Aeromonas salmonicida

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Aeromonas salmonicida is a pathogenic bacterium that severely impacts salmonid populations and other species. It was first discovered in a Bavarian brown trout hatchery by Emmerich and Weibel in 1894 9. Aeromonas salmonicida’s ability to infect a variety of host, multiply, and adapt, make it a prime virulent bacterium. A. salmonicida is an etiological agent for furunculosis; a disease that causes septicemia, haemorrhages, muscle lesions, inflammation of the lower intestine, spleen enlargement, and death in freshwater fish populations. It is geographically found worldwide with the exception of South America 9. The major route of contamination is due to poor water quality; however, it can also be associated stress factors such as overcrowded areas, high temperatures, and trauma. Spawning and smolting fish are prime victims of Furunculosis due to their immuno-compromised state of being.


Morphology and Bacterial Characteristics

Aeromonas salmonicida is a gram-negative, facultatively anaerobic, non-motile bacterium. It is bacillus shaped, approximately 1.3-2.0 by 0.8-1.3 mm in size, and grows at an optimal temperature between 22˚-25˚C 9. The bacterium readily ferments and oxidizes glucose, is catalase, and cytochrome oxidase positive. Aeromonas salmonicida’s molecular properties consist of a special surface protein array called the A-layer, which is believed to be responsible for the bacteria’s virulent traits, and Lipopolysaccharide, the cell’s major cell envelope antigen 4. The A-layer consists of a 50 kD protein, and provides protection to the bacterium. The Lipopolysaccharide consists of three moieties: lipid A, a core oligosaccharide and an O-polysaccharide (O-antigen). The extracellular products of Aeromonas salmonicida consists of 25 proteins, enzymes and toxins, and many more 4. In addition, the genome is composed of a single circular chromosome (4,702,402 bp), two large and three small plasmids. The chromosome yields 58.5% of G+C pairs, has 4086 encoding proteins, and totals 4388 genes 15.

A. salmonicida isolates flourish when grown on blood agar or tyrosine. Large colonies will be observed along with a brown diffusible pigment within 2-4 days. Most typical strains are morphologically and biochemically homogenous with a few exceptions. Some of these exceptions include a distinguishable variation in pigment production, the bacteria’s ability to ferment selected sugars, and Voges-Proskauer assay results.

Cell Structure and Metabolism

Aeromonas salmonicida is a facultative anaerobe which means that it is capable of making ATP by aerobic respiration if oxygen is present but is also capable of switching to fermentation when oxygen is not present. It does not ferment sucrose or lactose, using glucose in this pathway instead; glucose fermentation creates gas. The bacterium grows optimally at temperatures between 22 and 25°C. The maximum temperature that it can grow at is 34.5°C. After about a 24 hour growth period the bacterial colonies reach about the size of a pin point. The colonies also have a brown pigmented color that appears after it has been growing for 48–72 hours.[1]


There are currently five “typical” subspecies of A. salmonicida according to Bergey's Manual of Systematic Bacteriology.

  • A. s. salmonicida
  • A. s. achromogenes
  • A. s. masoucida
  • A. s. smithia
  • A. s. pectinolytica

Host Range

  • Salmon
  • Trout
  • Cyprinid
  • Pike
  • Perch
  • Bullheads
  • Turbot
  • Halibut


Aeromonas salmonicida is an airborne pathogen that can travel 104 cm from its host into the atmosphere and back to the water (Wooster and Bowser 1996); thus making it difficult to control. The bacterium can maintain its pathogenicity in freshwater conditions for 6-9 months 10, and in saltwater conditions for up to 10 days without a host 16. Several direct count methods and other detection methods have found that the organism does not lose or reduces its titer concentrations.

