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Diseases of Aquatic Organisms

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DAO 75:51-59 (2007)  -  doi:10.3354/dao075051

Histopathological and ultrastructural observations of metacercarial infections of Diplostomum phoxini (Digenea) in the brain of minnows Phoxinus phoxinus

Bahram Sayyaf Dezfuli1,*, Silvia Capuano1, Edi Simoni1, Luisa Giari 1, Andrew Paul Shinn2

1Department of Biology, University of Ferrara, Via Borsari, 46, 44100 Ferrara, Italy
2Institute of Aquaculture, University of Stirling, Stirling FK9 4LA, UK

ABSTRACT: The spatial distribution and histopathological changes induced by metacercariae of the digenean trematode Diplostomum phoxini (Faust, 1918) in the brains of European minnows Phoxinus phoxinus (L.) from the River Endrick, Scotland, were studied by light and electron microscopy. Post-mortem examination of a sample of 34 minnows revealed that 50% (n = 17) of the population was infected with 13.7 ± 2.6 (mean ± SE; range 1 to 38) metacercariae per infected host. Serial histological sections of the infected minnow brains revealed that the metacercariae were unevenly distributed throughout the brain, with aggregations occurring in the cerebellum, the medulla oblongata and the optic lobes. In fish with highest intensities of infection, over 40% of the cerebellar area and about 30% of the medulla oblongata area were occupied by larvae. Metacercariae disrupt the integrity of brain tissue, with individuals being found in small pockets surrounded by cellular debris. Metacercariae were rarely encountered on the surface of the brain. Electron microscopic examination of infection sites revealed that the granular layer surrounding metacercariae was necrotic, exhibited nuclear degradation and was marked by vacuolation of the cytoplasm. Rodlet cells, the only inflammatory cell types recorded in this study, were found only in parasitized brains and in close proximity to the teguments of metacercariae. It is hypothesised that secretions released from the teguments of metacercariae are a counter response to protect the metacercariae from the fish brain’s cellular defence mechanisms.

KEY WORDS: Brain infection · Digenean trematode · Phoxinus phoxinus · Rodlet cells · Histopathology · Ultrastructure

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