1

Furunculosis And Other Diseases 

Caused By Aeromonas salmonicida

Rocco C. Cipriano

U.S. Geological Survey/Leetown Science Center

National Fish Health Research Laboratory,

1700 Leetown Road, Kearneysville, West Virginia 25430

and

Graham L. Bullock

The Freshwater Institute, Post Office Box 1889, 

Shepherdstown, West Virginia 25443

Fish Disease Leaflet 66

2001

Revison of “Furunculosis and other diseases caused by Aeromonas salmonicida,” by G. L. 

Bullock, R. C. Cipriano, and S. F. Snieszko, 1983.
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HOST AND GEOGRAPHIC RANGE

After Emmerich and Weibel (1890) first described Aeromonas salmonicida (syn. Bacillus 

salmonicida, Bacterium salmonicida, Bacterium trutta) among trout in German hatcheries, it 

was initially believed that A. salmonicida was a pathogen exclusive for instensively cultured

salmonid fishes. Current knowledge, however, indicates that relatively few cultured or feral fish

in freshwater, brackish or even marine environments are immune to the deleterious effects of this 

pathogen. Let it suffice to say that all species of salmon, trout, charr and grayling are

susceptible to infection. Furthermore, the number of non-salmonid hosts that have become

infected with this bacterium has steadily multipled commensurate with the increased conduct of

epidemiological investigations. Present indications suggest that there are at least four subspecies

of A. salmonicida; - salmonicida, achromogenes, masoucida and smithia (Holt et al. 1994). 

Strains of A. salmonicida subsp. salmonicida induce typical furunculosis and cause severe

septicemia with resultant mortality especially within coldwater fishes. The other subspecies

produce atypical forms of disease that are often characterized by dermal ulcerations and external

pathology with or without subsequent septicemia. The number, diversity and distribution of fish

species that are susceptible to A. salmonicida enhances this bacterium’s distribution worldwide. 

However, both typical and atypical subspecies may not be common to all geographic areas. For 

example, A. salmonicda was not reported within New Zealand or Australia until 1974, when

atypical variants of A. salmonicida were introduced into Australia by an importation of diseased 

ornamental goldfish (Trust et al. 1980; Humphrey and Ashburner 1993). Since that

introduction, atypical isolates of A. salmoncida have become endemic even among feral

populations of goldfish (Whittington et al. 1987), but A. salmonicida subsp. salmonicida has not 

yet been reported within Australian fishes. Similarly, only A. salmonicida subsp. salmonicida

has reported from salmonids in Nova Scotia, Canada (Hammel 1995). It may be argued,

however, that such distinctions are somewhat controversial because atypical isolates of A. 

salmonicida obtained from goldfish can be virulent in Atlantic salmon (Salmo salar) and induce 

pathology indicative of classical furunculosis (Carson et al. 1988). 

PATHOLOGICAL CONDITIONS
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Salmonid Furunculosis

Aeromonas salmonicida subsp. salmonicida causes severe septicemia and acute mortality in

susceptible salmonid hosts. The mode of infection, nature of pathology, and the degree of

mortality, however, is interrelated with the quality of environmental parameters and furthermore

affected by the age and innate resistance of the host. Peracute infections most often occur in

fingerling fish, which may darken in color and die without showing marked clinical indications

of disease. Only a slight exophthalmia may be evident. Acute infections often occur in juvenile 

and adult fish that darken in color and hemorrhage at the base of fins and oral cavity. Internal

hemorrhages may be evident in the abdominal walls, viscera, and heart of affected fish. The

spleen is enlarged, and the liver can have subcapsular hemorrhages, or focal necrosis of

parenchymatous tissue. Affected fish may display erratic swimming behavior, become sluggish,

and stop feeding. Consequently, the stomach and intestine are usually devoid of food, and the 

lumen may contain sloughed epithelial cells, mucus, and blood. The reproductive organs are

commonly hemorrhaged and the intestine is often severely congested (Scott 1968). The chronic 

form of furunculosis usually occurs in older fish that have become more refractive to the disease 

or among species that have greater innate resistance to infection by A. salmonicida. One or more 

furuncle-like lesions may be present on the dermis and ulcers may extend deep into the

musculature. Internally, chronically infected salmonids show a general visceral congestion and

peritonitis. Hemorrhages may occur over the pyloric area and liver, and kidneys are soft or

friable (McCarthy and Roberts 1980).

