Proliferative Gill Disease of Fish from the Tennessee-Tombigbee Waterway,Mississippi

Abstract

Proliferative gill disease (PGD), a condition not previously reported in wild fish, was found in two channel catfish Ictalurus punctatus sampled from the Tennessee-Tombigbee Waterway in Mississippi during June and July 1989. The parasite thought to cause PGD was observed in only one of the fish, but the distinctive lesions associated with this disease were prominent in both of the channel catfish. Organisms resembling the PGD parasite were also found in the gills of 4 of 18 largemouth bass Micropterus salmoides and 6 of 20 bluegills Lepomis macrochirus, but there was little or no host response to these parasites.     

Experimental Induction of Proliferative Gill Disease in Specific-Pathogen-Free Channel Catfish

Abstract

Specific-pathogen-free channel catfish Ictalurus punctatus were exposed to sediment and mud from a pond containing channel catfish with proliferative gill disease. In one experiment, fish were to exposed to mud and sediment for 2 months in water maintained at 19°C. Fish were necropsied weekly, and certain tissues were examined histologically and ultrastructurally. Four trials were conducted with sediment samples from different epizootics of proliferative gill disease. In a second experiment, fish were exposed to sediment for 7 d in water maintained at 16, 19, or 26°C; the fish were then moved to clean water held at 16, 19, or 26°C. Fish were necropsied before transfer to clean water and weekly thereafter for 2 months. Channel catfish held at 19°C developed proliferative gill disease within 2 d of exposure to sediment. Primary cells of a uninucleate myxosporean parasite were present in the gills at the base of lamellae. These developed into plasmodia with numerous secondary cells, and some primary cells disintegrated, releasing their internal secondary cells. Similar development was observed in internal organs 1 week after appearance of the parasite in gills. Complete sporogony did not occur over the 2 months of this study. Plasmodia became necrotic and were not detected after 60 d. In fish exposed to sediment for 7 d at 16, 19, and 21°C, similar organisms were detected, but clinical disease occurred only at 19 and 26°C. Proliferative gill disease may be attributed to extrasporogonic stages of a myxosporean resembling Sphaerospora spp.     

Induction and Evaluation of Proliferative Gill Disease in Channel Catfish Fingerlings

Abstract

Proliferative gill disease (PGD) was first reported in channel catfish Ictalurus punctatus at commercial farms in 1981 and is caused by the myxozoan parasite Henneguya ictaluri. The disease affects the gills and is characterized by severe branchial inflammation, epithelial hyperplasia, lamellar fusion, and lysis of chondrocytes. Presumptive diagnosis is based on the presence of lytic areas in the cartilage of the primary lamellae on microscopic examination and is confirmed histologically by the presence of the organism. In these trials, PGD was induced by exposing channel catfish fingerlings to fresh or aged infectious water collected from a pond containing fish diagnosed with severe PGD. The severity of disease was graded by histological scoring and microscopic examination of wet mounts to determine the percentage of gill filaments containing chondrolytic lesions. Exposure of fish to infectious pond water was shown to produce pathological lesions consistent with PGD, and the percentage of gill filaments containing chondrolytic lesions was positively correlated with histological scoring of gill pathology. The number of trophozoite stages in the gills was shown to increase with the severity of the disease. In most cases, however, parasitic cells were not observed in tissue samples with chondrolytic lesions during the early stages of infection. These observations indicate that pathology and lysis of chondrocytes can occur prior to detection of the organism by histopathology. Exposing fish to infectious pond water that was aged for 1 d produced negligible gill pathology and implies that the infectivity of the H. ictaluri actinospore stage is short lived. Removing fish from the source of infection promoted repair of damaged gill tissue; within 14 d of fish transfer to clean water, gill pathology associated with the acute infection was negligible.     

