Microbiome dynamics associated with Hematodinium sp. infection in Norway lobster (Nephrops norvegicus)

  • 1Institute of Aquaculture, University of Stirling, Stirling, FK9 4LA, UK.
  • 2Faculty of Aquatic and Fisheries Sciences, Kafrelsheikh University, Kafr El Sheikh City, 33516, Egypt.
  • 3Weymouth Laboratory, Centre for Environment, Fisheries and Aquaculture Science (Cefas), Weymouth, Dorset, DT4 8UB, UK.
  • 4Sustainable Aquaculture Futures, Biosciences, College of Life and Environmental Sciences, University of Exeter, Stocker Road, Exeter, UK.
  • 5Institute of Aquaculture, University of Stirling, Stirling, FK9 4LA, UK. amaya.albalat@stir.ac.uk.

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Abstract

BACKGROUND

The parasite Hematodinium sp. causes morbidity and seasonal mortality events in more than 40 decapod species globally and therefore, it is now recognised as a significant threat to the future sustainability of shellfish fisheries and aquaculture worldwide. Among these, Norway lobster (Nephrops norvegicus), an important representative of the marine benthos and supporting the most valuable shellfish fishery in the UK, experience yearly seasonal Hematodinium sp. patent infections. Currently, little is known about the N. norvegicus microbiome and potential role during Hematodinium sp.

INFECTION

Therefore, in this study we investigated the microbiome dynamics of N. norvegicus associated with Hematodinium sp. infection and disease progression in the haemolymph and gut. N. norvegicus were sampled from the Clyde Sea Area, Scotland during the peak of the Hematodinium sp. patent infection. The presence and intensity of Hematodinium sp. infection were determined using the body colour method (BCM), pleopod method (PM), histology (heart, gonads, hepatopancreas, gills and muscle) and molecular tools (PCR).

RESULTS

Marked shifts in the bacterial richness of the haemolymph and significant alterations in the overall bacterial community composition of both tissues were observed in infected lobsters. These changes, observed even at subpatent levels of infection (only positive by PCR), indicate a prompt and persistent microbiome shift associated with Hematodinium sp.

INFECTION

Furthermore, smaller healthy animals (25.2 ± 1.20 mm CL) known to be particularly susceptible to high severity infection displayed a decreased microbiome richness in the haemolymph suggesting a potential link between the host microbiome and susceptibility to disease progression, a possibility that merits further research.

CONCLUSIONS

This study offers the first insights into the pathobiome of N. norvegicus due to Hematodinium sp. infection and disease that in turn provides a foundation for further studies on the pathogenesis of this important parasitic disease.

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