Figure 1: Brook trout (Salvelinus fontinalis) 

showing a furuncle like lesion near its dorsal fin

caused by infection with Aeromonas salmonicida

subsp. salmonicida. Photograph by R. Cipriano.

The development of the characteristic “furunclelike” lesion is not a consistent finding, but is most 

often associated with chronic infections. When

these lesions are present, they consist of tissue fluid exudate, necrotic tissue, and some

macrophages. Thus, the furunculosis lesion differs from the true furuncle associated with

homeothermic vertebrates, which is characterized by a necrotic mass of polymorphonuclear

leukocytes. Degeneration of myofibrils, fragmentation of muscle fibers, and hemorrhage of the

entire muscular tissue is evident within the swelling

lesion and leads to a colliquative necrosis of the

musculature in the most serious lesions (Sakai

1978). Bacteria may also colonize the gill

epithelium on or between the secondary lamellae

(Bruno 1986) where they may be enclosed within a 

membrane that is continuous with the basement

membrane of the lamellar epithelium (McArdle et

al. 1986). Bacterial embolisms may develop in gill 

lamellae causing a further proliferation of branchial

epithelial cells and a subsequent fusion of gill

lamellae that impairs circulation (Miyazaki and

Kubota 1975a).
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Figure 2: Ulceration deep into the musculature of a brook trout (Salvelinus fontinalis) caused by 

Aeromonas salmonicida subsp. salmonicida. Photograph by R. Cipriano.

Trout Ulcer Disease

Fish (1934) described an Ulcer Disease in Trout among salmonids from a hatchery in Cortland

(New York), which he believed was similar to but distinct from the clinical picture observed in

typical salmonid furunculosis. He also noted that similar pathology was previously reported

among trout at two other New York hatcheries on Long Island (Calkins 1889) and Cold Spring 

Harbor (Marsh 1905). In each of these cases, disease manifested itself as an external bacterial

infection without involvement of the blood, liver, spleen, and kidneys, but the posterior intestine

was often congested. Lesions were infrequently observed in the kidneys or livers of affected fish 

and, if present, they were consistently sterile by culture on nutrient agar. Snieszko (1952) did

imply that an internal pathology similar to that described for typical salmonid furunculosis might

develop in the most acute cases. Because specific pathogen free fish were not readily available 

for his experimental purposes, it is difficult to determine if the internal pathology alluded to by

Snieszko was actually a clinical indication of ulcer disease or the expression of an underlying A. 

salmonicida subsp. salmonicida infection. 

The external clinical pathology that was observed in cases of Ulcer Disease, however, was quite 

dissimilar to typical salmonid furunculosis. Patches of the epidermis initially thickened and then

enlarged to form white epidermal tufts from 0.5 to 1.0 mm in diameter. The development of

these tufts progressed until the underlying dermis was eroded and a finely delineated dark red or 

gray ulcer became apparent. Bacteria multiplied within the necrotic debris of the exposed

subepithelial connective tissue but did not necrotize or penetrate deeply into the musculature. 

The lesions, therefore, remained shallow and developed from the outside in. By contrast, the

furuncles of typical salmonid furunculosis developed from the inside out and were evident deep 

into the musculature. Other ulcers were also present on the fins, jaw, or in the oral cavity where 

the soft tissue covering the roof of the mouth was eroded (Wolf 1938). 

Figure 3: Shallow ulceration on the dermis of 

a brook trout (Salvelinus fontinalis) that is

characteristic of the lesions observed in Trout

Ulcer Disease caused by Aeromonas 

salmonicida subps. achromogenes. The

etiology of this condition was formerly

ascribed to Hemophilus piscium. Photograph

courtesy of S. F. Snieszko personal collection.

