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30 September 2002 : Vol 1 : No 5         

CONTENTS
- KHV Verdict Shock British Trade

- Aquatic Animal Health Code

- What Shall I Do?

- Bacterial Gill Disease

- Koi Producers Meeting

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"KHV VERDICT" RATTLE THE TEA CUPS

The British Koi Trade was rocked to their roots when the Judge ruled in favour of the Claimant in the recent court case in which a UK Koi hobbyist sued a supplier for damages resulting from losses due to KHV infection. The Claimant (Ronald Craven) bought fish from a Japanese breeder on a buying trip that was organised by the Defendant (TMI). The fish were shipped by TMI to the UK and held in their care before being collected by Mr Craven. What followed was an outbreak of KHV at both TMI and Mr Cravens ponds. Needless to say, he lost the bulk of his collection.

Judge McGonigal awarded damages amounting to £74,928.68 plus costs to the Claimant. In paragraph 5.17 of his judgement he concluded:

"I find therefore that one or more of the Tewin Fish was not of satisfactory quality or fit for the purpose of being kept by a koi carp hobbyist when they were delivered to Mr Craven on 5 January 2001. The KHV infection in such fish spread to the other Tewin Fish and to the other fish in Mr Craven's covered and uncovered pond and to those in his quarantine and hospital tanks. If a seller sells fish suffering from an infectious disease to a buyer knowing that the fish will be kept with other fish, the seller is liable for the deaths of other fish that become infected with the disease (see Smith v Green (1875) 1 CPD 92). It was in the contemplation of the parties that Mr Craven would put the Tewin Fish into ponds containing other fish and that, if any of the Tewin Fish was infected with KHV, then KHV would spread to other fish in any pond where the Tewin Fish were put and could spread to adjoining ponds. I find that Tewin's breach of the terms implied by Section 14 of the Sale of Goods Act 1979 caused the death of those fish." (My highlighting: Ed)

The immediate reaction from the Trade was that of utter disbelief and shock. Should each and every fish now be sold with a contract limiting liability? Should they be importing and selling Koi at all? Was the financial risk not too high? How can Producers be tied down?

But, while the Craven v TMI case carries a special set of circumstances that may not apply to the way most Koi are sold, it offers a warning to the Trade in live fish in general. 

The highlighted parts above is of particular significance to each and every Trader of Koi in the UK and they should reconsider the way in which they conduct their business in future in order to minimize their risk. Likewise, the Producers of Koi worldwide should take notice of developments and bring their house in order. 

The Judge did not come to any conclusion regarding the origin of the TMI KHV infection, but there was a common denominator lurking ominously in the pages of the transcript. 

The full transcript of the court case is available at www.koiherpesvirus.co.uk courtesy the claimant.

AQUATIC ANIMAL HEALTH CODE

The OIE has just released International Aquatic Animal Health Code Edition 2002. The Office International des Epizooties (OIE) is an intergovernmental organisation that was established in 1924 in order to promote world animal health. It is in the interest of everyone involved with the production and trade of aquatic animals to acquaint themselves with contents of these documents that can be found on the OIE site.

International Aquatic Animal Health Code
and
Diagnostic Manual for Aquatic Animal Diseases

... crucial reading for anybody involved in aquatic animal health certification, diagnosis, quarantine, risk analysis or movement issues... These publications will be indispensable for veterinary administrators... should serve as useful reference books to all fish/shellfish disease specialists.  Australian Veterinary Journal

... the concise and accurate description of diagnostic techniques contained in this Manual is indispensable for anyone involved in the control of aquatic animal diseases.  Vlaams Diergeneeskundig Tijdschrift

Prepared by the OIE Fish Diseases Commission, the aim of the International Aquatic Animal Health Code is to facilitate trade in aquatic animals and aquatic animal products. The Code provides detailed definitions of the minimum health guarantees required of trading partners in order to avoid the risk of spreading aquatic animal diseases, includes sections on import risk analysis, import/export procedures and gives detailed rules for ‘Diseases notifiable to the OIE’. Less detailed chapters cover additional diseases classified as ‘Other significant diseases’ (of lesser economic importance, limited geographical distribution, or defined too recently to justify inclusion in the first list). The Code also contains sections on health control and hygiene, and model international health certificates for trade in live and dead aquatic animals.