Communications: Experimental Production of Proliferative Gill Disease in Channel Catfish Exposed to a Myxozoan-Infected Oligochaete,Dero digitata

Abstract

Specific-pathogen-free fry of channel catfish Ictalurus punctatus raised in well water were exposed to Dero digitata (an oligochaete) collected from ponds where catfish have had proliferative gill disease (PGD) and where D. digitata is known to be infected with the triactinomyxid myxozoan Aurantiactinomyxon sp. These fry developed gill lesions and parasites characteristic of PGD. Fry exposed to suspensions of mature Aurantiactinomyxon spores obtained from squashes of infected D. digitata also developed PGD. Fry exposed to oligochaetes other than Dero spp., non-oligochaete benthic macroinvertebrates, or suspensions of squashes of D. digitata without identifiable myxozoans did not develop PGD.     

Observations on the Occurrence of Bacterial Gill Disease and Amoeba Gill Infestation in Rainbow Trout Cultured in a Water Recirculation System

Abstract

Spontaneous outbreaks of bacterial gill disease (BGD) occurred in 17-44-g rainbow trout Oncorhynchus mykiss after they were placed in a water recirculation system. In each of five groups stocked from September 1991 through July 1992, BGD occurred within 6–8 d after stocking. In each instance, BGD was followed by a secondary amoeba infestation. The spontaneous BGD outbreaks did not occur among previously stocked groups that had recovered from earlier BGD disease outbreaks. Examination of gill tissue by Gram stain and indirect fluorescent antibody technique showed increased numbers of filamentous bacteria associated with BGD after the rainbow trout were stocked into the system. Bacterial numbers decreased after a 1-h treatment with chloramine-T at concentrations of 9–15 mg/L but increased within 2 d after treatment. Although the chloramine-T treatments controlled mortality related to BGD, the amoeba infestation persisted. Histological examination of gills showed some focal hyperplasia before the rainbow trout were placed into the recirculation system, but hyperplasia became more extensive and lamellar fusion and mild telangiectasis developed within a week after placement in the system. The density at which the fingerling rainbow trout were stocked and the suspended solids present in tank water may have contributed to the BGD outbreaks. Exposure of juvenile rainbow trout to tank water from the recirculation system before they were placed into the system did not afford them protection against BGD after stocking.     

猪增生性肠炎研究进展

猪增生性肠炎是由胞内劳森氏菌引起的猪的接触性传染病,本文介绍了其病原学、流行病学、临床症状、发病机理、病理变化以及实验室诊断等方面的研究现状.     

Small Subunit rRNA Gene Comparisons of Four Actinosporean Species to Establish a Polymerase Chain Reaction Test for the Causative Agent of Proliferative Gill Disease in Channel Catfish

Abstract

Proliferative gill disease (PGD) causes high morbidity and mortality in cultured channel catfish Ictalurus punctatus. The presence of the myxozoan Aurantiactinomyxon ictaluri (class Actinosporea) is strongly associated with PGD. This parasite, shed as an actinospore from the aquatic oligochaete Dero digitata, infects channel catfish by an undetermined route. Several other actinosporeans have been identified that are shed from D. digitata isolated from catfish ponds, including those designated A. mississippiensis, Helioactinomyxon sp., and the actinospore stage of Henneguya exilis. By the use of multiple sequence alignment of polymerase chain reaction (PCR)-amplified small subunit ribosomal RNA (SSU rRNA) genes of A. ictaluri, A. mississippiensis, and H. exilis, we identified two variable regions. The largest variable region was PCR amplified, sequenced from the Helioactinomyxon sp., and used in addition to the other three sequences in multiple-sequence alignment comparison to develop PCR primers specific for A. ictaluri. This PCR specific for A. ictaluri produced 104-base-pair products from a plasmid clone containing the SSU rRNA gene of A. ictaluri, spore DNA of A. ictaluri, and DNA prepared from channel catfish gill and D. digitata infected with A. ictaluri. The PCR assay was able to detect as few as 100 copies of the cloned gene. There was no detectable product from the genomic DNA of H. exilis, A. mississippiensis, or Helioactinomyxon sp., specific pathogen-free channel catfish gill, and noninfected D. digitata. The PCR assay will be useful as a diagnostic tool for PGD in channel catfish and will aid in the elucidation of the life cycle of A. ictaluri.     

