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**Fish Disease Leaflet 84****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 Leaflet62 (1981), same title, by S. F. Snieszko.)*
- **Introduction**  **Etiology****Pathology**
- **Diagnosis**  **Host and Geographic Range****Source and Reservoir of Infection**
- **Incubation and Communicability**  **Control**- *Prevention*  ***Treatment*****Bibliography**
**Introduction**
Fish gills function as both respiratory and excretory organs.Basically they consist of a network of capillaries where bloodis separated from the surrounding water by only one or two layersof cells. Proliferation of epithelial tissue, and later the lossof surface by the clubbing and fusing of lamellae, impair respirationand the excretion of nitrogenous waste materials, and disturbosmotic balance. Because these changes adversely affect the healthof fish, the prevention and treatment of gill diseases are importantin fish culture.
Pathologic changes in gill tissues have been divided into fivecategories: (1) bacterial gill disease (BGD) of salmonids andpondfishes, caused by filamentous bacteria that have yellow pigmentin their cell walls; (2) nutritional gill disease, caused by adeficiency of pantothenic acid; (3) hemorrhagic gill disease,in which an apparent hemorrhagic condition is really a dilationof lamellar vessels (telangiectasia), caused by toxic agents orphysical injury; (4) mycotic gill necrosis in pondfishes, causedby the fungus *Branchiomyces* (Meyer and Robinson 1973; Nieshand Hughes 1980); and (5) proliferative gill disease of unknownetiology in pondfishes and rainbow trout, *Oncorhynchus mykiss*(Daoust and Ferguson 1985). Bacterial gill disease, the most lethalof these categories, is discussed here.**Etiology**
Outbreaks of BGD are triggered by stressors that result from intensiveculture. Although crowding, low dissolved oxygen concentrations,and ammonia buildup may contribute to epizootics, the exact roleof these and other stressors is not known. However, when properstressors are present, gill tissues are colonized by filamentousyellowpigmented bacteria that damage gill tissue and cause deathof the fish. Davis (1927) first observed the bacteria and gilldamage in trout at a Vermont hatchery. Later, Rucker et al. (1949,1952) and Bullock (1972) isolated several strains of yellowpigmentedbacteria from infected gill tissue but none could be shown tobe the causative agent. Wakabayashi (1980) isolated a differentyellowpigmented bacterium and experimentally produced BGD withthis organism. The bacterium, named *Flavobacterium branchiophila*by Wakabayashi et al. (1989), is probably the cause of most BGDoutbreaks in salmonids.
Gill lesions in warmwater pond fish are produced by *Cytophaga*(formerly *Flexibacter*) *columnaris*, the causativeagent of columnaris disease. Although columnaris disease is typicallycharacterized by fins and body lesions, gill pathology involvingthis bacterium has been reported (Foscarini 1989; Farkas and Olah1986).**Pathology**
In disease caused by *F*. *branchiophila*, a proliferativehyperplasia develops in the epithelium of the gill lamellae. Ina typical case, electron microscopic studies of affected gillsshow hypertrophy of lamellar epithelium in the early stages ofthe disease, which results in a transfiguration of flat epithelialcells into cuboidal or columnar cells and oval chloride cells.As the disease progresses, the epithelium proliferates, causingclubbing and fusing of gill lamellae. Also, staining of gill tissuewith ruthenium red reveals bacterial cells adhering to the outermostepithelial layer (Kudo and Kimura 1983a) . The adhesion of *F*.*branchiophila* to gill tissue may be significant becauseKudo and Kimura (1983b) demonstrated that an extract from *F*.*branchiophila* produced the pathological changes seen ina natural outbreak. Later, the same authors (Kudo and Kimura 1983c)found that, after treatment, 5 weeks were required for completerecovery of gill tissue.
