In the gilt-head seabream, it is manifested as a chronic disease that provokes anorexia, delayed growth with weight loss, cachexia, reduced marketability and increased mortality.

In contrast to this complex life cycle, spontaneous, direct fish-to-fish transmission has been demonstrated for E. leei and other species belonging to the genus Enteromyxum in various marine fish.

Common field observations include loss of appetite, poor food conversion rates and difficulties to reach commercial size.

Emaciation can be imperceptible in very susceptible species and/or at high temperatures (e.g. D. puntazzo infections with E. leei), because fish die before reaching a caquexic condition.

At dissection, macroscopical signs include intestinal focal congestion and haemorrhages, and it can appear fragile and semi-transparent, often filled with mucous liquid with reduced perivisceral fat deposits, pale internal organs and occasionally green liver.

In advanced GSB infections with E. leei, the intestine displays hypertrophy of the lamina propria-submucosa and loss of the epithelial palisade structure, together with an intense local inflammatory response.

Confirmatory diagnosis usually consists of the detection of Enteromyxum spores or other proliferative stages in smears of the intestine, either fresh or stained with diff-quick or May-Grunwald Giemsa.

The examination of histological sections of intestine is the standard procedure, with the help of some stainings, such as periodic acid-Schiff (PAS), Giemsa or toluidine blue, or some lectins.

This procedure has been validated against a gold standard (histological observation of the whole digestive tract), with a high sensitivity (0.96) and specificity (Palenzuela, unpublished data).

Once the parasite becomes established, they are generally eradicated only with aggressive actions that include eliminating infected fish, disinfecting tanks, sea cages, drying ponds, etc.

In addition, epidemiological studies are being conducted in the Mediterranean basin to determine the true impact of enteromyxosis and the host/farm factors that enhance or mitigate its extension.

Chronic exposure to the parasite stimulates gene expression related to interferon signalling and antigen processing and presentation in the intestine of exposed non-parasitized fish, which may point to the local triggering of immune resistance mechanisms against the infection.

[41] Interleukin (IL) expression during GSB enteromyxosis is modulated from a pro-inflammatory to an anti-inflammatory profile, and this shift is apparently driven by the up-regulation of il10.

[43] More recently, the involvement of cytotoxic T cells in the clearance of the parasite has been suggested from the higher expression of cd8 in exposed but non-parasitized fish intestines.