草鱼细菌性烂鳃病病原菌的分离及其特异性卵黄抗体的初步研究

试验从患典型烂鳃病草鱼病变部位分离到1株柱状黄杆菌(FC-3株),采用0.4%甲醛灭活制成免疫原,接种健康120日龄桃源蛋鸡,收集鸡蛋并提纯卵黄抗体(IgY),并以此IgY为基础建立间接ELISA方法。结果:用FC-3株制备的IgY经初步提纯后电泳分离可见重链和轻链2条蛋白条带,获得了IgY多克隆抗体。建立的间接ELISA方法检测柱状黄杆菌纯培养液的检出限值为1×10^7cfu/mL,抗原包被最佳浓度和抗体最佳工作浓度分别为1∶100和1∶512,辣根过氧化物酶标记兔抗鸡IgY最佳工作浓度为1∶4000。结论:建立的间接ELISA方法对柱状黄杆菌有明显的检测特异性,与其他菌株无交叉反应,重复性好。     

Hatchery Efficacy Trials with Chloramine-T for Control of Bacterial Gill Disease

Abstract

Three hatchery trials were carried out to determine the efficacy of chloramine-T for the control of bacterial gill disease in rainbow trout Oncorhynchus mykiss, ranging in weight from 2.5 to 54 g. In each trial, we used a single flow-through treatment of 8.5 mg chloramine-T/L. The single treatment provided effective control in all three trials; however, results were best when treatment was begun in the early stages of an outbreak. A second or third treatment may be required if an outbreak is in an advanced stage or if fish are under stress.     

Gill Infection Model for Columnaris Disease in Common Carp and Rainbow Trout

Challenge models generating gill lesions typical for columnaris disease were developed for the fry of both Common Carp Cyprinus carpio and Rainbow Trout Oncorhynchus mykiss by means of an immersion challenge and Flavobacterium columnare field isolates were characterized regarding virulence. Carp inoculated with highly virulent isolates revealed diffuse, whitish discoloration of the gills affecting all arches, while in trout mostly unilateral focal lesions, which were restricted to the first two gill arches, occurred. Light microscopic examination of the gills of carp exposed to highly virulent isolates revealed a diffuse loss of branchial structures and desquamation and necrosis of gill epithelium with fusion of filaments and lamellae. In severe cases, large parts of the filaments were replaced with necrotic debris entangled with massive clusters of F. columnare bacterial cells enwrapped in an eosinophilic matrix. In trout, histopathologic lesions were similar but less extensive and much more focal, and well delineated from apparently healthy tissue. Scanning and transmission electron microscopic observations of the affected gills showed long, slender bacterial cells contained in an extracellular matrix and in close contact with the destructed gill tissue.

This is the first study to reveal gill lesions typical for columnaris disease at macroscopic, light microscopic, and ultrastructural levels in both Common Carp and Rainbow Trout following a challenge with F. columnare. The results provide a basis for research opportunities to examine pathogen–gill interactions.

Received January 10, 2014; accepted July 27, 2014     

Blood Parameters and Immune Status of Rainbow Trout with Proliferative Kidney Disease

Abstract

Blood parameters, disease resistance, and the immune response were sequentially evaluated in rainbow trout Oncorhynchus mykiss with proliferative kidney disease (PKD). The fish were maintained under laboratory conditions, and the study group went through a full cycle of the disease. Hematological and serological changes occurred primarily in those fish with severe kidney lesions. Fish infected with the parasite that causes PKD demonstrated a greater resistance to bacterial challenge, and their immune responses were heightened when compared with those of uninfected fish. These data suggest that PKD alone is not a predisposing factor for secondary infections if the fish does not incur severe renal lesions.     

