Griffin Matt J, Camus Alvin C, Wise David J, Greenway Terrence E, Mauel Michael J, Pote Linda M
Thad Cochran National Warmwater Aquaculture Center, Mississippi Agricultural and Forestry Experiment Station and College of Veterinary Medicine, Mississippi State University, Box 197, Stoneville, Mississippi 38776, USA.
J Aquat Anim Health. 2010 Mar;22(1):21-35. doi: 10.1577/H09-030.1.
Proliferative gill disease (PGD) in channel catfish Ictalurus punctatus is caused by the myxozoan parasite Henneguya ictaluri. There is no effective treatment for PGD, and mortalities can exceed 50% in severe outbreaks. One approach to controlling losses would be to utilize a less susceptible ictalurid species in pond culture; alternatively, one could identify the traits that convey resistance and exploit them in a selective breeding program. Challenge studies have found less severe inflammatory responses in the gill tissue of blue catfish I. furcatus and fewer mortalities than in channel catfish. However, it remains unclear whether infection and subsequent plasmodial development progress the same way in the two species. To investigate this, we compared the dynamics of H. ictaluri infection in blue catfish, channel catfish, and channel catfish x blue catfish hybrids in continuous long-term (5-7-d) and short-term (24-h) pond challenges. After long-term challenge, 66.2% of the channel catfish and 63.6% of the hybrid catfish developed characteristic PGD lesions, compared with 3.7% of the blue catfish. Quantitative polymerase chain reaction analysis detected H. ictaluri in larger percentages of channel and hybrid catfish than blue catfish (98.7% and 95.7% versus 45.9%), with significantly greater parasite DNA equivalents in channel and hybrid catfish than blue catfish. Similar findings were obtained in the short-term exposures. Histologically, channel and hybrid catfish developed severe PGD accompanied by large numbers of developing plasmodia. While mild PGD was observed in some blue catfish, the progression of lesions lagged behind that in channel and hybrid catfish. Most importantly, developing plasmodia were not observed in blue catfish, and parasite DNA was not detected 14 d after removal from the source of infection. Our findings indicate that the resistance of blue catfish to H. ictaluri infection can be overcome by large numbers of infective actinospores but that infection appears to be eliminated before plasmodial development occurs.
斑点叉尾鮰的增殖性鳃病（PGD）由粘孢子虫寄生虫鮰单极虫（Henneguya ictaluri）引起。PGD没有有效的治疗方法，在严重爆发时死亡率可能超过50%。控制损失的一种方法是在池塘养殖中使用较不易感的鮰科鱼类；或者，可以识别出赋予抗性的性状并在选择性育种计划中加以利用。攻毒研究发现，蓝鲶（Ictalurus furcatus）鳃组织中的炎症反应不如斑点叉尾鮰严重，死亡率也低于斑点叉尾鮰。然而，尚不清楚这两个物种的感染及随后的孢原虫发育过程是否相同。为了对此进行研究，我们在连续长期（5 - 7天）和短期（24小时）池塘攻毒试验中，比较了蓝鲶、斑点叉尾鮰以及斑点叉尾鮰×蓝鲶杂交种中鮰单极虫感染的动态情况。长期攻毒后，66.2%的斑点叉尾鮰和63.6%的杂交鲶鱼出现了典型的PGD病变，而蓝鲶的这一比例为3.7%。定量聚合酶链反应分析检测到，斑点叉尾鮰和杂交鲶鱼中鮰单极虫的比例高于蓝鲶（分别为98.7%、95.7%和45.9%），斑点叉尾鮰和杂交鲶鱼中的寄生虫DNA当量显著高于蓝鲶。短期暴露试验也得到了类似的结果。组织学检查显示，斑点叉尾鮰和杂交鲶鱼出现了严重的PGD，并伴有大量正在发育的孢原虫。虽然在一些蓝鲶中观察到了轻度PGD，但病变进展落后于斑点叉尾鮰和杂交鲶鱼。最重要的是，在蓝鲶中未观察到正在发育的孢原虫，并且在从感染源移除14天后未检测到寄生虫DNA。我们的研究结果表明，大量感染性放线孢子可以克服蓝鲶对鮰单极虫感染的抗性，但感染似乎在孢原虫发育之前就被消除了。
