Aliivibrio salmonicida
From Wikipedia, the free encyclopedia
| Aliivibrio salmonicida | |
|---|---|
Scientific classification  | |
| Domain: | Bacteria |
| Kingdom: | Pseudomonadati |
| Phylum: | Pseudomonadota |
| Class: | Gammaproteobacteria |
| Order: | Vibrionales |
| Family: | Vibrionaceae |
| Genus: | Aliivibrio |
| Species: | A. salmonicida |
| Binomial name | |
| Aliivibrio salmonicida Håstein et al., 1978 | |
Aliivibrio salmoncida is a species of Gram-negative, rod-shaped, facultatively anaerobic marine bacterium in the family Vibrionaceae. It is the causative agent of cold-water vibriosis (Hitra disease), a systemic inection affecting Atlantic salmon (Salmo salar) and other marine fish.[1][2] This species is adapted to low-temperature marine environments and is primarily associated with aquaculture systems in northern regions, particularly the North Atlantic.[3]
The species was originally described as Vibrio salmoncida based on phenotypic and pathogenic characteristics observed in diseased salmon.[1] Subsequent phenogenetic analyses using 16S rRNA gene sequencing and multilocus data supported its reclassification into the genus Allivibrio, which groups several marine, often bioluminescent, Vibrionaceae species.[4]
Morphology and physiology
A. salmoncida is a curved rod-shaped bacterium that is motile by means of polar flagella. It stains Gram-negative and possesses a diderm cell envelope typical of members of the class Gammaproteobacteria.[2] The bacterium is oxidase-positive, catalase positive, and exhibits metabolic traits consistent with marine Vibrionaceae, including a requirement for sodium ions.
The organism is facultatively anaerobic and capable of both respiratory and fermentative metabolism depending on oxygen availability.[5] In laboratory conditions, this bacterium has a low optimal growth temperature (typically 4-12 °C), consistent with its ecological adaptation to cold marine environments.[2]
Genome and host adaptation
The genome of A. salmoncida has been sequenced and is characterized by a high number of insertion sequences and pseudogenes, indicating extensive genome decay.[3] Many genes involved in environmental survival and metabolic flexibility are disrupted, consistent with specialization toward a host-associated lifestyle.[3] Comparative analyses have shown loss or inactivation of pathways commonly retained in free-living Vibrionaceae.[3]
One of the pathways disrupted in A. salmonicida are those associated with chitin degradation and utilization, pathways that are typically conserved in environmental Vibrionaceae.[3] In related marine bacteria, chitin serves as both a nutrient source and a surface for environmental persistence.[6] Subsequent work demonstrated that some strains of A. salmoncida are able to degrade and metabolize chitin and utilize it as a carbon source despite not possessing a full chitinolytic pathway.[7]
Virulence & pathogenesis
Cold-water vibriosis is a systemic infection characterized by rapid dissemination of bacteria following entry into the host.[8] Experimental infection studies have demonstrated spread to the bloodstream and internal organs.[8]
The lipopolysaccharide O-antigen is required for full virulence, as mutants lacking genes necessary for O-antigen synthesis showed reduced virulence in Atlantic salmon.[9] Flagellar components also contribute to pathogenicity. Deletion of dlagellar genes reduced virulence in immersion challenge models, although motility itself is not required for invasion.[10]
