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Coral Reef or Velvet Disease, Amyloodiniumiasis, A Virulent Dinoflagellate Disease of Saltwater Fishes

by Bob Fenner

A Maroon Clown with Velvet

 

Marine Velvet is one of the two most important biological diseases of coral reef and marine aquariums. Its host incidence and importance is of critical concern to the marine aquarium industry. The causative organism, Amyloodinium ocellatum (formerly Oodinium ocellatum) is found in all oceans, and is very common on wild and newly-collected fishes, including sharks and rays. Death from infection may occur within a day of symptoms (e.g. fast breathing), detection. Amyloodiniumiasis has been identified as a source of mass mortalities, epizootics in home aquariums, commercial settings, and public aquariums since its original description by Brown in 1931, most cases being hard to diagnose initially, and rapidly becoming deadly. 

    In a related genus, Oodinium pillularis and O. limnecitum are the causative agents of freshwater rust or velvet disease (Jacobs 1946). 

Taxonomy/Nutrition:

    Amyloodinium is a Dinophycean (Dinoflagellate), of the same order as Gymnodinium breve (red tide organism), family Peridineae. This parasitic species derives all nutrition from its host; lacks photosynthetic chloroplasts (Unlike freshwater species of Oodinium). Marine velvet absorbs cytoplasmic fluid by means of a pseudopod that appears to have histolytic properties. Primarily it is a gill parasite, but may attach to the body (Blasiola 1978)

Clinical Signs/Pathology:

    Tissue ulceration and hypersecretion of mucus are obvious microscopically. Hyperplasia and filament adhesion, with the feeding stage burrowing deep into the fish host's subcutaneous skin layer. Infected fishes have a white, tan, golden or gray dusty or powdery appearance over their outside. May not be seen till late stage as the gill filaments are primary sites, therefore rapid breathing is a key initial symptom. Always display rapid breathing (more than 80 openings per minute). Additionally, infected fishes generally swim near the surface, "flash" or scratch against the bottom, decor and refuse food. All fish in the system will have the disease to a varying degree. Loss of life is said to come about from interference with respiration, but many dead fish examined have few parasites on their gills, so the question of toxin involvement is raised. 

    Identification of Amyloodinium is attained through a skin slime smear (or gill section if the fish is dead) with a spatula or glass slide, cover glass. Dinospores can be seen at 150 times magnification locomoting in wavy, bee-line tumbling motion. They are bell-shaped, have a mid-line constriction, about ten microns in length. Vegetative forms are about 60 microns, slightly oblong, dark colored, containing large starch granules that stain easily with iodine. 

    Actual "Dinoflagellate" appearance is only apparent in the disseminative (off-fish) dinospore stage.

Life Cycle of Amyloodinium:

This parasite is most often "brought in" to a new system from newly acquired infected fish/es, but may be acquired and passed on invertebrates, live rock, algae... most anything wet. Hence the need for diligence in selection, acclimation and quarantine. It's life cycle is almost identical to the more-familiar Cryptocaryon (Saltwater Ich) protozoan.

Almost always, the gills of fishes are affected... way ahead of apparent marks on the body or fins. Rapid gilling, apparent inflammation and irritation of the gills, followed by labored breathing, sedentary behavior, may occur so rapidly (hours to a day or two) that no other macroscopic evidence of its presence may show. Light, resident infestations in captivity (unlike Crypt) are rare... With most captive cases resulting in rapid reproduction, re-infestation, gill necrosis, hemorrhage and death.

Free-swimming infective  dinospores, have an apical flagellum and one at the waistline in a groove, red eye spot, measure  9-15 microns. According to Bower (1987) dinospores  can usually live for 7-8 days without finding a host and are infective for 6, remaining alive and infective even longer at lower temperatures. She recounts that though most emerge from encystation within 5 days and survive another 7 to 9 days, some dinospores were present in their test tanks (at 75-80 F.) some 37 days later. 

Non-motile feeding stages (trophozoites) that parasitize the host fish (become attached to gill epithelium or skin, lose flagella, develop a funnel-shaped aperture at one end through which projects rhizoids to obtain nutrition. As Trophozoites grow, internal structure becomes obscured by globular starch granules. Trophozoites range in size from 15 to 150 microns, have a round to oval macronucleus. Their cell wall membrane is sharp and clearly visible, contains chitin.

When they mature (3 days to a week) they drop off and fall to the substrate where they encyst. Cysts are formed by the cells retracting rhizoids and sealing the opening with a cellulose cap. Here what are now known as tomonts undergo vegetative (non-sexual) division. Internally dividing cells called...

Palmella stage. Asexual division results in 2,4,8,16... 256 individuals formed. There is no division below 50 degrees F., slow rate 68-77 F. Optimal above 77 F.  (25 C.) Hosts rapidly show signs of infection 6-7th day at 77 F. Note: there is no dormant or resting stage. One strain lasted w/o fish for 4 weeks, but not eight at 78 F. Invertebrates can carry this disease. 

Prevention:

    Extended quarantine (20 days or more), and prophylactic dips/baths (Freshwater, pH-adjusted, w/ or w/o additions like Formalin) exclude most cases of Amyloodiniumiasis, but not entirely. There is evidence of some acquired immunity... Thus far there are no vaccines sold in the U.S. for this disease.

     Ultraviolet Radiation will kill free-swimming dinospores... but I hesitate to endorse it as carte-blanche insurance, as many trophonts may still sufficiently develop these stages re-infesting your fishes, and sufficiently debilitating them to result in morbidity, mortality.