The Manual describes diagnostic techniques for all the diseases that appear in the Code, and includes bibliographical references and a list of OIE Reference Laboratories for fish, mollusc and crustacean diseases. Draft texts for the Code and Manual were circulated to all OIE Member Countries for comment from their aquatic animal health experts, and these observations were taken into account in finalising the contents.

The Code and the Manual are available in two separate volumes.

The Code  and Manual are available online and free of charge.

WHAT SHALL I DO?

The European Association of Fish Pathologists (EAFP) has produced a very handy booklet: What Shall I Do? A Practical Guide for the Fresh Water Fish Farmer  Their aim was to provide a quick treatment guide to some of the common diseases affecting farmed fish. It is richly illustrated throughout with plenty colour pictures. The guide also includes contact details for technical support services throughout the EU region and national health coordinators.

While covering most of the diseases Koi farmers deal with, of interest is also Section 43: Diseases and Problems of Koi Carp and other Cold-water Ornamentals and Section 44: Disinfection in Aquaculture.

The cost is 12 UK pounds including postage, outside Europe 16 UK pounds. Please contact the EAFP General Secretary, David Bruno, for further information. 

BACTERIAL GILL DISEASE  

"Gill Rot is the most common disease in Koi" claims Dr Toshihisa Oguma in the July edition of Nichirin (2002-3 No 415). He should know because he is a veterinary surgeon practising in Niigata, the heart of Koi country. Unfortunately, the complexity of gill diseases is mostly misunderstood by Koi farmers. I reproduce here Fish Disease Leaflet 84 (1990) lifted from the Colorado Koi site, otherwise obtainable from the US Dept of the Interior, Fish and Wildlife Service.

Bacterial Gill Disease of Freshwater Fishes

G. L. Bullock

U.S. Fish and Wildlife Service, National Fisheries Research Center-Leetown, National Fish Health Research Laboratory, Box 700, Kearneysville, West Virginia. 25430.

UNITED STATES DEPARTMENT OF THE INTERIOR, Fish and Wildlife Service. 1990.

(Revision of Fish Disease Leaflet 19 (1970) and Fish Disease Leaflet 62 (1981), same title, by S. F. Snieszko.)

Introduction

Fish gills function as both respiratory and excretory organs. Basically they consist of a network of capillaries where blood is separated from the surrounding water by only one or two layers of cells. Proliferation of epithelial tissue, and later the loss of surface by the clubbing and fusing of lamellae, impair respiration and the excretion of nitrogenous waste materials, and disturb osmotic balance. Because these changes adversely affect the health of fish, the prevention and treatment of gill diseases are important in fish culture.

Pathologic changes in gill tissues have been divided into five categories: (1) bacterial gill disease (BGD) of salmonids and pondfishes, caused by filamentous bacteria that have yellow pigment in their cell walls; (2) nutritional gill disease, caused by a deficiency of pantothenic acid; (3) hemorrhagic gill disease, in which an apparent hemorrhagic condition is really a dilation of lamellar vessels (telangiectasia), caused by toxic agents or physical injury; (4) mycotic gill necrosis in pondfishes, caused by the fungus Branchiomyces (Meyer and Robinson 1973; Niesh and Hughes 1980); and (5) proliferative gill disease of unknown etiology in pondfishes and rainbow trout, Oncorhynchus mykiss (Daoust and Ferguson 1985). Bacterial gill disease, the most lethal of these categories, is discussed here.

Etiology

Outbreaks of BGD are triggered by stressors that result from intensive culture. Although crowding, low dissolved oxygen concentrations, and ammonia buildup may contribute to epizootics, the exact role of these and other stressors is not known. However, when proper stressors are present, gill tissues are colonized by filamentous yellowpigmented bacteria that damage gill tissue and cause death of the fish. Davis (1927) first observed the bacteria and gill damage in trout at a Vermont hatchery. Later, Rucker et al. (1949, 1952) and Bullock (1972) isolated several strains of yellowpigmented bacteria from infected gill tissue but none could be shown to be the causative agent. Wakabayashi (1980) isolated a different yellowpigmented bacterium and experimentally produced BGD with this organism. The bacterium, named Flavobacterium branchiophila by Wakabayashi et al. (1989), is probably the cause of most BGD outbreaks in salmonids.

Gill lesions in warmwater pond fish are produced by Cytophaga (formerly Flexibacter) columnaris, the causative agent of columnaris disease. Although columnaris disease is typically characterized by fins and body lesions, gill pathology involving this bacterium has been reported (Foscarini 1989; Farkas and Olah 1986).