Snieszko and Friddle (1948) originally isolated and Snieszko et al. (1950) then described

Hemophilus piscium as the etiologic agent of Ulcer Disease in Trout. Paterson et al. (1980a) later 

suggested that this bacterium was actually an atypical, achromogenic strain of A. salmonicida by 

showing that DNA:DNA hybridization results for H. piscium were similar to those of A. 

salmonicida, but beyond acceptable limits for the genus Hemophilus. These workers further
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showed that strains of H. piscium were (1) sensitive to A. slmonicida bacteriophage; (2)

serologically identical to A. salmonicida; and (3) phenotypically analogous to achromogenic

strains of A. salmonicida. Unfotunately, the original isolates described by Snieszko and Friddle 

(1948) and Snieszko et al. (1950) were not available for comparison. Thornton et al. (1999) also 

showed the SSU rRNA gene sequence identity between H. piscium and A. salmonicida subp. 

salmonicida is 99.6%. This information strongly argues that the pathology observed in Trout

Ulcer Disease is caused by atypical, achromogenic strain of A. salmonicida.

Goldfish Ulcer Disease

Goldfish ulcer disease was first described by Mawdesley-Thomas (1969), who termed the

condition furunculosis of goldfish because A. salmonicida was isolated from skin lesions.

However, the organism in those studies was actually a typical biotype of the bacterium, A. 

salmonicida subsp. salmonicida and, therefore, the clinical pathology described by MawdsleyThomas is quite different than that which is observed in the majority of reports concerning

Goldfish Ulcer Disease. True Goldfish Ulcer Disease, however, was actually introduced into

goldfish farms in the United States during the 1970’s. Although other investigators attributed the 

etiology of this disease to a fungus (oomycete), a yellow pibmented bacterium (Flavobacterium 

columnarae), or a protozoan (Epistylis longicorpia), Elliott and Shotts (1980a, b) established the 

causal agent to be another atypical, achromogenic variant of A. salmonicida. 

Figure 4: A dermal ulceration on a goldfish (Carrasius 

auratus) indicative of Goldfish Ulcer Disease caused by an

atypical variant of Aeromonas. salmonicida. Photograph by

R. Cipriano.

The role of ectoparasites in creating a portal of entry for A. salmonicida remains unclear, but A. 

salmoncida preferentially adhered to mucus and dead or damaged cells in the dermis. Early

infections appeared as white proliferations on the epithelium of fishes. These areas developed

peripheral hemorrhages beneath the scales and. as the lesion develops, scales in the affected area 

were sloughed, the dermis became necrotic, and there was significant degeneration of the

musculature. There was also a marked leukocyte infiltration at the site of trauma within 24 – 48 

h. Unlike typical salmonid furunculosis, the infiltration persisted throughout a 21-day 

observation period and consisted of acidophilic, heterophylic, and basophilic granulocytes,

lymphocytes, and macrophages. There was no evidence, however, that A. salmonicida was

phagocytized by the leukocytes. Septecemia caused by A. salmonicida was most likely to be 

found if fish had well-developed dermal lesions. The causative bacterium was most readily

isolated just below the dermis at the peripheral margin of the lesion. 
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Carp Erythrodermatitis 

Carp erythrodermatitis is a subacute to chronic skin disease that occurs at temperatures from 4 to 

30°C (Pol et al. 1980). This disease was historically associated with Carp Dropsy Syndrome 

until Fijan (1972) showed that Carp Dropsy actually involved two infections: Spring Viremia of

Carp caused by Rhabdovirus carpio and Carp Erythrodermatitis. Consequently, the etiologic

agent of Carp Erythrodermatitis was isolated and described as an atypical, achromogenic variant 

of A. salmonicida (Bootsma et al. 1977; Bootsma and Blommaert 1978). Although A. 

salmonicida is now recognized to cause Carp Erythrodermatitis, it is important to note that other 

species of bacteria may also induce external lesions in carp that are macroscopically similar to

those that are caused by A. salminicida (Schultz 1980).

Figure 5: A dermal ulceration in the mirror carp

(Cyprinus carpio) indicative of the pathology

observed in Carp Erythrodermatitis, as caused by an 

atypical Aeromonas salmonicida. Photograph from

NFHRL collection courtesy of R. Bootsma.