Treatment:

    It cannot be over-emphasized that diagnosis and treatment must not be delayed... lest all fish livestock be lost. The free-living dinospore stage is susceptible to chemical treatment, but the on-fish stages (trophonts and tomonts) are not.

    Infestations have occurred in systems with salinities ranging from 3-45 ppt. (Noga, 1996). Hyposalinity as a bath/dip is only effective in so much that lowered specific gravity causes the trophonts to drop off their hosts and encyst. Further, Clorox (tm) bleach at concentrations of 3 tsp. per four gallons have proven to not kill these resting stages. Obviously the pH-adjusted freshwater must need be drained and discarded between dips.

    Copper (either citrated, chelated or not) at standard dosages of 0.15-0.20 have been shown to neither prevent division nor kill dinospores. However, trophonts are affected at treatment concentrations. Hence continuous copper use is often helpful in controlling Amyloodinium, but not eradicating it from systems, unless administered carefully over time.

    Noga and Levy (1995) reported success using Chloroquine diphosphate (an antimalarial medicine) at 5-10 mg/L for 10 days. Like copper, this compound is toxic to invertebrates and algae, and unlike copper, quite expensive.

    Formalin exposure (100-200 mg/l aka ppm.) for 6-9 hours will result in the shedding of trophonts... but unless some efficacious treatment is continued these will later develop dinospores and re-infest the fish-hosts. Re-examination of hosts is required...

    Many other substances/treatments have been investigated, and indeed there are many such products on the market that claim to prevent and/or cure Amyloodiniumiasis... none have proven absolutely efficacious.

Infested systems can be cured in one of three ways:

1) Leaving the tank "fallow" (without fish hosts) for 6 to 8 weeks. This process can be sped up by elevating water temperature. A figure stated by Bower (1987) is perhaps 2 weeks at 35 C. (95 F.).

2) Bleaching the system with a minimum of 3 tsp. per gallon of chlorine bleach for 24 hours, then dumping, freshwater rinsing... 

3) Draining the system and letting it dry thoroughly. 

Prevention of introduction of the parasite is the single best method of control. Along with freshwater bath protocols in the acclimation, introduction of new fishes, a good two week or more period of isolation, examination of new fish livestock will all but guarantee success in avoiding this parasite. 

Environmental factors like degree of crowding, presence of filter feeders and filtration methods like ultraviolet sterilization and diatomaceous earth have been discussed in reducing the likelihood of infection, removal of a percentage of dinospores. 

Other promising treatments have included the use of hydrogen peroxide as a bath (75 to 150 ppm for thirty minutes), fresh seawater used to flush (http://www.soest.hawaii.edu/SEAGRANT/Makai/nov98/2.html).

None of these is 100% effective in eradicating Amyloodinium from a system. 

Related Articles on WWM:

http://www.wetwebmedia.com/acclimat.htm

http://www.wetwebmedia.com/quaranti.htm

http://www.wetwebmedia.com/dips_baths.htm

Bibliography/Further Reading:

Amlacher, E. 1970. Textbook of Fish Diseases. TFH Publ. N.J. p. 157

Blasiola, George C. 1978. Coral reef disease, Oodinium ocellatum. Marine Aquarist 8(7):50-59

Bower, Carol E. 1987. Update on Amyloodinium ocellatum. SeaScope Fall 87. 

Brown, E.M. 1931. Notes on a new species of dinoflagellate from the gills and epithelium of marine fishes. Proc. Zool. Soc. Lond. 1931(1):345-346

Cheung, P.J. , R.F. Nigrelli, G.D. Ruggieri. 1979. Scanning electron microscopic observations on the various stages of the life cycle of O. ocellatum. Brown. Osborn Labs of Mar. Sci. N.Y. Aq., N. Y. Zool. Society, Brooklyn, N.Y. T. Am. Micros. 98(1): 157

Jacobs, D. L. 1946. A new parasitic dinoflagellate from freshwater fish. Trans. Am. Micr. Soc. 65:1-17

Kingsford, M.D. 1975. Treatment of Exotic Marine Fish Diseases. Palmetto Publ. Co. Florida 1,4, 16-18, 21-26, 40, 40-49

Noga E.J. and Levy M.G. 1995. Dinoflagellida (Phylum Sarcomastigophora) In: P T K Woo (ed.) Fish Diseases and Disorders. Volume 1: Protozoan and Metazoan Infections. CAB International, Wallingford, Oxon. pp 1-25.

Noga, Edward J. 1996. Fish Disease, Diagnosis and Treatment. Mosby-Year Book Inc., St. Louis. 367pp.

Noga, E.J., Z. Fan and U. Silphaduang. 2001. Histone-like proteins from fish are lethal to the parasitic dinoflagellate Amyloodinium ocellatum. Parasitology 123:57-65.

Reichenbach-Klinke, H. and E. Elkan. 1965. The Principle Diseases of Lower Vertebrates. Book 1, Diseases of Fishes. TFH Publ., N.J. 30-35

Schubert, G. 1974. The velvet touch. TFH 22(6):91-96

Sindermann, C.J. 1970. Principle Diseases of Marine Fish and Shellfish. Acad. Press, N.Y. pp. 6, 228, 231

Wilkerson, Joyce D. 1998. Clownfishes. A Guide to Their Captive Care, Breeding & Natural History. Microcosm, VT.




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