# Changes in the gill and gut microbiota of koi infected with carp edema virus

## TL;DR

This study explores how carp edema virus affects the gill and gut microbiota in koi and how it impacts the host's immune response and stress levels.

## Contribution

The study reveals how CEV infection alters microbiota and gene expression in gills and gut, potentially explaining secondary bacterial infections.

## Key findings

- CEV infection significantly alters gill microbiota with increased opportunistic bacteria like Chryseobacterium and Aeromonas.
- Stress response is activated in CEV-infected fish, indicated by elevated cortisol and glucose levels in blood plasma.
- Histopathological changes in gills include intralamellar space occlusion and apoptotic cells, while gut changes are minor.

## Abstract

Carp edema virus (CEV) is a contagious pathogen affecting mostly the gills of common carp (Cyprinus carpio) and impairing the functions of this organ. Moreover, CEV was reported to cause stress activation and modulation of the hosts immune system. Last but not least, secondary bacterial infections often occur during CEV infection. In this study, we assessed the impact of CEV infection on the microbiota in the gills, foregut, and hindgut of koi. Moreover, we studied expression of genes encoding antiviral proteins, proinflammatory cytokines, mucins, and tight junction proteins. We observed increased levels of cortisol and glucose in the blood plasma of CEV-infected fish, suggesting activation of stress response. Histopathological analysis of the gills showed occlusion of the intralamellar space with the presence of apoptotic cells in CEV-infected fish, while in the gut only minor histopathological changes were recorded. Microbiota of the gills was significantly altered during infection with increased absolute abundance of several bacteria genera, including opportunistic bacteria e.g. Chryseobacterium, Flavobacteria, Aeromonas, and Pseudomonas. In the foregut, we did not observe changes in the absolute bacterial abundance between control and CEV-infected fish, while in the hindgut only absolute abundance of Aeoromonas was increased in infected fish. Moreover, CEV infection differentially altered expression of studied genes, including for example upregulation of expression of mxa, vig, il-1b, and cldn 7 in studied organs. Our study explores the effect of CEV infection on the host microbiota, which may partly explain the occurrence of secondary bacterial infections during infection with this virus.

The online version contains supplementary material available at 10.1186/s13567-025-01700-y.