Clinical indicatications of Carp Ertythrodermatitis become evident as small inflamed

hemorrhagic areas on the skin that develop into white erosions surrounded by a narrow red zone 

and darkened pigmentation. Extensive hemorrhage in the dermis is followed by a necrosis of

the epidermis with strong infiltration by polymorphonuclear leukocytes. Edema in the dermis

displaces “knots” in the epidermis while hemorrhage occurs around the veins inducing a

persistent inflammatory infiltration that extends into the stratum compactum, subdermis and

underlying musculature. Irregular, hemorrhagic, ulcers proliferate in the central necrotic areas

(Gayer et al. 1980). 

Common carp with extensive lesions may also exhibit exophthalmia, hemorrhage in the gills,

abdominal distention and anemia. In more advanced cases, a transudate may be present within

the abdominal cavity, and the internal organs may become edematous (Fijan 1972). The

causative bacterium is present exclusively in lesions between the dermis and epidermis (Bootsma 

et al. 1977), but is not cultured from the kidneys of infected carp. 

TAXONOMY AND CLASSIFICATION

In the ninth edition of “Bergey’s Manual of Determinative Bacteriology,” Holt et al. (1994)

recognize four subspecies of A. salmonicida; - namely, salmonicida, masoucida, achromogenes 

and smithia (Table 1). Although phenotypic (Griffin 1954; Popoff 1969; Dalsgaard et al. 1994; 
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Hanninen et al. 1995) and genotypic (Belland and Trust 1988; Umelo and Trust 1998; Boyd et 

al. 1994; Nielsen et al. 1994; Garcia et al. 2000; O’Hici et al. 2000) characterizations have 

consistently indicated that strains of A. salmonicida subsp. salmoncida form a homogeneous

clonal group, more variation exists among “atypical” isolates (Powell et al. 1998; Hoie et al.

1999; Yamada et al. 2000). In fact, molecular and genotypic analyses have not necessarily

correlated with phenotypic subspeciation (Austin et al. 1998) and the degree of heterogeneity is 

sufficiently greater among atypical isolates than that which is apparent within the three 

subspecies masoucida, achromogenes and smithia (O’Hici et al. 2000). In fact, Austin et al. 

(1989) have shown that numerical taxonomy and DNA: DNA hybridization techniques divided

A. salmonicida into five phena. In their studies, subspecies masoucida, salmonicida, 

achromogenes, and smithia grouped within phena 10, 11, 12, and 14, respectively. Phenon 13 

contained an additional group of atypical isolates that did not group within any of the recognized 

subspecies. Isolates from this phenon have been obtained from both salmonid and non-salmonid 

sources, can induce ulcers and septicemia in rainbow trout and goldfish, and produce brown

pigment. Unlike all previously reported isolates of A. salmonicida, most (87%) of the isolates in 

phenon 13 grow at 37oC (Austin 1993). 

Pavan et al. (2000) have also proposed a new subspecies, “pectinolytica,” based upon phenotypic 

and DNA: DNA hybridization studies of isolates obtained from polluted waters of the Mantanza 

River, near Buenos Aires, Brazil. Their isolates were unusually dissimilar to hitherto reported

isolates of A. salmonicida in their ability to ferment sorbitol and degrade polypectate. Analysis 

of 16S rDNA sequences indicated that these isolates constituted a tightly knit genomic group that 

was most closely related to A. salmonicida subspp. salmonicida, masoucida and achromogenes. 
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Table 1: Phenotypic Differentiation Of Different Subspecies Of Aeromonas salmonicida 

described in “Bergey’s Manual od Determinative Bacteriology”, 9th ed. (Holt et al 1994)

Aeromonas salmonicida subp.

Characteristic salmonicida achromogenes masoucida smithia

Indole production - + + -

Methyl Red + + + -

Vogues Prokauer - - + -

H2S production - - + +

Lysine decarboxylase d d d -

Arginine dihydrolase + + + [-]

D-Glucose acid + + + [+]

D-Glucose gas + - + [+]

L-Arabinose acid + - +

D-Galactose acid + + + -

Glycerol acid d d d [-]

Maltose acid + + + -

D-Mannitol acid + - + -

Sucrose acid - + + d

Trehalose acid + + + -

Esculine hydrolysis + - + -

Lipase (corn oil) + + + -

ONPG d d d +

Brown pigment + - - -

+ = 90% or more strains are positive; - = 90% or more strains are negative; [-] = 0-10% are 

positive; d = 11-75% of strains are positive; [+] = 76-89% of strains are positive.
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DETECTION AND DIAGNOSIS

Presumptive diagnoses of typical and atypical variants of A. salmonicida from clinically diseased 

or moribund fish are based on clinical indications of disease, the type and number of species

infected, and the clinical history of disease within the affected population or facility.

