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1.
Abstract. The range of branchial lesions associated with bacterial gill disease (BGD) in rainbow trout, Oncorhynchus mykiss (Richardson), was investigated through the ultrastructural examination of 23 separate outbreaks of the disease condition within commercially reared stocks. Diseased branchial tissues had a large and diffusely distributed monomorphic population of filamentous bacteria which were strictly epicellular. Although bacterial colonization was restricted to the branchial cavity, it was neither site nor cell specific: epithelial and chloride cells of the lamellae, filaments and lining tissues of the branchial cavity were all uniformly affected. The bacteria possessed an extensive glycocalyx which appeared to facilitate adhesion to the apices of the microridged sub-unit modifications of the cell surface. Sites of colonization were accompanied by a diffuse pattern of cellular degeneration and necrosis that was generally restricted to the outer layers of epithelium. The polarity and nature of these changes suggest that the mechanism of interaction between the bacteria and host cells includes progressive hydropic change as a sequel to primary membrane damage and consequent increased cell permeability. These cellular changes were accompanied by the range of stereotypical responses of the gill to damage frequently reported for BGD including lamellar fusion, epithelial hyperplasia, and squamous and mucous cell metaplasia, in addition to lamellar spongiosis.  相似文献   

2.
An unusual form of bacterial gill disease (BGD) was identified which affected five species of cultured salmonids from Canada (i.e. rainbow trout, chinook salmon and Atlantic salmon), Norway (i.e. brown trout) and Chile (i.e. coho salmon). All outbreaks occurred at low water temperatures (< 10 °C) and with clinical presentations distinct from classical BGD, which is caused by Flavobacterium branchiophilum. In contrast to classical BGD, fish did not show marked respiratory distress with flaring of the opercula, the animals did not orientate at the surface of the water column near inflow water or at the margins of the tanks, and the feed response of the fish was varied. While mortality was increased, it was not precipitous as in classical BGD. Eight outbreaks were examined in greater detail using histopathology, scanning electron microscopy, bacteriology and immunohistochemistry. Large numbers of small bacterial rods were seen adhering to the lamellar epithelium of affected gills from all outbreaks. Histologically, the lamellar epithelium appeared swollen, often with evidence of single cell degeneration and exfoliation. In more severe instances, the formation of lamellar synechiae was seen, usually associated with sequestration of bacteria between fused lamellae. By contrast with typical BGD, overt epithelial hyperplasia, lamellar fusion and filamental clubbing were not common sequelae to infection; instead, the end result was shortened and somewhat stubby lamellae covered with swollen epithelial cells. The predominant bacterium recovered from affected gills was a small, Gram-negative, motile, fluorescent pigment-producing rod that shared phenotypic characteristics with Pseudomonas fluorescens. Polyclonal antisera prepared against three representative isolates indicated a weak antigenic similarity among them. Immunohistochemistry corroborated this finding, in that the antisera reacted strongly with gill sections containing the homologous bacteria, but not against morphologically similar bacteria in heterologous sections. A Gram-negative, yellow pigmented bacterium (YPB), identified as Flavobacterium psychrophilum, was also recovered, but only from the gills in the Ontario outbreaks. Antiserum prepared against this YPB indicated an antigenic similarity among isolates recovered from the Ontario outbreaks, but immunohistochemistry failed to recognize antigenically related bacteria on the gills of fish from the other outbreaks. Based on the unusual clinical presentation and the histopathological appearance of the gills, in conjunction with the absence of filamentous bacteria associated with and recovered from affected gills, the present authors have called this condition ‘atypical bacterial gill disease’ or ABGD.  相似文献   

3.
氯氰菊酯暴露对草鱼4种器官组织结构的影响   总被引:1,自引:0,他引:1  
通过氯氰菊酯对草鱼(Ctenopharyngodon idellus)幼鱼(9.30±0.48)g的急性毒性实验及对鳃、肝、肾、脾的组织学研究,探讨了随着氯氰菊酯浓度的增加以及暴露时间的延长草鱼组织结构损伤的变化趋势.结果显示:氯氰菊酯对草鱼种的48 h-LC50和96 h-LC50分别为55.21μg/L和25.00...  相似文献   

