso), due to Microgemma hepaticus gen.nov. sp.nov.

Abstract. Microgemma hepaticus gen.nov. sp.nov. is described from the liver of juvenile grey mullet, Chelon labrosus (Risso). Development occurs within xenomas (diameter 500μm) which have microvillar surfaces, encircling bands of mitochondria and a reticulate hypertrophic nucleus. Vegetative developmental stages, meronts, are plasmodial and divided by plasmotomy. These stages are enclosed by host membranes. Sporogonic stages are free in the cytoplasm and divide by multiple exogenous budding. Uninucleate spores (2·4μm × 4·2μm) possess 7–9 coils of the polar filament and a lamellar polaroplast. Xenomas are associated with liver connective tissue, and cause necrosis of adjacent liver cells in certain circumstances. Host response to infection involves leucocyte infiltration and granuloma formation, with spores being destroyed by repeated macrophage phagocytosis and necrosis and resulting in gradual resolution of the lesion. Although juveniles apparently tolerate large parasite burdens there is some evidence of a contribution by the parasite to stress-related mortality. The transmission of the disease and its potentially high pathogenicity to larval fishes is discussed.     

Gill filament necrosis in farmed Japanese eels, Anguilla japonica (Temminck & Schlegel), infected with Herpesvirus anguillae

A herpesviral gill disease accompanied by mass mortality occurred in Japanese eels, Anguilla japonica (Temminck & Schlegel), reared in warm water ponds from 1993 to 1995. Diseased fish displayed marked haemorrhage and congestion within gill filaments and destruction at the tips of affected filaments with necrosis and inflammation in the central connective tissue and the central sinus. Electron microscopy revealed herpesvirus particles in infected fibrocytes within the filamental connective tissue. The isolate was identified as Herpesvirus anguillae by a neutralization test. Infectivity experiments with the isolates revealed that the virus was pathogenic.     

Histopathology of leech, Austrobdella bilobata Ingram, infestation on the yellowfin bream, Acanthopagrus australis (Günther), in northern New South Wales

Abstract. The histopathology of leech, Austrobdella bilobata , infestation on the upper palate and pelvic fin of the yellowfin bream, Acanthopagrus australis (Günther), is described. The feeding site was often haemorrhagic and swelling surrounded the attachment site. Histological examination revealed massive cellular infiltration (predominantly lymphocyte and macrophage) in the submucosa beneath the feeding and attachment sites. The latter also had a complete erosion of the integument beneath the parasite. Localized proliferation of connective tissue fibres and zones of necrosis and oedema were present in some cases.     

Pathology of bacterial gill disease: sequential development of lesions during natural outbreaks of disease

Abstract. This study examines the sequential pattern of bacterial colonization and the sequential development of branchial lesions during typical outbreaks of bacterial gill disease (BGD) among four groups of commercially reared rainbow trout fingerlings, Oncorhynchus mykiss (Richardson). During a 5-month monitoring regime, prior to the onset of natural outbreaks of BGD, gill morphology of examined fish remained unaltered. Bacterial colonization of the gills was immediately preceded by several gill changes which were widely present in fish from all groups under study. These changes, which were detectable at the ultrastructural level only, included cytoplasmic blistering and degeneration of the microridges of the superficial filament epithelium, in addition to slight topographical irregularity of the filament tips suggestive of mild hyperplasia. Bacterial colonization began at these altered filament tips before spreading to more proximal regions of the filament and adjacent lamellar surfaces. Explosive increases in proportional morbidity and mortality coincided with the development of the following gill lesions: extensive bacterial colonization of lamellar surfaces, lamellar epithelial hydropic degeneration and necrosis, and lamellar oedema. In contrast, gill lesions such as lamellar fusion, epithelial hyperplasia and various metaplastic responses were detected later either as subacute (3–5 days) or chronic (7–14 days) changes. The role of epithelial necrosis as an important event during BGD is discussed as a possible mechanism leading to the development of sub-acute and chronic gill lesions.     

虹鳟肝脂肪变性病病理学的初步观察

肝脂肪变性病是虹鳟常见的营养缺乏疾病,可使养殖产量罹致重大损失。取虹鳟(Salmo gairdneri)的肝脏和血液进行光学显微镜和电子显微镜观察;血液经常规和生化检验(分析)。石蜡切片病鱼肝细胞大量坏死,结缔组织增生,使肝组织变性破坏,已无法辨认。冰冻切片P.A.S.阴性,空泡中没有脂肪和糖元。电镜扫描与透射观察,病鱼肝细胞坏死,可见大量脂肪滴和空泡。血液常规红血球比数下降,淋巴球数下降,中性白血球和单核球增多。生化指标麝香草酚浊度(TTT)均在2单位以下,麝香草酚絮状(TFT)阴性,谷丙转氨酶(GPT)明显增高;胆固醇下降,血清总蛋白含量下降,白蛋白与球蛋白的比例倒置。     

