Ronza Paolo, Robledo Diego, Bermúdez Roberto, Losada Ana Paula, Pardo Belén G, Martínez Paulino, Quiroga María Isabel
Departamento de Anatomía, Producción Animal y Ciencias Clínicas Veterinarias, Universidade de Santiago de Compostela, Lugo, Spain.
Royal (Dick) School of Veterinary Studies, The Roslin Institute, The University of Edinburgh, Midlothian, United Kingdom.
Front Genet. 2019 Jan 31;10:26. doi: 10.3389/fgene.2019.00026. eCollection 2019.
Enteromyxosis, caused by , is one of the most devastating diseases stemming from myxozoan parasites in turbot ( L.), being a limiting factor for its production. The disease develops as a cachectic syndrome, associated to catarrhal enteritis and leukocytic depletion, with morbidity and mortality rates usually reaching 100%. To date, no effective treatment exists and there are different unknown issues concerning its pathogenesis. The gross and microscopic lesions associated to enteromyxosis have been thoroughly described, and several morphopathological studies have been carried out to elucidate the mechanisms of this host-parasite interaction. More recently, efforts have been focused on a multidisciplinary approach, combining histopathology and transcriptome analysis, which has provided significant advances in the understanding of the pathogenesis of this parasitosis. RNA-Seq technology was applied at early and advanced stages of the disease on fishes histologically evaluated and classified based on their lesional degree. In the same way, the transcriptomic data were analyzed in relation to the morphopathological picture and the course of the disease. In this paper, a comprehensive review of turbot enteromyxosis is presented, starting from the disease description up to the most novel information extracted by an integrated approach on the infection mechanisms and host response. Further, we discuss ongoing strategies toward a full understanding of host-pathogen interaction and the identification of suitable biomarkers for early diagnosis and disease management strategies.
由[病原体名称未给出]引起的肠道黏孢子虫病，是大菱鲆（Scophthalmus maximus L.）黏孢子虫寄生虫引发的最具毁灭性的疾病之一，是其生产的限制因素。该病以恶病质综合征形式发展，与卡他性肠炎和白细胞减少有关，发病率和死亡率通常达到100%。迄今为止，尚无有效的治疗方法，关于其发病机制存在不同的未知问题。与肠道黏孢子虫病相关的大体和微观病变已得到充分描述，并且已经开展了多项形态病理学研究以阐明这种宿主 - 寄生虫相互作用的机制。最近，研究工作集中在多学科方法上，将组织病理学和转录组分析相结合，这在理解这种寄生虫病的发病机制方面取得了重大进展。RNA测序技术应用于疾病的早期和晚期阶段，对根据病变程度进行组织学评估和分类的鱼类进行研究。同样，转录组数据也根据形态病理学图像和疾病进程进行分析。本文对大菱鲆肠道黏孢子虫病进行了全面综述，从疾病描述开始，直至通过综合方法提取的关于感染机制和宿主反应的最新信息。此外，我们讨论了为全面理解宿主 - 病原体相互作用以及鉴定用于早期诊断和疾病管理策略的合适生物标志物而正在进行的策略。