4.
Abstract. Organ samples were collected from plaice, Pleuronectes platessa L., captured in the highly oiled Aber Wrac'h and Aber Benoit at five intervals during the period 1978-1980, following the Amoco Cadiz crude oil spill. Reference plaice were obtained along the western and southern coasts of Brittany. Tissue samples were fixed, processed and stained by routine histologic procedures for qualitative and quantitative histopathological examination. The predominant lesions and conditions which characterized fish from the oiled estuaries were: fin and tail necrosis, hyperplasia and hypertrophy of gill lamellar mucous cells, gastric gland degeneration, decreased hepatocellular vacuolation (lipid), increased concentration of hepatic macrophage centres and lateral trunk muscle fibre degeneration. Dilation of Bowman's space, glomerular hypertrophy and abdominal muscle fibre degeneration were pronounced at the last sampling interval. Other types of lesions were seen at a lower frequency: hyperplasia and fusion of gill lamellar epithelium, telangiectasis of gill capillaries, hepatopancreatic degeneration and hepatic necrosis. Fish muscle and liver collected for biochemical analysis to detect the presence or absence of petroleum hydrocarbons were negative for Amoco Cadiz oil fractions. At the same time oysters, Crassostrea gigas Thunberg, collected from the oiled estuaries throughout the study period, showed high levels of Amoco Cadiz oil fractions. These data, along with the type and frequency of lesions observed, suggested that the plaice had been chronically-exposed to petroleum hydrocarbons of Amoco Cadiz origin. Some relief from chronic pollutant exposure was indicated by a decrease in gill mucous cell concentration at the last sampling interval. An increase in abdominal muscle fibre degeneration and an increase in the frequency of dilation of Bowman's space with glomerular hypertrophy at the last sampling interval suggested a latent response to the polluting agent.  相似文献   

5.
为进一步了解氨氮对团头鲂幼鱼的毒性毒理影响,以体质量为(14.27±0.01)g的团头鲂幼鱼为研究对象,研究了氨氮胁迫对其鳃、肝、肾组织结构的影响。实验首先进行96h的氨氮胁迫,得出96h LC50,在此基础上,设置对照组(0.472 mg/L)和实验组(25 mg/L)两个氨氮浓度处理组,进行0、6、12、24、48h的氨氮胁迫,取样后剩余团头鲂幼鱼移入曝气自来水进行96h的毒后恢复实验。结果表明:96h LC50为56.492 mg/L;三种组织观察表明,氨氮胁迫6h,鳃丝毛细血管扩张,上皮组织增生;肝细胞肿胀,细胞核肿大,肝细胞空泡化;肾小球萎缩,肾小囊腔膨大,肾小管管腔缩小;胁迫12h,泌氯细胞增生,呼吸上皮细胞出现部分脱落;肝细胞水样变性、血窦扩张、细胞轮廓模糊,形成点状病灶;肾小管上皮细胞肿大、水样变性、浊肿;胁迫24h,鳃小片融合、变短,呼吸上皮细胞大面积脱落;肝细胞水样变性、血窦扩张严重,形成局部病灶;肾组织淋巴细胞浸润严重,充血,肾小球坏死,肾小管坏死;胁迫48h,鳃小片卷曲,上皮细胞部分脱落;肝细胞部分溶解、血窦扩张,形成点状病灶;肾小管上皮细胞坏死,肾小球坏死;96h恢复后,泌氯细胞和上皮组织增生严重;肝组织大面积细胞核肿大,血窦扩张;肾组织淋巴细胞浸润严重,肾小管坏死,肾小球坏死。实验表明,不同的器官之间病症的损伤程度是不同的,肝组织的损伤最严重,然后依次是鳃和肾。随着胁迫时间延长,鳃、肝和肾组织受到的损害增加,同时鱼体也产生防御反应,但96h的恢复期不足以让团头鲂幼鱼在胁迫中完全恢复,而恢复能力最差的是肾组织。  相似文献   

6.
Epitheliocystis infection affecting the gill and the pseudobranch of the cultured amberjack, Seriola dumerili Risso, is described. In hyperinfected fish, proliferative cell response around the epitheliocystis capsule resulted in gill and pseudobranch lamellar fusion, which led to mass mortalities in the 0+age class. Histopathological and scanning electron microscope observations showed that the target cell was the chloride cell since (1) epitheliocystis organisms were first found within the chloride cell; (2) chloride cells underwent degeneration in the filament epithelium, proliferated along the lamellae, and hypertrophied; and (3) cysts were found only in the trailing edge of the gill filament and in the interlamellar spaces where, in healthy fish, chloride cells are mainly located. In some cases, the pseudobranch of infected fish was much more severely affected than the gill. It is therefore suggested that, for diagnostic purposes, the pseudobranch should also be sampled when epitheliocystis disease is suspected.  相似文献   