Pathology

In disease caused by F. branchiophila, a proliferative hyperplasia develops in the epithelium of the gill lamellae. In a typical case, electron microscopic studies of affected gills show hypertrophy of lamellar epithelium in the early stages of the disease, which results in a transfiguration of flat epithelial cells into cuboidal or columnar cells and oval chloride cells. As the disease progresses, the epithelium proliferates, causing clubbing and fusing of gill lamellae. Also, staining of gill tissue with ruthenium red reveals bacterial cells adhering to the outermost epithelial layer (Kudo and Kimura 1983a) . The adhesion of F. branchiophila to gill tissue may be significant because Kudo and Kimura (1983b) demonstrated that an extract from F. branchiophila produced the pathological changes seen in a natural outbreak. Later, the same authors (Kudo and Kimura 1983c) found that, after treatment, 5 weeks were required for complete recovery of gill tissue.

Necrosis of gill tissue rather than hyperplasia occurs in BGD infections caused by C. columnaris. Farkas and Olah (1986) described three stages of C. columnaris infection of gills (termed gill necrosis) in common carp (Cyprinus carpio). The first stage is characterized by gills that are either pale or dark purple, caused by stressors such as ammonia, unfavorable temperatures, or toxins. No C. columnaris cells can be seen in stage I but are present in damaged gills in stage 2 and cause necrosis and mortality. In stage 3 (if fish survive), C. columnaris disappears but the necrotic area does not become functional. Funahashi (1980) reported different pathological changes in gill infections of the European eel (Anguilla anguilla) and Japanese eel (A. japonicus). In Japanese eels, there was hyperplasia of gill epithelium, and in advanced cases, filaments became necrotic and were sloughed off. In European eels, the clubbing of filaments was caused by hyperplasia of mucous cells but necrosis was not seen. Foscarini (1989) found that pathological changes in gill tissue of eels caused by C. columnaris infections resulted in alterations in cardiac performance. Bradycardia occurred when gills were hyperplastic, and a compensatory tachycardia developed as gill tissue became necrotized. He hypothesized that a combination of impaired gill circulation and cardiac performance results in the death of fish.

Diagnosis

Preliminary diagnosis of BGD in salmonids is based on the behavior of affected fish: they usually stop feeding,swim at the surface, and often orient themselves upstream (against the current) to ensure efficient water flow over gill surfaces. Because these behavior patterns usually do not occur in pondfishes with BGD, the disease cannot be diagnosed until mortalities begin. Definitive diagnosis is based on the examination of wet mounts of gill tissue for hyperplasia or necrosis and the presence of long, thin gramnegative bacteria. The causative agent is identified as F. branchiophila or C. columnaris by isolation and application of definitive biochemical tests. A fluorescent antibody test has been developed for F. branchiophila (Huh and Wakabayashi 1987).

Host and Geographic Range

Bacterial gill disease has been reported from a broad range of cultured coldwater and warmwater fishes. All cultured species are probably susceptible because disease outbreaks are closely associated with stress caused by intensive culture. Although the original description of BGD was made in North America, the condition occurs worldwide .

Source and Reservoir of Infection

The source of F. branchiophila is not known. The bacterium may be a normal inhabitant of the water or gills. Although C. columnaris can live in water and mud, fish probably serve as the main reservoir of infection.

Incubation and Communicability

The incubation period for either F. branchiophila or C. columnaris is variable because disease outbreaks depend on the presence of stressors. Bullock (1972) induced BGD in fingerling rainbow trout in 10 to 14 days when the fish were subjected to crowding, dissolved oxygen concentrations of 4 to 5 ppm, and ammonia concentrations of 1 ppm.

Control

Prevention

Prevention of BGD in hatchery salmonids is difficult because the fish are constantly stressed. Sanitation and application of the

proper cultural practices is helpful, but does not eliminate outbreaks. To help reduce such outbreaks, many fish culturists use prophylactic chemotherapy with chemicals (described later) once or twice a month.

Prevention of BGD is more difficult in pondfishes than in hatchery fishes, because C. columnaris usually occurs in the water source.

Treatment

Several chemicals have been used to treat BGD in hatchery salmonids. The most widely used are quaternary ammonium compounds, such as benzalkonium chlorides, available as Hyamine 1622 (98.8% active ingredient) and Hyamine 3500 (50% active ingredient). Another compound of this type is Roccal, available in 10% or 50% concentrations. Benzalkonium chlorides are used in concentrations of 1 to 2 ppm (calculated on the basis of the active ingredient) as a 1h bath or continuous flow treatment. Caution is necessary because the margin of safety is narrow, particularly in soft water.

