English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background  Swim bladder inflammation (SBI) is an important disease of common carp fingerlings in Central Europe. In the 1980s, its etiology was ascribed to multicellular proliferative stages of the myxozoan parasite  Sphaerospora dykovae  (formerly  S. renicola ).  S. dykovae  was reported to proliferate in the blood and in the swim bladder prior to the invasion of the kidney, where sporogony takes place. Due to the presence of emerging numbers of proliferative myxozoan blood stages at different carp culture sites in recent years we analysed cases of SBI, for the first time, using molecular diagnostics, to identify the myxozoan parasites present in diseased swim bladders.    Methods  We amplified myxozoan SSU rDNA in a non-specific approach and compared the species composition in swim bladders at culture sites where carp demonstrated 1. No signs of SBI, 2. Minor pathological changes, and 3. Heavy SBI. Based on DNA sequences, we determined the localisation and distribution of the most frequent species by  in situ  hybridisation, thereby determining which myxozoans are involved in SBI.    Results  Large multicellular myxozoan swim bladder stages characterised heavy SBI cases and were identified as  S. dykovae,  however, blood stages were predominantly represented by  Sphaerospora molnari , whose numbers were greatly increased in carp with mild and heavy SBI, compared with SBI-free fish.  S. molnari  was found to invade different organs and cause inflammatory changes also in the absence of  S. dykovae . One site with mild SBI cases was characterised by  Buddenbrockia  sp. infection in different organs and a general granulomatous response.    Conclusions  We provide evidence that the etiology of SBI can vary in relation to culture site and disease severity and that emerging numbers of  S. molnari  in the blood represent an important co-factor or precondition for SBI.

Molecular fingerprinting of the myxozoan community in common carp suffering Swim Bladder Inflammation (SBI) identifies multiple etiological agents