Amoebic Gill Disease

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Also Known As: AGD — Amoebiasis — Amoebic Gill Infection — Amoebosis — Paramoebiasis

Caused By: Neoparamoeba pemaguidensis — Neoparamoeba perurans


Amoebic gill disease is caused by Neoparamoeba perurans, the most important pathogenic amoeba in fish. The disease causes large economic losses in marine cultured salmonids.[1] [2] It can also affect turbots.

Neoparamoeba perurans, a newly described amoeba is also known to colonize fish gills which results in amoebic gill disease in salmonids [2]. More careful comparative field (e.g. susceptibility of different fish species under various environmental conditions) and laboratory studies (e.g. biochemical, molecular) using cloned isolates of the two species are required to more clearly determine the etiological agent(s) of AGD.


Tasmania, Australia, Ireland, France, North America and Spain suffer the most significant losses due to AGD.

Although small numbers of the amoeba have been found on the gills of wild fish, it is unknown if they can be source of infection in cage-cultured salmonids.


Atlantic salmon and rainbow trout are most susceptible to disease.

Turbot, brown trout, bass, bream, sea urchins[3] and crabs[4] can also be infected, causing morbidity and mortality.

The amoeba will also readily colonise severe injuries such as jellyfish stings, clubbed lamellae and necrotic gill syndrome lesions.

Clinical AGD is always associated with water temperatures of 12-20⁰C and high salinities of ≥32 ppt. [5] Amoeba numbers also rise in the Summer.

Clinical Signs

AGD causes mucus to build up on the gills of infected fish and hyperplasia of the gill tissues to occur. The secondary lamellae may fuse together. Fish often swim close to the surface and gulp air as they become dyspnoeic. Opercular movements will increase. They may swim belly upwards in the terminal stages. Diseased fish usually stop feeding become lethargic and mortalities are common.


Finding N. pemaguidensis is not always pathological and it is important to distinguish in which cases it is the aetiological agent. The presence of multiple, typical mucoid patches on the gills is highly suggestive of AGD.

Wet mounts of gill tissue can be tested with immunofluorescent antibody testing(IFAT), Quick Dip®[6] and dot-blot techniques[7] which is used for mass screening.

Histologically, amoebae can be seen attaching to the gill epithelium with haematoxylin & eosin stain. PCR is also available.

On necropsy, multifocal patches of white to grey swollen gill tissue with excessive mucus associated is characteristic of AGD. This is particularly evident in the dorsal gill arches.[8] These changes tend to be more diffuse in rainbow trout than in salmon.

Histopathological features are similar in all species affected and feature essentially hyperplasia and hypertrophy of the gill epithelium.[9] Gill lamellae are often fused and tissues spongiotic.


Freshwater baths are used as therapy but are very stressful for the fish. Current treatment method in Scotland and Ireland is a bath in hydrogen peroxide[10] .

Chloramine, chlorine dioxide and levamisole have also been used.


Lack of information about transmission and carriers of the disease has made control difficult to design and implement.

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  1. Munday, B. L., Zilberg, D., Findlay, V (2001) Gill disease of marine fish caused by infection with Neoparamoeba pemaquidensis. J Fish Diseases, 24(9):497-507
  2. 2.0 2.1 Young, N.D. Crosbie, P.B.B., Adams, M.B., Nowak, B.F., and Morrison R.N. (2007) Neoparamoebae perurans n.sp., an agent of amoebic gill disease in Atlantic salmon (Salmo salar). International Journal of Parasitology 37, 1469-1481.
  3. Jones, G. M., Scheibling, R. E (1985) Paramoeba sp. (Amoebida, Paramoebidae) as the possible causative agent of sea urchin mass mortality in Nova Scotia. J Parasitology, 71:559-565
  4. Johnson, P. T (1977) Paramoebiasis in the blue crab, Callinectes sapidus. J Invertebrate Pathology, 29(3):308-320
  5. Rodger, H. D., McArdle, J. F (1996) An outbreak of amoebic gill disease in Ireland. Veterinary Record, 139(14):348-349
  6. Zilberg, D., Nowak, B., Carson, J., Wagner, T (1999) Simple gill smear staining for diagnosis of amoebic gill disease. Bulletin of the European Association of Fish Pathologists, 19(5):186-189
  7. Douglas-Helders, M., Carson, J., Howard, T., Nowak, B (2001) Development and validation of a new dot blot test for the detection of Paramoeba pemaquidensis (Page) in fish. J Fish Diseases, 24(5):273-280
  8. Adams, M. B., Nowak, B. F (2001) Lesion distribution and structure in the gills of Atlantic salmon (Salmo salar L.) affected with amoebic gill disease. In: Battaglene SC, Cobcoft JM, eds. The First Scientific Conference of the Atlantic Salmon Subprogram Handbook. Hobart, Tasmania, Australia: CSIRO Marine Laboratories, 28-29
  9. Zilberg, D., Munday, B. L (2000) Pathology of experimental amoebic gill disease in Atlantic salmon, Salmo salar L., and the effect of pre-maintenance of fish in sea water on the infection. J Fish Diseases, 23(6):401-407
  10. Mark D. Powell, Heather Mlynarski, Joy A. Becker1, James A. Mackie (2009) Effects of oral administration of AquaciteTM and Beta-becTM, two commercial β-glucan-based nutritional supplements in Atlantic salmon (Salmo salar) during an outbreak of Amoebic Gill Disease.. Fiskehelse, 11. årgang nr. 1, 26-34

Zilberg, D. and Munday, B.L. (2006). Phylum Amoebozoa. In: Fish Diseases and Disorders, Volume 1: Protozoan and Metazoan Infections, 2nd edition (ed. P.T.K. Woo), CABI, Wallinford, UK. pp. 1-15


This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project.

The datasheet was accessed on August 08, 2011.

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