7.
Evaluations of histopathological lesions in gill tissue were carried out in the freshwater fish Macropsobrycon uruguayanae following 30 and 60 days of exposure to 1.5 mg 1-1 of cadmium. The study was conducted on both fed and starved animals in order to determine the influence of feeding condition on cadmium toxicity. The main lesions observed and quantified were: (1) hyperplasia of primary lamellar epithelium; (2) hyperplasia of secondary lamellar epithelium; (3) separation of respiratory epithelium; (4) shortening of secondary lamellae; (5) epithelial necrosis; (6) fusion of adjacent secondary lamellae; (7) hypertrophy of respiratory epithelium; (8) lamellar telangiectasis; (9) hyperplasia of chloride cells; (10) mucinous metaplasia; and (11) inflammatory infiltration. Lesions 6, 8, 9 and 11 were only induced by exposure to cadmium, while lesion 4 could be produced only by starvation. Starved fish also showed a reduction in total body weight and length. Lesion 2 was shown to be non-specific, and produced by either cadmium, starvation or even exposure time. The possible mode of action of the experimental factors are discussed in relation to the observed pathologies.  相似文献   

8.
Lake trout Salvelinus namaycush (Walbaum) raised for stocking experienced yearly (2011–13) winter epizootics of epitheliocystis. Affected fish were dispersed on the bottom of the tank, had decreased feed and fright response, and mortality often reached 40%. Peak mortality occurred within 3 weeks of the appearance of clinical signs, and outbreaks typically lasted 6 weeks. Affected fish had no gross lesions but histologically had branchial epithelial necrosis and lamellar hyperplasia, with small to large numbers of scattered epithelial cells containing 10‐ to 20‐μm inclusions. A longitudinal study was undertaken of one annual outbreak, and lamellar hyperplasia was most closely associated with mortality. The number of inclusions was statistically greater (P < 0.05) before and during peak mortality, but inclusions were present in low numbers before clinical signs occurred. Results of histochemical staining, immunohistochemistry and transmission electron microscopy supported the presence of a β‐proteobacteria rather than a Chlamydiales bacterium within inclusions. PCR primers to identify Chlamydiales did not give consistent results. However, the use of universal 16S rDNA bacterial primers in conjunction with laser capture microdissection of inclusions demonstrated that a β‐proteobacteria was consistently associated with affected gills and is more likely the cause of the disease in lake trout.  相似文献   

9.
Abstract. Since 1977, repeated outbreaks of infestation by Amyloodinium ocellatum (Dinoflagellida) in cultured gilthead bream Sparus aurata L. and seabass Dicen-trarchus labrax (L.) resulted in sporadic and mass mortalities. Fingerlings and yearlings as well as breeders were affected and, since 1978, larval and post-larval S. aurata in the hatchery. Infestations in juvenile and breeder fish were located predominantly on the gills and mucosal integument but in larval fish only the skin rather than the gills was infested. Histopathological changes of the infested gills are described. Vacuolar degeneration of the cells penetrated by the parasites' rhizoids was evident at the site of attachment and cloudy swelling was apparent in the surrounding epithelial cells. In heavy infestations the entire epithelium of the gill filaments underwent hyperplasia with consequent fusion of the lamellae. Where hyperplasia was extensive the cells gradually degenerated while the inner epithelial layer showed distinct spongiosis and in some cases completely disintegrated. All heavily infested gills lacked mucous cells.  相似文献   

10.
草鱼细菌性烂鳃病的组织病理研究   总被引:7,自引:2,他引:7  
草鱼细菌性烂鳃病是一种危害严重的常见鱼病。其组织病理变化可以分为慢性和急性两种类型。鳃组织病理变化,经过炎性水肿、细胞增生和坏死三个进程。慢性型以增生为主;急性型的鳃组织病理变化,由于病程短,炎性水肿迅速转入坏死,增生不严重或几乎不出现,以炎性水肿和坏死为主。患细菌性烂鳃病的草鱼的肝脏、肾脏也发生病理变化。肝细胞发生颗粒变性、水样变性、醣元颗粒消失,以至坏死;其肾组织主要发生近曲小管上皮细胞颗粒变性、水样变性、坏死,在坏死的肾小管周围的造血组织中的一些细胞核固缩,个别肾小球萎缩。人工感染患细菌性烂鳃病的当年草鱼的白细胞数显著地低于对照组,而红细胞数和血红蛋白量虽低于对照组,但没有显著性差异.  相似文献   