传染性法氏囊病病毒变异E株对法氏囊生长发育的影响

本试验全面而系统地观察了传染性法氏囊病病毒变异Ｅ株,通过泄殖腔、鼻腔和尿囊腔接种雏鸡和鸡胚后不同时间法氏囊的组织形态学变化。结果表明,病毒感染后１２～４８小时,雏鸡法囊粘膜上皮细胞肿胀、坏死脱落,淋巴滤泡髓质部及皮质部淋巴细胞不同程度变性、坏死、排空,形成腺管样结构或囊状空泡,接毒后７２～１４４小时,法氏囊淋巴滤泡淋巴细胞坏死排空,淋巴滤泡萎缩,网状结缔组织大量增生,而胚胎发育时期,法氏囊粘膜上皮肿胀变性,法氏囊淋巴滤泡形成延迟或不完整,淋巴滤泡内淋巴细胞缺乏或空虚。探讨了传染性法氏囊病病毒对胚胎发育时期的雏鸡发育时期法氏囊生长发育的影响。     

铅染毒和新城疫疫苗免疫对鹌鹑生长发育的影响

采用2×5因子设计,新城疫(ND)疫苗免疫分为免疫组和未免疫组,铅染毒按饮水中的醋酸铅浓度分为0、50、500、1 000和2 000 mg/L 5个组,将90只14日龄黄羽鹌鹑随机分组,实行自由饮水和采食,研究铅染毒和ND免疫对鹌鹑生长发育的影响.结果表明,ND免疫在1～2周内能显著降低鹌鹑的体重(P<0.01);ND免疫可导致肝脏指数增大,血清透明质酸含量升高;2 000 mg/L醋酸铅能显著降低试验期鹌鹑的体重(P<0.01),至试验第5周(7周龄)所有铅染毒组的鹌鹑体重均显著低于对照组(P<0.01).铅能导致鹌鹑采食量下降、脱毛、性腺发育受阻和血清透明质酸含量升高.性腺发育不良是鹌鹑铅中毒的一个重要标志,透明质酸含量可作为检测鹌鹑群体是否经过ND疫苗免疫和遭受铅污染的指标.     

The Effect of Tramadol and Indomethacin Coadministration on Gastric Barrier Function in Dogs

Background

Tramadol is a centrally acting analgesic that is often used in conjunction with nonsteroidal anti‐inflammatory drugs (NSAIDs). The effect of coadministration of tramadol and indomethacin on gastric barrier function in dogs is unknown.

Hypothesis/Objectives

That coadministration of a nonselective NSAID (indomethacin) and tramadol would decrease recovery of barrier function as compared with acid‐injured, indomethacin‐treated, and tramadol‐treated mucosa.

Animals

Gastric mucosa of 10 humanely euthanized shelter dogs.

Methods

Ex vivo study. Mounted gastric mucosa was treated with indomethacin, tramadol, or both. Gastric barrier function, prostanoid production, and cyclooxygenase expression were quantified.

Results

Indomethacin decreased recovery of transepithelial electrical resistance after injury, although neither tramadol nor the coadministration of the two had an additional effect. Indomethacin inhibited production of gastroprotective prostanoids prostaglandin E₂ (acid‐injured PGE ₂: 509.3 ± 158.3 pg/mL, indomethacin + acid injury PGE ₂: 182.9 ± 93.8 pg/mL, P < .001) and thromboxane B₂ (acid‐injured TXB ₂: 233.2 ± 90.7 pg/mL, indomethacin + acid injury TXB ₂: 37.9 ± 16.8 pg/mL, P < .001), whereas tramadol had no significant effect (PGE ₂ P = .713, TXB ₂ P = .194). Neither drug had an effect on cyclooxygenase expression (COX‐1 P = .743, COX‐2 P = .705). Acid injury induced moderate to marked epithelial cell sloughing, which was unchanged by drug administration.

