Genetic decay showing transition to a life as a host dependant-fish pathogen?

Aliivibrio salmonicida is a gram-negative proteobacteria in the family Vibronaceae, responsible for the disease cold-water vibriosis. This disease presents a huge issue in marine aquaculture, often causing breakouts in livestock population. Characteristics of the disease in-vivo include degradation, hemolysis and sepsis (presence of harmful bacteria in tissue).

Hjerde et al., (2008) shotgun sampled the entire genome of environmental A.salmonicida strain LFI1238. The sample came from cod supplied by the Norwegian institute of fisheries and aquaculture.

They identified a total of 4,286 protein sequences and found that the genome was split into 6 parts. These 6 parts comprised 2 groups of chromosomes and 4 of plastids. The genome was found to be highly fragmented due to high levels of insertion sequence (IS) elements. These are short sequences of DNA that acts as a transposable element, meaning it can change its position within the genome. These elements can be linked to processes such as evolution and the events associated with it for example acquisition, gene loss and rearrangement of chromosomes. Horizontal gene transfer may give new functional capabilities to A.salmonicida in areas such as protein secretion and iron acquisition, both of which hold the potential for pathogenicity. However, along with these new functions, degeneration of 370 genes suggests decreased metabolic and physiological capacities. This is also suggested by a loss of function in comparison to other Vibrionaceae.

The genome of the bacteria has a mosaic structure, with the majority of the acquired DNA being flanked by IS elements. Perhaps the most important finding is the bacteria losing several genes whose function resides in the utilization of the homopolymer chitin, importantly making A.salmonicida unable to grow on the polymer form of chitin. This presents issues for the bacteria, as chitin is a key component of marine systems, important for the attachment of bacteria to carrier organisms. Consequently, this may limit the number of organisms that can act as a carrier to A.salmonicida. Acquiring new genes and losing old functions may to some extent explain the emergence of A.salmonicida as a fish pathogen, a new niche that has no need for certain functional genes. The genome observed here shows similarities to other host-restricted pathogens and so suggest that A.salmonicida has also converted to fulfill this niche of being a fish pathogen.

This study by Hjerde et al., (2008) presents hugely interesting information concerning A.salmonicida and potential for how it may have gotten rid of certain genes and their genetic function in order to make the transition to a niche of a fish pathogen. This is clearly shown by the expansion of IS elements being directly related to genome reduction of the bacteria. The fact that the bacteria have seemingly lost the ability to grow on chitin is of huge importance. This suggests that the numbers of organisms that can act as a carrier are surely reduced. I find this hugely interesting, as I assume that this would put the bacteria at a significant disadvantage, narrowing its niche. However, with horizontal gene transfer giving new functions, together with the loss of old ones, the transition to a fish pathogen is strongly supported. The shift has also been shown in Mycobacterium leprae, Salmonella Typhi and others. The loss of these genes, along with the potential for new functional capabilities, shows these bacteria have become host specific. As a whole I feel this research is extremely useful in presenting evidence for certain bacteria species becoming host-dependant fish pathogens.

Reference:

Hjerde, E., Lorentzen, M., Holden, M., Seeger, K., Paulsen, S., Bason, N., Churcher, C., Harris, D., Norbertczak, H., Quail, M., Sanders, S., Thurston, S., Parkhill, J., Willassen, N., Thomson, N. (2008). The genome sequence of the fish pathogen Aliivibrio salmonicida strain LFI1238 shows extensive evidence of gene decay. BMC Genomics. 9, 616.