Necrosis of gill tissue rather than hyperplasia occurs in BGDinfections caused by *C*. *columnaris*. Farkas and Olah(1986) described three stages of *C*. *columnaris* infectionof gills (termed gill necrosis) in common carp (*Cyprinus**carpio*). The first stage is characterized by gills thatare 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 gillsin stage 2 and cause necrosis and mortality. In stage 3 (if fishsurvive), *C*. *columnaris* disappears but the necroticarea does not become functional. Funahashi (1980) reported differentpathological changes in gill infections of the European eel (*Anguillaanguilla*) and Japanese eel (*A*. *japonicus*). InJapanese eels, there was hyperplasia of gill epithelium, and inadvanced cases, filaments became necrotic and were sloughed off.In European eels, the clubbing of filaments was caused by hyperplasiaof mucous cells but necrosis was not seen. Foscarini (1989) foundthat pathological changes in gill tissue of eels caused by *C*.*columnaris* infections resulted in alterations in cardiacperformance. Bradycardia occurred when gills were hyperplastic,and a compensatory tachycardia developed as gill tissue becamenecrotized. He hypothesized that a combination of impaired gillcirculation and cardiac performance results in the death of fish.**Diagnosis**
Preliminary diagnosis of BGD in salmonids is based on the behaviorof affected fish: they usually stop feeding,swim at the surface,and often orient themselves upstream (against the current) toensure efficient water flow over gill surfaces. Because thesebehavior patterns usually do not occur in pondfishes with BGD,the disease cannot be diagnosed until mortalities begin. Definitivediagnosis is based on the examination of wet mounts of gill tissuefor hyperplasia or necrosis and the presence of long, thin gramnegativebacteria. The causative agent is identified as *F*. *branchiophila*or *C*. *columnaris* by isolation and application ofdefinitive biochemical tests. A fluorescent antibody test hasbeen developed for *F*. *branchiophila* (Huh and Wakabayashi1987).**Host and Geographic Range**
Bacterial gill disease has been reported from a broad range ofcultured coldwater and warmwater fishes. All cultured speciesare probably susceptible because disease outbreaks are closelyassociated with stress caused by intensive culture. Although theoriginal description of BGD was made in North America, the conditionoccurs worldwide .**Source and Reservoir of Infection**
The source of *F*. *branchiophila* is not known. Thebacterium may be a normal inhabitant of the water or gills. Although*C*. *columnaris* can live in water and mud, fish probablyserve as the main reservoir of infection.**Incubation and Communicability**
The incubation period for either *F*. *branchiophila*or *C*. *columnaris* is variable because disease outbreaksdepend on the presence of stressors. Bullock (1972) induced BGDin fingerling rainbow trout in 10 to 14 days when the fish weresubjected to crowding, dissolved oxygen concentrations of 4 to5 ppm, and ammonia concentrations of 1 ppm.**Control*****Prevention***
Prevention of BGD in hatchery salmonids is difficult because thefish 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 prophylacticchemotherapy with chemicals (described later) once or twice amonth.
Prevention of BGD is more difficult in pondfishes than in hatcheryfishes, because *C*. *columnaris* usually occurs inthe water source.***Treatment***
Several chemicals have been used to treat BGD in hatchery salmonids.The most widely used are quaternary ammonium compounds, such asbenzalkonium chlorides, available as Hyamine 1622 (98.8% activeingredient) and Hyamine 3500 (50% active ingredient). Anothercompound 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 bathor continuous flow treatment. Caution is necessary because themargin of safety is narrow, particularly in soft water.
Another chemical is the herbicide Diquat. It has been used ata 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 DrugAdministration for disease control in food fishes. Efforts areunder way to have chloramineT registered as a treatment for BGD.This compound was found effective for BGD when used at 8.5 ppmfor I h (From 1980). In hatchery tests conducted by the NationalFish Health Research Laboratory, one treatment effectively controlledBGD when it was given early in an outbreak. However, two or moretreatments are required for advanced outbreaks.