Presumptive diagnosis of atypical A. salmonicida infections in salmonids or nonsalmonids is

more difficult than the diagnosis of typical furunculosis because clinical signs vary and dermal

lesions are often contaminated with opportunistic fungi and bacteria. Definitive diagnosis of all

A. salmonicida infections requires isolation and identification of the causative bacterium. 

Pigmented typical A. salmonicida strains can be readily isolated from kidney tissues of dead or 

moribund fishes using commercial media such as trypticase soya agar or brain-heart infusion

agar. Differentiation of colonial types that grow upon primary isolation can be facilitated by the 

simple addition of 0.1% (weight: volume) Coomassie Brilliant Blue (CBB) R-250 into either of

the aforementioned media. When cultured on CBB agar, the A-layer protein that is present in

virulent strains of A. salmonicida will absorb the Coomassie Brilliant Blue protein-specific dye. 

Consequently, virulent A. salmonicida develop dark blue to deep violet, friable colonies on CBB 

agar (Cipriano and Bertolini 1988; Cipriano and Blanch 1989). Although CBB agar facilitates 

presumptive identification, it is not a selective medium and a definitive diagnosis should be

confirmed via additional biochemical tests (Teska and Cipriano 1993). 

Figure 6: Growth on Coomassie Brilliant Blue (CBB) agar

differentiates between A-layer positive colonies (blue) and A-layer 

negative colonies (white) of Aeromonas salmonicida. Most isolates 

from fish contain the A-layer and the characteristic blue growth of

such colonies on CBB agar also facilitates presumptive diagnosis.

Photograph by R. Cipriano.

Atypical pigmented or nonpigmented strains of A. salmonicida are fastidious on initial isolation

from lesion material and the presence of biotic contaminants may interfere with an accurate

diagnosis. McCarthy (1977a) suggested, therefore, that isolation should be attempted from early 

and advanced lesions using a minimum of six fish from each epizootic. Elliott and Shotts

(1980a) found that primary isolation of atypical isolates causing Goldfish Ulcer Disease was

facilitated on blood agar. Additionally, Bootsma et al. (1977) suggested that diagnosis of Carp

Erythrodermatitis should be enacted first by experimentally infecting healthy common carp by

contact with diseased carp; and second, by inoculation of lesion material from experimentally

infected carp onto a medium consisting of tryptose blood agar base (DIFCO), 10% blood serum, 

and filter decontaminated ampicillin and polymyxin B sulfate to final concentrations of 50

μg/mL and 50 IU/mL, respectively. These fastidious atypical isolates have a specific

requirement for haem that is essential for the initiation of growth, especially when the bacteria

are in low concentrations within the initial inoculum. Incorporation of haematoporphyrin and

haemoglobin into the medium may, therefore, provide a suitable for of haem and increase plating

efficieny (Ishiguro et al. 1986).
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Following primary isolation, purified clones of typical and atypical strains of A. salmonicida are 

readily confirmed if resultant bacteria are gram-negative nonmotile rods that are cytochrome

oxidase positive, ferment glucose, and differentiate according to the biochemical criteria listed in

Table 1. Dalsgaard et al. (1998) noted that the identification of atypical isolates is particulary

troublesome unless biochemical tests are interpreted within a standardized time frame. It is also 

important to note, that some strains of A. salmonicida may be cytochrome oxidase negative; - a 

result that is inconsistent for this species (Chapman et al. 1991; Pedersen et al. 1994; Wiklund et 

al. 1994). A number of polymerase chain reaction (PCR) assays have also been developed that 

can be used either to achieve an initial diagnosis of furunculosis in clinically infected samples

(Gustafson et al. 1992; Calabrez et al 1993; Mooney et al. 1995; Høie et al. 1997) or to confirm 

the identity of isolates that have been cultured subsequent to primary isolation (Hiney et al. 1992; 

Miyata 1996; Oakey et al. 1998). Because PCR-assays may often detect concentrations of

bacteria below those obtained by culture, predictive validation and interpretation of results in the 

absence of definitive culture-positive results is often problematic (Hiney and Smith 1998).

