Monday, 18 December 2017

Winter is coming... and so is Cold Water Vibriosis (CWV)

Aliivibrio salmonicida causes Cold Water Vibriosis (CWV) and is the most important bacterial disease effecting salmon aquaculture. Standardized fish feeding in the late 1970’s and vaccinations against major bacterial pathogens in the 1980’s lead to global production (mostly from Norway, Scotland and Icelandic farms) of Atlantic salmon reaching 80,000 tonnes in 1986. Motivated by a CWV outbreak in 2011, this 2017 review gives a concise summary of our knowledge of the bacterial pathogen A. salmonicida from the past 30 years of study; including its genetics, virulence, pathogenesis and vaccinations.

Virulence factors
There are few studies describing the role of different virulence factors of A. salmonicida. Regulation of this pathogen appear to be related to the lux operon, and as with most vibrios, limited by iron availability. A. salmonicida is able to grow in iron-limiting conditions due to 1) iron acquisition systems that can operate in a wide range of temperatures; 2) major siderophore Bisucaberin induced at temperatures below 10°C. Proliferation in colder waters is likely attributed to the components of non-siderophore iron acquisition being suppressed at temperatures above 15°C. Cell division of A. salmonicida is highest on solid substrate at 15°C and highest in liquid media at 10°C. Salinity also effects expression of flagellins leading to impaired motility at low salinities. This motile pathogen is capable of sensing and moving towards fish mucus as well as bacterial quorum-sensing molecules.
Pathogenesis
It is assumed, but not known, that the lifecycle of
A. salmonicida (like other vibro spp.) consists of free-living and facultative pathogenic phases, with the production of their own bio-film allowing their persistence in the environment for >1 year. Since motility is effected by salinity, salinity impacts their pathogenicity. 12 Norwegian fish farms were sampled from October – June, revealing the persistence of A. salmonicida in the environment, even when no outbreaks of CWV occurred. A further study expanded on this, revealing the pathogen to be consistently present within a 200-250 m radius from aquaculture sites. A. salmonicida enters the host’s blood stream via intact skin, avoiding detection by muting its gene expression. It can alter its microbe-associated molecular patterns (MAMPs), changing them to environmental MAMPs, which go undetected by the Toll-like receptors (TLRs) of Atlantic salmon.
Vaccination
Early vaccinations involved immersion of Atlantic salmon in formalin-treated bacterin (immersion immunisation), giving limited and short lived protection. All subsequent vaccination involved injection of formalin-treated cells, giving longer lasting protection. Physiological state of the fish and water temperature during immunisation is very important to its success, owing to antibody production being greatest in relatively warm waters.

In conclusion, this paper is useful for highlighting gaps in the knowledge of CWV. The full life cycle, as well as its environmental source remains unknown and avoidance of the hosts TLR system needs further investigation. I feel this review could be more detailed and assumes a lot of the knowledge of the reader without providing referral to supporting material or much explanation. Lastly, the economic impacts of A. salmonicida are not discussed which I think could be used to add to the importance of this study and motivation for further research.

Reference

Kashulin, A., Seredkina, N. and Sørum, H. (2016). Cold-water vibriosis. The current status of knowledge. Journal of Fish Diseases, 40(1), pp.119-126. 

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