Tenacibaculum maritimum

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A Microbial Biorealm page on the genus Tenacibaculum maritimum

Classification

Higher order taxa

Bacteria; Bacteroidetes/Chlorobi group; Bacteroidetes; Flavobacteriia; Flavobacteriales; Flavobacteriaceae; Tenacibaculum

Species

NCBI: Taxonomy

Tenacibaculum maritimum

Description and significance

Tenacibaculum maritimum is a pathogenic bacterium found in diseased fish species and causes symptoms of rotten fins, skin lesions, and internal organ paleness. This bacterium lives in a host-associated ecosystem, specifically in fish kidneys. The bacterium may reside inside the fish kidneys but it causes the disease, tenacibaculosis, which shows symptoms of lesions and necrosis on almost all surfaces of the infected fish [1]. The cells of T. maritimum stain gram-negative and use gliding motility. While grown in the laboratory, the bacterium appears pale yellow, with uneven edges. This is a filamentous bacterium that is rod-shaped and approximately 0.5 µm wide by 2 to 30 µm long [4]. Cell lengths vary, however each cell is distinctly rod-shaped. Spheroplast forms of the cell are not common and rarely observed. This bacterium is categorized as mesophilic and prefers temperatures between 15-34 ̊C [4]. This bacterium is of importance because it is linked to the disease, tenacibaculosis, which is one of the most threatening infections to marine fish populations. The disease affects populations of fish species that have marketable value in different areas across the globe [4]. T. maritimum can cause infection in entire communities of fish and drastically impact fishing industries worldwide.

Genome structure

The entire genome of T. maritimum has been sequenced using Illumina HiSeq 1000 technology. The total length of the genome is 3,225,035 base pairs, contains a protein count of 2,759 and 31.8 GC%. The genome contains 159 contigs and does not contain any chromosomes or plasmids. [3]

Cell and colony structure

T. maritimum cells are gram-negative and rod-shaped with uneven edges. The bacterium possesses no flagella or pili and therefore uses gliding motility. This is a filamentous bacterium that is rod-shaped and approximately 0.5 µm wide by 2 to 30 µm long [4]. Spheroplast forms of the cell are not common and rarely observed. The lipopolysaccharide (LPS) structure of the bacterium shows that various strains have common O-specific chains which are antigenically related to one another [1].

Metabolism

The membranes of this bacterium contain iron-regulated proteins. There are two distinct iron-uptake systems of this bacterium. One pathway involves the synthesis of siderophores and the other directly binds to heme groups as an iron source [2]. Iron acts as an external electron donor for the bacterium’s metabolic pathways. The bacterium sources iron from the hemoglobin of its host. The various strains of this bacterium are able to grow under anaerobic conditions [4]. In laboratory studies, all strains of T. maritimum were positive for catalase and oxidase. There is little known information on the specific metabolic processes of T. maritimum.

Ecology

This bacterium resides in the kidneys of marine species and causes necrosis of its host’s tissues. The bacterium causes infection of disease, tenacibaculosis, in its host and this often results in death of the infected fish. Outbreaks of the disease, tenacibaculosis, can be due to the bacterium and result in vast mortalities in fish species populations.


Pathology

This bacterium is the particular organism which can cause the ulcerative disease known as tenacibaculosis, in marine fish species. [1] T. maritimum causes disease in fish such as turbot, sea bream, Atlantic salmon, Pacific sardine, rainbow trout, Japanese flounder, sea bass and sole.[1] Fish that are diseased by this bacterium will show signs of an eroded mouth, paleness of internal organs, rotten fins, and superficial skin lesions. [4] In order for the bacterium to successfully colonize to the hosts’ tissue, adhesion must occur. Because the bacterium does not have pili, flagella or fimbriae; these structures are not involved in adhesion to the hosts’ cells. The bacterium uses the collaboration of toxins and enzymes that are present in the extracellular products. These enzymes and toxins interact to dissociate and alter the tissues of the host, making colonization possible. [1] The bacterium’s extracellular products are able to perform proteolysis on nucleases, amylase, gelatin and casein. [1] Lipopolysaccharides with an O-chain composition are produced by this bacterium and add to the progression of biofilms in the fish tissues, which allows for increase adhesion for the bacterium. [1]

References

1. Avendaño-Herrera R1, Toranzo AE, Magariños B. (2006) Tenacibaculosis infection in marine fish caused by Tenacibaculum maritimum: a review 71: 255–266 doi:10.3354/dao071255

2. Avendaño-Herrera, R., Toranzo, A. E., Romalde, J. L., Lemos, M. L., & Magariños, B. (2005). Iron Uptake Mechanisms in the Fish Pathogen Tenacibaculum maritimum. Applied and Environmental Microbiology, 71(11), 6947–6953. http://doi.org/10.1128/AEM.71.11.6947-6953.2005

3. Genome Assembly. (2013, October 28). Retrieved December 6, 2015, from http://www.ncbi.nlm.nih.gov/assembly?LinkName=genome_assembly&from_uid=16243

4. Piñeiro-Vidal M, Riaza A, Santos Y (2008) Tenacibaculum discolor sp. nov. and Tenacibaculum gallaicum sp. nov., isolated from sole (Solea senegalensis) and turbot (Psetta maxima) culture systems, IJSEM 58(1):21-25 doi:10.1099/ijs.0.65397-0


Edited by Alexandra Andrews of Dr. Lisa R. Moore, University of Southern Maine, Department of Biological Sciences, http://www.usm.maine.edu/bio