11.
Abstract. Nodular gill disease characterized by severe multifocal epithelial hyperplasia was diagnosed in a group of rainbow trout, Salmo gairdneri Richardson, fingerlings. Gills of a large proportion of fish transferred from the affected tank to smaller aquaria showed a marked decrease in severity of the lesions after 2 months. Repair of hyperplastic lesions may occur in various forms of proliferative gill disease, provided that the basement membrane lining the primary and secondary disease, provided that the basement membrane lining the filaments and lamellae remains intact.  相似文献   

12.
铜在鲤体内的蓄积及毒性的研究   总被引:1,自引:0,他引:1  
采用半静态法将鲤(Cyprinus carpio)暴露于不同浓度的铜溶液中,研究了铜在鱼体中的吸收富集及毒性。结果表明:铜在鲤肝、肾、鳃和肌肉中的积累量均随着铜浓度的升高而增加。鲤各部位对铜的蓄积能力依次是肝、肾、鳃、肌肉,且肝、肾中铜的积累量明显高于鳃和肌肉,鲤对铜具有较强的蓄积毒性。中毒鱼体色变黑,生长受到抑制,临死前出现神经症状;鳃小片上皮增生、变性、坏死;肝细胞和肾小管上皮细胞空泡变性、溶解性坏死。  相似文献   

13.
Atlantic salmon were exposed to amoebic gill disease (AGD) immediately following their acclimatization to sea water (group 1), or following a 2 week period of maintenance in sea water (group 2). Three fish from each group were sampled on days 0, 1, 2, 4, 7, 14 and 28 post-infection. Characteristic gill lesions began to occur between days 2 and 4, and dramatically increased by day 7. The number of gill lesions on fish from group 2 was significantly higher than on fish from group 1 on days 7 and 14 ( P <0.001), but the two groups did not differ in any other parameter. Histologically, Paramoeba sp., the aetiological agent of AGD, could be seen on the gills of fish as soon as 1 day post-exposure, attached to healthy-appearing gills. Gill pathology in the form of hyperplasia and lamellar fusion followed shortly. AGD infection was accompanied by a significant increase in the number of gill mucous cells ( P =0.002). Different methods for the diagnosis of AGD are discussed.  相似文献   

14.
Freshwater bathing is essential for control of amoebic gill disease (AGD) during the marine phase of the Tasmanian Atlantic salmon production cycle, a practice that is costly, production limiting and increasing in frequency. Although the pathogenesis of gill infection with Neoparamoeba sp. in naïve Atlantic salmon, Salmo salar, is now understood, the progression of re‐infection (post‐treatment) required elucidation. Here, we describe the weekly histopathological progression of AGD from first to second freshwater bath. Halocline cessation and increased water temperature appeared to drive the rapid onset of initial infection prior to bathing. Freshwater bathing cleared lesions of attached trophozoites and associated cellular debris. Subsequent gill re‐infection with Neoparamoeba sp. was evident at 2 weeks post‐bath and had significantly increased (P < 0.001), in severity by 4 weeks post‐bath. No significant difference in gross pathology was observed until 4 weeks post‐bath (P < 0.05). The re‐infective progression of AGD was characterized by localized host tissue responses juxtaposed to adhered trophozoites (epithelial oedema, hypertrophy and hyperplasia), non‐specific inflammatory cell infiltration (macrophages, neutrophils and eosinophilic granule cells) and finally advanced hyperplasia with epithelial fortification. During the post‐bath period, non‐AGD lesions including haemorrhage, necrosis and regenerative hyperplasia were occasionally observed, although no evidence of secondary colonization of these lesions by Neoparamoeba sp. was noted. We conclude that pathogenesis during the inter‐bath period was identical to initial infection although the source of re‐infection remains to be established.  相似文献   

15.
Twelve tanks of juvenile rainbow trout, Oncorhynchus mykiss (Walbaum), were treated twice weekly for an 11- week period with a one-hour static bath of chloramine-T (10 mg l–1). The morphometric indices of gill damage and the histochemical characteristics of gill mucous cells of fish from treated and paired untreated tanks were compared. The use pattern of chloramine-T in this study evoked a slight increase in mean lamellar width, but it did not induce a greater degree of lamellar oedema, lamellar fusion, tissue infiltration, epithelial hyperplasia, chloride cell metaplasia or thrombosis of pillar channels in treated fish. Treatment caused a trend towards an increased number of mucous cells on lamellae, associated with a significant shift from neutral mucin to acid mucin production based on histochemical characteristics.  相似文献   