The production of a brown water soluble pigment remains a principal phenotypic characteristic

in the presumptive identification of most A. salmonicida subsp. salmonicida. Griffin et al.

(1953) noted that the incorporation of L-phenylalanine and L-tyrosine in media (pH = 6.5 to6.8) 

enhanced pigmentation. However, the presence of fermentable sugars (e.g. – maltose), 10%

carbon dioxide, simply tightening the caps of test tubes, or incubation of cultures above 22oC 

delayed pigmentation (Griffin 1953). The incorporation of 0.1% glucose in bacteriological

media may not only inhibit pigmentation but also cause an overall reduction in the size of the

bacterial colonies (Altman et al. 1992). Although the presence of brown pigment may facilitate 

diagnosis, similar pigments are also produced by other aquatic aeromonads (Ross 1962) and

pseudomonads (Hamilton-Miller 1975; Altman et al. 1992). 

A number of different serological techniques may be used for identification (Rabb et al. 1964;

McCarthy and Rawle 1975; McCarthy 1975b; McCarthy and Whitehead 1977; Eurell et al.

1979). Sakai et al. (1986) noted that enzyme immunoassays (ELISA) amplified with secondary

and tertiary antibodies may detect as little as 100 colony forming units (cfu) of A. salmonicida per 

mL. They also found that normal ELISA and immunofluorescence assays detected a minimum

of 102 and 103 cfu of the pathogen, respectively; but it required as many as 107 cfu for detection 

using either the latex agglutination or coagglutination procedures. Adams and Thompson (1990) 

also demonstrated that the threshold limit for detection of A. salmonicida by a normal ELISA test 

was approximately 103 cfu/mL. 

Fish may be covert carriers of A. salmonicida even when culture or other methods of diagnosis are 

negative (Hiney et al. 1997). In such cases, the stress induced furunculosis test as described by

Bullock and Stuckey (1975) and modified by McCarthy (1977b) has proven to be the most reliable 

procedure for detection of A. salmonicida among carrier fish (Hiney et al. 1994; Cipriano et al. 

1997). In this procedure, fish are injected with 20 mg of prednisolone acetate per kilogram of fish 

and maintained for 14 d in water at 18oC. All mortality is cultured to confirm the presence or 

absence of A. salmonicida. If no fish die, the observation period may be extended or all fish may be 

sacrificed and cultures are then prepared from their kidneys. Stress inducible furunculosis may be 

seasonal or transient in nature and can be enhanced by certain physiological (Scallan and Smith

1993) and environmental stressors (Scallan et al. 1994). Filtration (Maheshkumar et al. 1990; Ford 

1994) or PCR (O’Brien et al. 1994) analyses may also be adapted to detect and monitor

concentrations of A. salmonicida in culture water or facility effluents. 

BACTERIAL ECOLOGY
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Rose et al. (1990a) have indicated that within most microcosms, viability of A. salmonicida (as 

measured by cultivation on bacteriological media) was generally less than 10 days, which is

consistent with the obligate nature of this pathogen. Using a streptomycin-resistant mutant of A. 

salmonicida, McCarthy (1977b) determined that the bacterium survived 24 days in natural

brackish water, 17 days in nonsterile freshwater, and 8 days in seawater. He also found that A. 

salmonicida survived on wet or dry nets for 6 days and in tissues or carcasses of fish that died 

from furunculosis for 32 days. On fish husbandry equipment, the bacterium may adhere more

preferentially to plastics than it does to stainless steel (Carballo and Seoane 2000). Sakai (1986) 

has shown that virulent strains may survive for more than 15 weeks in the presence of humic

acid, tryptone, and cleaned river sand but cells were not viable within five weeks in the absence 

of sand. 