Transmission of furunculosis mainly occurs through fish-to-fish contact via the skin or by ingestion. Rainbow trout have been found to carry A. salmonicida up to 2 years post initial infection without reexposure. A study by Bullock and Stuckey 3 concluded that chemically immunosuppressed fish compared with temperature stressed fish had a 73% mortality as opposed to a 33% mortality rate, respectively. Naturally occurring trout infections consisted of a 5-6% mortality rate per week with an 85% rate in untreated populations. McCarthy 8 found that some clinical furunculosis survivors of an infected trout population became A. salmonicida carriers. When comparing furunculosis epidemics with depressed oxygen levels, Kingsbury 6 discovered that when oxygen concentrations were decreased to less than 5 mg/L, A. salmonicida concentrations increased. While observing chum salmon in a density of 14.7 fish per square meter, 12.4% were infected with A. salmonicida. Whereas, densities consisting of 4.9 fish per square meter were infection free 13. Additionally, Aeromonas salmonicida concentrations were considerably elevated in water with low dissolved oxygen (6-7 mg/L), compared to water with higher dissolved oxygen (10 mg/L) 13. High density-low oxygen water resulted in survival rates that were roughly 40% less than in those consisting of low density-high oxygen conditions 13.


The bacterium is pathogenic for fish, and causes a disease known as furunculosis.[2] The symptoms the fish show are external and internal hemorrhaging, swelling of the vents and kidneys, boils, ulcers, liquefaction, and gastroenteritis. Furunculosis is commonly known as tail rot in fish and is common in gold and koi fish. Infected fish with open sores are able to spread the disease to other fish.[1]

It is also one of several bacteria that can cause bald sea urchin disease.[3] Since A. salmonicida can't grow at 37°C, it is not pathogenic in humans.[4]

Clinical Symptoms and Disease Diagnosis

Furunculosis is classified into four categories based on severity: acute, subacute, chronic, or latent. When fish are infected they become listless and weak until they die. Other characteristics observed include anorexia, lethargic movement, and they may exhibit a darkened pigment. Deep or shallow ulcers, exophthalmia, bloody spots, distended abdomen, and petechia at the base of the fin may also occur. Internally the infected fish may suffer from gastroenteritis, hemorrhagic septicemia, edematous kidney, and an enlarged spleen. The liver may appear pale in color and the spleen may be darkened. The peritoneal cavity may also be bloody and inflamed.

Bacteria must be isolated to positively identify the disease. Isolates are retrieved from muscle lesions, kidney, spleen or liver and then grown on trypticase soy agar and brain-heart infusion agar incubated at 20-25˚C. Colonies of A. salmonicida will appear as hard, friable, smooth, soft, and dark in color.

While cultural procedures produce good results, serological procedures produce more rapid results by utilizing serum agglutination, fluorescent antibody, or enzyme linked immunosorbent assay (ELISA) on infected tissue or cultured bacterium 2. Mooney et al 11 developed a DNA probe with polymerase chain reaction (PCR) to detect A. salmonicida DNA; results were successful in 87% of wild Atlantic salmon.


A. salmonicida tests negative for indole formation, coagulase, hydrolysis of starch, casein, triglycerides, and phospholipids, hydrogen sulfide production, citrate utilization, phenylalanine and the Voges–Proskauer (butanediol fermentation) test. It tests positive for oxidase, lysine decarboxylase, methyl red, gelatin hydrolysis, and catalase.[1]

Cited sources

1 Amos, 2011

2 Austin, 1986

3 Bullock & Stuckly, 1975

4 Chart, Shaw, Ishguro, and Trust, 1984

5 Ishiguro, Kay, Ainsworth, Chamberlain, Austen, Buckley, and Trust, 1981

6 Kingsbury O, 1961

7 McCarthy D and Roberts R, 1980

8 McCarthy D, 1980

9 Merck Animal Health, 2009

10 Michel and Dubosis-Darnaudpey, 1980

11 Mooney et al, 1995

12 Munn, Ishiguro, Kay, and Trust, 1982

13 Nomura et al, 1992


15 Reith et al, 2008

16 Rose and Ellis, 1990

17 Strohmeyer, 2011


19 Verner–Jeffreys et al, 2007

20 Wooster and Bowser, 1996


1. Amos K. (2011). Disease interactions of wild and cultivated salmon. Available: Last accessed 11/06/2011.

2. Austin B, Bishop I, Gray C, Watt B, & Dawes J. (1986). Monoclonal antibody- based enzyme-linked immunosorbent assay for the rapid diagnosis of clinical cases of enteric redmouth and furunculosis in fish farms. Journal of Fish Disease. 9, 469-474.

