Seminar: Dr. Bartolomeo Gorgoglione, University of Toledo

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Seminar: Dr. Bartolomeo Gorgoglione, University of Toledo

September 20, 2017
at 3:00pm to at 4:00pm

Title: “From a complex Tetracapsuloides bryosalmonae life cycle, dissecting the elaborated trout immune response against PKD and upon co-infections with VHSV

Speaker: Dr. Bartolomeo Gorgoglione, University of Toledo

Abstract: Proliferative Kidney Disease (PKD) is a slow progressive disease of major importance to ecosystems and aquaculture in the central-northern areas of Europe and USA, considered an emergent economically important disease for salmonids. The myxozoan parasite Tetracapsuloides bryosalmonae undergoes a peculiar two-host life cycle. Infective spores produced during overt infections in the coelomic cavity of Phylactolaemata bryozoans, undertake coelozoic sporogony into renal tubules of salmonid, to generate malacospores infective for bryozoans. Increasing water temperatures due to climate change events, together with the recently discovered migrating zooids formation in Fredericella sultana, will provide more suitable conditions to extend their enzootic range, enhance life cycle reproducibility and exacerbate PKD pathogenesis. T. bryosalmonae extrasporogonic proliferation, within the kidney interstitium, causes instead a tumor-like chronic lymphoid hyperplasia, with granulomatous-like lesions resulting in the whole kidney swelling. In rainbow trout (Oncorhynchus mykiss), host with elevate susceptibility, PKD pathogenesis is shaped by an anti-inflammatory phenotype, a profound B-cell/antibody response and a complex interplay between T-helper subsets driving to dysregulated activities. Brown trout (Salmo trutta) is more resistant to PKD, showing milder clinical symptoms and a sustained inflammatory reaction with reduced immunosuppression. Hosts affected by PKD show an increased susceptibility to secondary or opportunistic pathogens, thus novel interactions are likely to happen when considering T. bryosalmonae is moving northward. The first heterogeneous lab-based co-infection model was set up between PKD and Viral Haemorrhagic Septicaemia (VHS), an OIE notifiable listed disease caused by a Novirhabdovirus, worldwide responsible for high morbidity and mortality. Pro-inflammatory and antimicrobial peptide genes are modulated upon virus co-infection, with an earlier activation of cellular and humoral responses, a stronger up-regulation of Th-1 and antiviral genes.

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