硫酸锌慢性毒性胁迫下克氏原螯虾的组织病理

将克氏原螯虾(Procambarus clarkii)成虾在Zn2+质量浓度为0、0.40 mg/L、4.04 mg/L和40.37 mg/L的硫酸锌溶液中浸浴21 d,分别于第7、14和21天时每组随机抽取5只虾,采集肝胰腺、鳃、触角腺、性腺、肌肉及消化道组织,于Bouin′s液中固定24 h。采用石蜡切片和HE染色的方法,观察其组织的病理变化,从组织学水平研究硫酸锌对克氏原螯虾的慢性毒性作用。结果显示,浸浴时各Zn2+浓度组肝胰腺、触角腺细胞质中出现被染成红棕色的颗粒,且颗粒的数量与浸浴浓度及时间成正相关。0.40 mg/L组在浸浴期间各组织均未出现其他明显病变;4.04mg/L组及40.37mg/L组从浸浴第7天开始肝胰腺、触角腺、鳃组织出现出血、细胞坏死等病变,随浸浴浓度增大和时间延长坏死细胞比例增大。40.37 mg/L组第14天时精母细胞开始出现坏死;第21天时精巢、卵巢严重出血,精、卵细胞出现大面积坏死,肝细胞大量坏死脱落,肝小管结缔组织增生,大量脱落的细胞塞满管腔使肝胰腺表面形成肉眼可见的红棕色颗粒状斑点。结果表明在Zn2+质量浓度高于4.04 mg/L的硫酸锌浸浴21 d后,克氏原螯虾肝胰腺、触角腺、鳃、性腺组织均出现不同程度的病变,表明其代谢系统、呼吸系统、生殖系统等受到较严重的损伤,因此长期暴露在Zn2+质量浓度高于4.04 mg/L的环境中会严重威胁克氏原螯虾的生存和繁殖。     

单环刺螠精巢年周期发育及精子发生

采用组织学方法观察了单环刺螠(Urechis unicinctus)精巢的形态结构及其年周期发育,并利用超微技术观察了精子的发生过程。结果表明,单环刺螠的精巢呈条带状,位于虫体尾部,两端通过肌束分别与呼吸肠管壁外侧和体壁内侧相连。精巢由生精细胞团与结缔组织组成,结缔组织位于精巢中央,精原细胞团分布于结缔组织外周,精母细胞团散布于结缔组织内,各级精母细胞脱离精巢落入体腔液中,历经精母细胞、精细胞,最后形成精子脱离细胞团进入肾管。根据精巢的组织学特征,将单环刺螠的精巢年周期发育划分为增殖期、生长期、成熟期、排放期和休止期5个时期。光镜和电镜下观察了精巢和体腔液中精子发生各时期的结构变化,包括细胞核形态的变化、顶体发生以及尾部的形成。本研究揭示了单环刺螠的精巢发育特点、精子发生历经的场所和分化特征。     

Localization of major yolk protein in the digestive tract of the sea urchin <Emphasis Type="Italic">Strongylocentrotus intermedius</Emphasis>

In the present study, we examined the localization of the major yolk protein (MYP) in the intestine of the sea urchin Strongylocentrotus intermedius. First, partial MYP complementary DNA was isolated from the sea urchin intestine. The expression level of MYP messenger RNA (mRNA) along the sea urchin digestive tract is highest in the intestine, so we performed in situ hybridization and immunohistochemical analysis using this tissue. No MYP mRNA was detected in the luminal epithelium, connective tissue, muscle tissue, or coelomic epithelium by in situ hybridization analysis. Positive immunohistochemical staining was observed in the luminal epithelium, inner epithelium and connective tissue, the signal being strongest in the latter. We conclude that MYP synthesized in the inner epithelial cells is moved to and stored in connective tissue and the luminal epithelium, before being secreted into the body cavity and the inner digestive cavity of the sea urchin.     

南方大口鲶寄生鲶盘虫一新种——拟凶恶鲶盘虫↑（*）

本文报道了采自南方鲶SilurusmeridionalisChen鳃上之寄生鲶盘虫1新种,定名为拟凶恶鲶盘虫Silurodiscoidesparasotisp.nov.。其后固着器由2对中央大钩和7对发育不完全的雏形边缘小钩组成;雄性交接器由弯曲似长号状交接管和“6”字形片状支持器组成。并与相似种进行了比较研究,同时对南方大口鲶苗期鲶盘虫病进行了研究。