3. Bullock & Stuckly H. (1975). Aeromonas salmonicida detection of asymptomatically infected trout. The Progressive Fish-Culturist. 37, 237-239.

4. Chart H, Shaw D, Ishguro E, &Trust T . (1984). Structural and Immunochemical Homogeneity of Aeromonas salmonicida Lipopolysaccharide. Journal of Bacteriology. 158 (1), 16-22.

5. Ishiguro E, Kay W, Ainsworth T, Chamberlain J, Austen R, Buckley J, & Trust T. (1981). Loss of Virulence During Culture of Aeromonas salmonicida at High Temperature. Journal of Bacteriology. 148 (1), 333-340.

6. Kingsbury O. (1961). A possible control of furunculosis. The Progressive Fish-Culturist. 23, 136-137.

7. McCarthy D & Roberts R. (1980). Furunculosis of fish- The state of our knowledge. Advances in Aquatic Microbiology, Droop M & Janasch H, 293-341. London. Academic Press.

8. McCarthy D. (1980). Some ecological aspects of the bacterial fish pathogen Aeromonas salmonicida. Aquatic Microbiology. 299-324.

9. Merck Animal Health. (2009). The Disease. Available: Last accessed 11/06/2011.

10. Michel C & Dubosis-Darnaudpey A. (1980). Persistence of the virulence of Aeromonas salmonicida strains kept in river sediments. Annual Rech Veterinary. 11, 375-386.

11. Mooney J, Powell E, Clabby C, & Powell R. (1995). Detection of Aeromonas salmonicida in wild Atlantic salmon using a specific DNA probe test. Diseases of Aquatic Organisms. 21. 131-135.

12. Munn C, Ishiguro E, Kay W, & Trust T. (1982). Role of Surface Components in Serum Resistance of Virulent Aeromonas salmonicida. Infection and Immunity. 36 (3), 1069-1075.

13. Nomura T, Yoshimizu M, & Kimura T. (1992). An epidemiological study of furunculosis in salmon propagation. Salmonid Diseases, T. Kimura. Hakodate, Japan: Hokkaido University Press, 187.

14. Northeast Salmon Team. (2011). Survey of North Atlantic Fishes for Salmonid Pathogens. Available: Last accessed: 11/06/2011.

15. Reith M, Singh R, Curtis B, Boyd J, & Bouevitch A. (2008). The genome of Aeromonas salmonicida subsp. salmonicida A449: insights into the evolution of a fish pathogen. BMC Genomics. 9 (427), 1-15.

16. Rose A & Ellis E. (1990). The survival of Aeromonas salmonicida subsp. salmonicida in sea water. The Journal of Fish Disease. 13, 205-214.

17. Strohmeyer C. (2011). Treatment and Identification of Aeromonas and Vibrio in Aquariums and ponds. Available: Last accessed 11/06/2011.

18. The Scottish Government. (2011). Furunculosis in salmon . Available: Last accessed 11/06/2011.

19. Verner–Jeffreys D, Algoet M, Pond M, Virdee H, Bagwell N, & Roberts E . (2007). Furunculosis in Atlantic salmon (Salmo salar L.) is not readily controllable by bacteriophage therapy. Science Direct. 270, 475-484.

20. Wooster G & Bowser P. (1996). The aerobiological pathway of a fish pathogen: survival and dissemination of Aeromonas salmonicida in aerosols and its implications in fish health management. Journal of the Worlds Aquaculture Society. 27 (1), 7-14.


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  4. Altwegg, M., A. G. Steigerwalt, R. Altwegg-Bissig, J. Lüthy-Hottenstein, and D. Brenner. 1990. Biochemical identification of Aeromonas genospecies isolated from humans. Journal of Clinical Microbiology 28:258-264.

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