16.
军曹鱼淋巴囊肿的病理学研究   总被引:8,自引:0,他引:8  
应用病理组织学和电镜方法,对患疑似淋巴囊肿病的军曹鱼(Rachycentron canadum)的各器官进行观察.结果表明,患病军曹鱼的皮肤囊肿组织由一些淋巴囊肿细胞集合体组成,这些囊肿细胞排列紧密,直径为10~150 μm,细胞呈圆形、锥形不规则状;细胞外有一层厚的囊膜;细胞质内散布有大量的嗜碱性包涵体,且多数集中在细胞的边缘部分;电镜观察到囊肿细胞质中有大量二十面体的病毒粒子,病毒颗粒直径220 nm.据此确认该病为病毒性淋巴囊肿病.其他器官主要组织病理学变化有:在心脏、肝脏、脾脏和头肾中也存在囊肿细胞,心肌纤维水肿;肾间质淋巴细胞增生,巨噬中心出现,肾小管上皮细胞变性和坏死;脾淋巴细胞增生,脾髓质出血;肝脂肪变性;鳃上皮肿胀.根据观察结果可以认为,该病毒不仅损伤鱼的皮肤,致使病鱼外观异样而严重影响其商品价值,而且对鱼的内脏和免疫器官也造成严重的致命损伤.  相似文献   

17.
Abstract. The normally free-living amoeba Paramoeba sp. is associated with epithelial hyperplasia on the gills of Atlantic salmon, Salmo salar L., in Tasmania. Gill-attached paramoebae were significantly larger than cultured ones. Unlike cultured paramoebae, gill-attached ones had small electron-dense, cytoplasmic deposits and small surface projections at the host-parasite interface. Examination of sequential samples of Tasmanian salmon gills from spring to summer indicated that pathological changes in the gill filaments were associated only with the presence of Paramoeba ; the parasite was also associated with necrosis of surface epithelial cells, and cytoplasmic processes passed into and between surface cells of hyperplastic gill epithelium. The evidence points to the paramoebae as primary opportunistic pathogens causing mechanical and possibly chemical damage. Based on size and ultrastructure, the Paramoeba sp. most closely resembles P. pemaquidensis Page.  相似文献   

18.
Two trials were conducted to assess the effects of repeated prophylactic formalin treatments on the gill structure of salmonids. In trial 1, which involved Atlantic salmon, Salmo salar L., approaching smoltification in a commercial facility, fish were treated with either 167 or 250 mg l-1 formalin for 90 min every 2 weeks for 12 weeks. Formalin-treated salmon had slight, but not significant, increases in the frequency of lamellar fusion, numbers of lamellar mucous cells, and numbers of an endemic gill ciliate, Trichophyra piscium, after 6 and 12 weeks of treatment. In trial 2, which involved juvenile rainbow trout, Oncorhynchus mykiss (Walbaum), fish were treated with 200 mg l-1 formalin for 60 min twice weekly for 12 weeks. Significant effects were limited to an increase in the numbers of mucous cells present on gill lamellae. In both trials, there was no evidence of lamellar oedema or necrosis of lamellar epithelial cells.  相似文献   

19.
黄颡鱼腹水病的组织病理研究   总被引:3,自引:0,他引:3  
本文应用组织病理学的方法,对患有腹水病的黄颡鱼(Pseudobagrus fulviddco)的各器官进行观察.结果表明各器官主要组织病理学变化有:鳃小片上皮细胞肿胀、增生、肥大,并有脱落、变性、坏死现象;肾小管上皮细胞出现肿胀,局部肾小管崩解坏死;肾小球结构模糊不清、松散,呈空泡样,部分区域肾小球的血管球肿胀、肾小球坏死;肾间质中可见局灶性坏死,局部区域可见颗粒管型和黑素-巨噬细胞沉着.肝细胞发生明显的水泡变性,部分病鱼肝组织可见局灶性坏死和血管充血.肠胃上皮细胞排列紊乱,并有脱落、变性、坏死现象.脾组织中毛细血管扩张、充血,严重区域破裂出血,形成血斑,部分病鱼脾组织可见弥散性坏死灶.  相似文献   

20.
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