New vaccination strategies are required for effective control of winter ulcer disease caused by emerging variant strains of Moritella viscosa in Atlantic salmon.

Moritella viscosa is one on the major etiological agents of winter-ulcers in Atlantic salmon (Salmo salar) in Norway. Outbreaks of ulcerative disease in farmed fish occurs across the North Atlantic region and is an impeding factor for sustainable growth within the industry. Commercially available multivalent core vaccines containing inactivated bacterin of M. viscosa reduce mortality and clinical signs related to winter ulcer disease. Two major genetic clades within M. viscosa have previously been described based on gyrB sequencing, namely typical (hereafter referred to as classic) and variant. Vaccination-challenge trials using vaccines including either variant and or classic isolates of M. viscosa show that classic clade isolates included in current commercial multivalent core vaccines provide poor cross-protection against emerging variant strains, while variant strains confer high level of protection against variant M. viscosa but to a lesser extent to classic clade isolates. This demonstrates that future vaccine regimens should include a combination of strains from both clades.

Effects of perfluorinated alkyl acids on cellular responses of MCF-10A mammary epithelial cells in monolayers and on acini formation in vitro.

Perfluorinated alkyl acids (PFAAs) are stable chemicals detected in tissue and serum from various species, including humans, and have been linked to adverse health outcomes. Experimental PFAA exposure in rodents has been associated with changes in mammary gland development. The estrogen receptor (ER)-negative human breast epithelial cell line, MCF-10A, can be grown as monolayer, but also has the ability to form three-dimensional acini in vitro, reflecting aspects of mammary glandular morphogenesis. Cells were exposed to five different PFAAs, perfluorooctane sulfonate (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), and perfluoroundecanoic acid (PFUnDA), both in monolayer and acini cultures. In monolayer cultures only the higher concentrations of PFOS, PFNA and PFDA (400-500µM) caused a significant increase in cell death, whereas PFOA and PFUnDA had no effect. Normal acini maturation was negatively impacted by PFOS, PFNA and PFDA already at the lowest concentration tested (0.6µM). Observed effects included loss of organization of the cell clusters and absence of a hollow lumen. Overall, this study demonstrated that PFAAs can interfere with cellular events related to normal development of glandular breast tissue through ER-independent mechanisms.