Although viable counts of A. salmonicida could not be detected after four weeks in loamy

sediment and after seven weeks in sandy sediment, naked DNA and DNA from released cells

were still present after 13 weeks (Deere et al. 1996). Viable cells of A. salmonicida were 

observed microscopically even when the bacterium could not be cultured on agar plates (Morgan

et al. 1993; Effendi and Austin 1994). These viable but nonculturable cells underwent major

morphological changes and lost pathogenicity for Atlantic salmon (Effendi and Austin 1995a)

and were considered to be dormant (Ferguson et al. 1995). Rose et al. (1990b) have argued 

against dormancy and suggested that a small number of cells, fewer than the sensiticvity of

detection by culture, remain viable and can be resuscitated by the addition of nutrient broth. 

Perez et al. (1995) have also supported the argument against dormancy indicating that A. 

salmonicida remained viable in filtered sea water for 23 to 90 days at 10oC and for 12 to 69 days 

at 20oC. After the addition of nutrients, Husevåg (1995) showed that a small percentage of A. 

salmonicida cells, previously starved for six months in a nutrient-free medium at 15oC, could be 

revived in liquid but not on agar media. Whether or not A. salmonicida enters a true dormancy, 

it is evident that nutrient flow within the environment could rejuvenate the growth and

replication of this bacterium so that, even a small number of non-culturable cells might become a 

potential reservoir of infection for naïve fish. 

TRANSMISSION

Fish that harbor latent infections of A. salmonicida and can transmit the pathogen horizontally by 

either physical contact or shedding the bacterium into the water column represent a significant 

threat for horizontal transfer of the pathogen to naïve fish within freshwater (Horne 1928) and

marine environments (Scott 1968; Nomura 1993). Epizootics are particularly troublesome at the 

beginning of marine culture if undetected A. salmonicida carrier smolts are transported into pens 

(Hammell 1995). Under such conditions, transport often facilitates contagion and the

physiological stress encountered with osmoregulation may enhance disease (Ezura et al. 1984). 

Contagion within natural waterways may be further enhanced by the escape of infected

individuals from culture facilities or sea farms and the subsequent movements of these infected

fish within the feral environment (Johnsen and Jenson 1994). Large aggregations of fish in deep 

pools or beneath waterfalls in response to favorable water temperatures may facilitate contagion

(Johnsen and Jensen 1994).

There is probably no one way in which A. salmonicida enters a susceptible host, but the

bacterium is readily transferred by the horizontal contact among infected fish that are cohabited

with naïve individuals (Nordmo et al. 1998). Although some workers have failed to transmit the 

disease via a gastrointestinal route (Krantz et al. 1964; McCarthy 1977b), Klontz and Wood

(1973) observed clinical furunculosis in sablefish that seemingly resulted from the ingestion of
12

infected coho salmon (Oncorhynchus kisutch). Miyazaki and Kubota (1975a,b) have provided

histopathological evidence for both perbranchial and percutaneous routes of infection. 

Present information suggests that the source and reservoir of infection and transmission of

atypical A. salmonicida is probably similar to that which has been described for typical strains 

(Wiklund and Dalsgaard 1998). Tuffery and Dehand (1979) were not able to isolate bacteria

from tissues of live or dead carp that had been injected with a Carp Erythrodermatitis variant of 

A. salmonicida. Elliott and Shotts (1980b) also found that goldfish injected with A. salmonicida 

isolated from clinical cases of Goldfish Ulcer Disease died without developing ulcers. However,

ulcers were produced if the goldfish were either exposed to the pathogen in the water or after

scarification in which a sample of scales was removed and the exposed dermis was swab

inoculated with bacteria. In studies conducted at the National Fish Health Research Laboratory, 

we also found that rainbow trout (Salmo gairdneri), brook trout (Salvelinus fontinalis), and

Atlantic salmon died after injection with atypical variants of A. salmonicida isolated from 

goldfish, without the development of dermal ulcerations. Removal of mucus, followed by skin

inoculation, produced ulcers in brook trout and Atlantic salmon, but not in rainbow trout. 