Another chemical is the herbicide Diquat. It has been used at a concentration of 8.4 to 16.8 ppm of the formulated material, or 2 to 4 ppm on the basis of active ingredient (Diquat cation).

None of these chemicals are approved by the U. S . Food and Drug Administration for disease control in food fishes. Efforts are under way to have chloramineT registered as a treatment for BGD. This compound was found effective for BGD when used at 8.5 ppm for I h (From 1980). In hatchery tests conducted by the National Fish Health Research Laboratory, one treatment effectively controlled BGD when it was given early in an outbreak. However, two or more treatments are required for advanced outbreaks. (see note below. Ed)

When BGD, caused by C. columnaris, occurs in pondfish, external treatments for the control of columnaris disease are used. The treatment with 8.5 ppm Diquat described above has been reported to be effective. Diquat, copper sulfate at 0.5 ppm, and potassium permanganate at 2 to 4 ppm can be added to ponds and allowed to dissipate over time. If copper sulfate or potassium permanganate are used, treatment levels may have to be adjusted, depending on water chemistry. In soft water, 0.5 ppm copper sulfate may be toxic; and if pondwater is high in organic material, potassium permanganate concentrations must be increased (Rogers 1971; Jee and Plumb 1981).

Bibliography

Bergey's Manual of Systemic Bacteriology. 1989. J. T. Staley, M. R. Bryant, N. Pfennig, and J. G. Holt, eds. Vol 3. William & Wilkins, Baltimore, Md. 2298 pp.

Bohn, M. 1974. Bacterial gill diseases in pond fish. Muench. Beitr. Abwasserfisch. Flussbiol. 25:89104.

Bootsma, R. 1974. Bacterial gill disease of carp (Cyprinus carpioL.). Tijdschr. Diergeneeskd. 99:143144.

Bullock, G. L. 1972. Studies on selected myxobacteria pathogenic for fishes and on bacterial gill disease in hatcheryreared salmonids. U.S. Fish Wildl. Serv., Tech. Pap. 60. 30 pp.

Daoust, P. Y., and H. W. Ferguson. 1985. Nodular gill disease: a unique form of proliferative gill disease in rainbow trout Salmo gairdneri Richardson. J. Fish Dis. 8:511522.

Davis, H. S. 1926. A new gill disease of trout. Trans. Am. Fish. Soc. 56:156160.

Davis, H. S. 1927. Further observations on the gill disease of trout. Trans. Am. Fish. Soc. 57:210212.

Farkas, J. 1985. Filamentous Flavobacterium sp. isolated from fish with gill diseases in cold water. Aquaculture 44:110.

Farkas, J., and J. Olah. 1986. Gill necrosis-a complex disease of carp. Aquaculture 58:1726.

Foscarini, R. 1989. Induction and development of bacterial gill disease in the eel Anguilla japonica experimentally infected with Flexibacter columnaris: pathological changes in the gill vascular structure and in cardiac performance. Aquaculture 78: 120.

From, J. 1980. ChloramineT for control of bacterial gill disease. Prog. FishCult. 42:8586.

Funahashi, N. 1980. Histopathological studies on gill-I. A bacterial gill disease of cultured eel. Fish Pathol. 14: 107115.

Herman, R. L. 1985. Striped bass fingerling mortality involves multiple factors. Fish Health News 14(3):iii-v.

Hoskins, G. 1976. Fusobacteria associated with bacterial gill disease of salmon. Prog. FishCult. 38:150151.

Huh, G. J., and H. Wakabayashi. 1987. Detection of Flavobacterium sp., a pathogen of bacterial gill disease, using the indirect fluorescent antibody technique. Fish Pathol. 22:215220.

Jee, L. K., and J. A. Plumb. 1981. Effects or organic load on potassium permanganate as a treatment for Flexibacter columnaris. Trans. Am. Fish. Soc. 110:8689.

Kimura, N., H. Wakabayashi, and S. Kudo. 1978. Studies on bacterial gill disease in salmonids-I. Selection of bacterium transmitting gill disease. Fish Pathol. 12:233242.

Kudo, S., and N. Kimura. 1983a. Transmission electron microscopic studies on bacterial gill disease in rainbow trout fingerlings Salmo gairdneri. Ultrastructural studies on bacterial gill disease in rainbow trout fingerlings-I. Jpn. J. Ichthyol. 30:247260.