When BGD, caused by *C*. *columnaris,* occurs in pondfish,external treatments for the control of columnaris disease areused. The treatment with 8.5 ppm Diquat described above has beenreported to be effective. Diquat, copper sulfate at 0.5 ppm, andpotassium permanganate at 2 to 4 ppm can be added to ponds andallowed to dissipate over time. If copper sulfate or potassiumpermanganate are used, treatment levels may have to be adjusted,depending on water chemistry. In soft water, 0.5 ppm copper sulfatemay be toxic; and if pondwater is high in organic material, potassiumpermanganate concentrations must be increased (Rogers 1971; Jeeand Plumb 1981).**Bibliography**
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Bohn, M. 1974. Bacterial gill diseases in pond fish. Muench. Beitr.Abwasserfisch. Flussbiol. 25:89104.
Bootsma, R. 1974. Bacterial gill disease of carp (*Cyprinuscarpio*
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Bullock, G. L. 1972. Studies on selected myxobacteria pathogenicfor 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 *Salmogairdneri* 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 oftrout. Trans. Am. Fish. Soc. 57:210212.
Farkas, J. 1985. Filamentous *Flavobacterium* sp. isolatedfrom fish with gill diseases in cold water. Aquaculture 44:110.
Farkas, J., and J. Olah. 1986. Gill necrosis-a complex diseaseof carp. Aquaculture 58:1726.
Foscarini, R. 1989. Induction and development of bacterial gilldisease in the eel *Anguilla japonica* experimentally infectedwith *Flexibacter columnaris*: pathological changes in thegill vascular structure and in cardiac performance. Aquaculture78: 120.
From, J. 1980. ChloramineT for control of bacterial gill disease.Prog. FishCult. 42:8586.
Funahashi, N. 1980. Histopathological studies on gill-I. A bacterialgill disease of cultured eel. Fish Pathol. 14: 107115.
Herman, R. L. 1985. Striped bass fingerling mortality involvesmultiple factors. Fish Health News 14(3):iii-v.
Hoskins, G. 1976. Fusobacteria associated with bacterial gilldisease 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 indirectfluorescent antibody technique. Fish Pathol. 22:215220.
Jee, L. K., and J. A. Plumb. 1981. Effects or organic load onpotassium permanganate as a treatment for *Flexibacter columnaris*.Trans. Am. Fish. Soc. 110:8689.
Kimura, N., H. Wakabayashi, and S. Kudo. 1978. Studies on bacterialgill disease in salmonids-I. Selection of bacterium transmittinggill disease. Fish Pathol. 12:233242.
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Kudo, S., and N. Kimura. 1983b. Extraction of a hyperplasia-inducingfactor. Bull. Jpn. Soc. Sci. Fish. 49:17771782.
Kudo, S., and N. Kimura. 1983c. Ultrastructural studies on bacterialgill 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 studieson 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 reuseon rainbow trout in hatcheries. Prog. FishCult. 35:28.
Meyer, F. P., and J. Robinson. 1973. Branchiomycosis: a new fungaldisease of North American fishes. Prog. FishCult. 35:7477.
Miyazaki, T., and Y. Jo. 1986. A histopathological study on bacterialgill 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 identifyand fight them. Fish Farming Ind. 2:2026.
Rucker, R. R., H. E. Johnson, and E. J. Ordal. 1949. An investigationof the bactericidal action and fish toxicity of two homologousseries of quarternary ammonium compounds. J. Bacteriol. 57:225234.
Rucker, R. R., H. E. Johnson, and G. M. Kaydas. 1952. An interimreport 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. Characteristicsof 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. *Flavobacteriumbranchiophila* sp. nov., a causative agent of bacterial gilldisease of freshwater fishes. Int. J. Syst. Bacteriol. 39:213216.
Wakabayashi, H., and T. Iwado. 1983. Effects of a bacterial gilldisease 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. FishPathol. 20:161165. *U.S. Department of the Interior**|| U.S. Geological Survey  11649 Leetown Road, Kearneysville, WV  25430, USA  URL: http://www.lsc.usgs.gov  Maintainer: lsc_webmaster@usgs.gov  Last Modified: February 26, 2004 dwnPrivacy Policy and Disclaimers || FOIA || Accessibility*