Conclusions and Clinical Importance

There was no apparent interaction of tramadol and a nonselective cyclooxygenase in this ex vivo model. These results suggest that if there is an adverse interaction of the 2 drugs in vivo, it is unlikely to be via prostanoid inhibition.     

Cellular Inflammatory Response of Rainbow Trout to the Protozoan Parasite that Causes Proliferative Kidney Disease

Abstract

The cellular inflammatory response of rainbow trout Oncorhynchus mykiss (formerly Salmo gairdneri) to the myxozoan parasite PKX that causes proliferative kidney disease was investigated. The response was studied from 3 to 20 weeks after the fish were injected with infected kidney homogenate. Kidney samples were examined by light and electron microscopy. In contrast to most myxosporeans, PKX provoked a severe host response. Parasites were found in peritubular capillaries and sinusoids 3 weeks postinjection. The initial response to PKX was hemopoietic hyperplasia followed by a marked granulomatous nephritis that was resolved by termination of the study at 20 weeks postinjection. The macrophage was the predominant cell type involved in the inflammatory response to PKX. We presume that the macrophage effectively interrupts the development of PKX and eliminates the parasite from the host.     

California Golden Trout Oncorhynchus mykiss aguabonita Are Susceptible to Proliferative Kidney Disease

Abstract

An outbreak of proliferative kidney disease affecting farmed California golden trout Oncorhynchus mykiss aguabonita in the United Kingdom is described. The fish displayed the clinical signs of the disease, such as characteristic swelling of the posterior kidney and spleen. Confirmation of infection with Tetracapsuloides bryosalmonae in the renal tissue was done by means of electron microscopy and immunohistochemistry using a monoclonal antibody specific to T. bryosalmonae.     

Gill myxosporeans on some Egyptian freshwater fish

Seven new species of myxosporeans are described from gills of seven freshwater species of fish from Egypt. The annual developmental cycle of the gills involves a period of summer invasion, followed in the autumn by development of cysts (plasmodia + host capsule) and initiation of sporogenesis, completion of sporogenesis in the winter, and the release of spores in the spring.     

新城疫中药多糖佐剂油乳苗对鸡免疫器官发育的影响

４２０只７日龄健康罗曼雏鸡随机分为７组,每组６０只。第１组肌注新城疫（ＮＤ）黄芪多糖佐剂油乳苗,第２组肌注ＮＤ香菇多糖佐剂油乳苗,第３组肌注ＮＤ复方多糖（１）佐剂油乳苗,第４组肌注ＮＤ复方多糖（２）佐剂油乳苗,第５组肌注ＮＤ复方多糖（３）佐剂油乳苗,第６组肌注ＮＤ油乳苗（对照）,第７组肌注生理盐水（空白对照）。分别于注苗后５、１０、１５、２５、３５ｄ,每组随机取１０只鸡称重,并取免疫器官脾、法氏囊用１０％福尔马林固定后称重,作统计学处理。结果表明,中药多糖作为新城疫油乳苗佐剂有明显的增加免疫器官重量的作用,复方中药多糖对脾、法氏囊的增重效果优于单一多糖。     

消炎痛抑制山羊黄体溶解

在山羊发情周期第１６～２１天，每天给４只山羊按每公斤体重注射消炎痛１２ｍｇ；另４只山羊注射相应体积的玉米油作为对照，用血浆孕酮水平来监视黄体溶解过程。将血浆孕酮水平降到每毫升１ｎｇ以下的时刻定为黄体完全溶解的时间。对照组山羊的黄体在周期的１９．７ｄ完全溶解；处理组山羊的血浆孕酮水平到周期的第２２天时仍无明显的下降趋势。每天按每公斤体重注射１２ｍｇ消炎痛完全阻止了山羊的黄体溶解。