Kudo, S., and N. Kimura. 1983b. Extraction of a hyperplasia-inducing factor. Bull. Jpn. Soc. Sci. Fish. 49:17771782.

Kudo, S., and N. Kimura. 1983c. Ultrastructural studies on bacterial gill disease in rainbow trout Salmo gairdneri fingerlings. 4. The recovery from hyperplasia in an artificial infection. Bull. Jpn. Soc. Sci. Fish. 49:16351642.

Kudo, S., and N. Kimura. 1984. Scanning electron microscopic studies on bacterial gill disease in rainbow trout Salmo gairdneri fingerlings. Jpn. J. Ichthyol. 30:393403.

Larmoyeux, J. D., and R. G. Piper. 1973. Effects of water reuse on rainbow trout in hatcheries. Prog. FishCult. 35:28.

Meyer, F. P., and J. Robinson. 1973. Branchiomycosis: a new fungal disease of North American fishes. Prog. FishCult. 35:7477.

Miyazaki, T., and Y. Jo. 1986. A histopathological study on bacterial gill disease. Fish Pathol. 21:207208.

Neish, G. A., and G. C. Hughes. 1980. Fungal diseases of fishes. Book 6 (159 pp) in S. F. Snieszko and H. R. Axelrod eds. Diseases of fishes. T F. H. Publication, Inc., Neptune, N.J.

Ostland, V. E., H. W. Ferguson, and R. M. W. Stevenson. 1989. Case report: bacterial gill disease in goldfish Carassius auratus. Dis. Aquat. Org. 6:179184.

Rogers, W. A. 1971. Principal diseases of catfish: how to identify and fight them. Fish Farming Ind. 2:2026.

Rucker, R. R., H. E. Johnson, and E. J. Ordal. 1949. An investigation of the bactericidal action and fish toxicity of two homologous series of quarternary ammonium compounds. J. Bacteriol. 57:225234.

Rucker, R. R., H. E. Johnson, and G. M. Kaydas. 1952. An interim report on gill disease. Prog. FishCult. 14:1014.

Wakabayashi, H. 1980. Bacterial gill disease of salmonid fish. Fish Pathol. 14:185189.

Wakabayashi, H., S. Egusa, and J. L. Fryer. 1980. Characteristics of filamentous bacteria isolated from a gill disease of salmonids. Can. J. Fish. Aquat. Sci. 37:14991504.

Wakabayashi, H., G. H. Huh, and N. Kimura. 1989. Flavobacterium branchiophila sp. nov., a causative agent of bacterial gill disease of freshwater fishes. Int. J. Syst. Bacteriol. 39:213216.

Wakabayashi, H., and T. Iwado. 1983. Effects of a bacterial gill disease on the respiratory functions of juvenile rainbow trout. Pages 153160 in A. E. Ellis, ed. Fish and shellfish pathology. Academic Press, Orlando, Fla.

Wakabayashi, H., and T. Iwado. 1985. Changes in glycogen, pyruvate, and lactate in rainbow trout with bacterial gill disease. Fish Pathol. 20:161165.

Chloramine-T treatments should take pH and hardness into consideration. Please see the article by Jill V. Spangenberg, DVM, PhD (Pharmacology and Toxicology), e-mail: jvspangenberg@ucdavis.edu Investigation of the Safety and Efficacy of Chloramine-T in the Treatment of External Fluke Infestations on the KoiVet website www.koivet.com. The article may deal primarily with fluke treatment, but the relative safety of the drug is also established and (according to the manufacturer) if you kill the fluke, you would have killed most bacteria as well.

KOI PRODUCERS MEETING?  

A suggestion came in that perhaps the time was right for a gathering of Koi Producers and Traders to discuss the problems facing our industry. It was suggested that the Aquarama 2003 Conference is used as venue for such a meeting. Are there any support or ideas for such a happening?

So. keep those Koi healthy.

Totsiens 

Servaas de Kock   

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OUR MISSION: This free Newsletter is intended to share information of interest to the Breeders, Exporters, Importers and Dealers of Koi internationally. It is not intended for the average hobbyist. Your feedback or criticism of whatever kind will be valued. If you want to update me on whatever is happening in your part of the world, I will be delighted. The idea is to serve the Koi industry and keep commercial content out. If I make mistakes, well, correct me if you can substantiate your claim. Please forward this to anyone you think might be interested in our subject matter.

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