Atypical isolates obtained from ulcerated flounders (Platichthys flesus) could reproduce dermal

ulcerations only if the bacterium was injected subdermally or if the skin of fish had been

scarified prior to waterborne challenge (Wiklund 1995). The importance of dermal scarification

is further emphasized by Takahashi et al. (1975), who concluded that the natural transmission of

Goldfish Ulcer Disease was most severe among fish whose dermis had been severely eroded by

either ectoparasites or handling. Aeromonas salmonicida has been isolated from the sea louse 

Lepeophtheirius salmonis (Nese and Enger 1993) in the marine environment and from Argulus 

corregoni (Shimura et al. 1983), and Tetrahymena pyriformis (King and Shotts 1988) within the 

freshwater environment. Because each of these parasites is capable of inducing severe branchial

or dermal damage, it has been theorized but not substantiated that infected ectoparasites may act 

as vectors in the spread of furunculosis. 

Horizontal transmission of A. salmonicida has also been demonstrated where mollusks have been 

co-cultured with susceptible hosts (Bjoershol 1999; Starliper 2001). Another novel application

of husbandry techniques that may effect the transmission of infection involves the use of wrasse

as cleaner fish to clear sea lice from Atlantic salmon in net pen culture. The wrasse may

themselves become infected with atypical variants of either by orally ingesting infected sea lice

or through horizontal exposures with other infected fish. Infected wrasse may, therefore, act as a 

further reservoir of contagion for salmon with which they are co-cultured (Collins et al. 1991;

Laidler et al. 1999). As a consequence of such infection, it was suggested that wrasse should not 

be released into the environment or transferred between facilities at the end of specific

production cycles (Treasurer and Laidler 1994). 

In addition to horizontal transmission via cohabitation or fish to fish contact, Wooster and

Bowseer (1996) found that viable cells of A. salmonicida can be dispersed in aerosol droplets at 

least 104.1 cm (limits of the test chamber used) in the air. Viable A. salmonicida was also 

recovered from the water of tanks that were exposed to an aerosol spray downwind of the

contaminant source. This study indicates that aerosol transmission of A. salmonicida may be

particularly problematic where culture systems utilize spray bars within raceways or aquaria in

close proximity to one another. These findings are also consistent with the report of Enger et al. 

(1992) which indicated that concentrations of A. salmonicida are selectively enriched within in

the lipid rich surface microlayer at the air-water interface. 

Mackie et al. (1930) noted the presence of A. salmonicida within the ovaries and testes of

infected fish, but failed to experimentally induce intra-ovum infections and vertically transmit

furunculosis between parent and offspring. Consequently, Mackie et al (1933) concluded that A. 

salmonicida contaminated the surface of the eggs and recommended that such eggs should be
13

disinfected to minimize or prevent further contagion (Mackie et al. 19933). McCarthy (1977b) 

indicated that vertical transmission was not a significant route of infection because A. 

salmonicida cells from infected parents were unlikely to survive in the eyed-egg stage.

Similarly, Bullock and Stuckey (1987) were unable to document vertical transmission of 

furunculosis among the progeny of parental stocks that had either survived furunsulosis

expizootics or had been experimentally injected with A. salmonicida prior to spawn. 

VIRULENCE FACTORS

Because clinical signs of furunculosis are readily produced in fish injected with extracellular

products produced during the growth of A. salmonicida (Ellis et al. 1981), an extensive body of 

research exists on mechanims of virulence associated with this pathogen. Such virulence has

been associated with structural components of the bacterial cell and with exotoxins that are

secreted during bacterial metabolism. Although it is phenotypically difficult to predict virulence

in vitro based upon the presence or absence of an individual bacterial component (Olivier 1990), 

the synergistic effect of each of these elements is indeed significant to the cumulative expression

of furunculosis in vivo. The nature of virulence in A. salmonicida is indeed complex and

apparently varies between strains. 

A-Layer Protein

Figure 10: Transmission electromicrograph of a virulent

Aeromonas salmonicida showing the presence of the Alayer (A) in relation to the bacterial outer membrane

(OM), rigid layer (R), plasma membrane (PM) and pililike appendages (B).

Udey (1978) showed that virulent A. salmonicida possessed an additional layer (A-layer) 

associated with the external surface of the membrane of the cell wall. Evenberg et al. (1981) 

determined that the A-layer consisted of a major additional cell envelope protein (ACE) that was 

immunologically similar among virulent isolates. The protein was water-insoluble, hydrophobic,

and similar to the K88 adhesive fimbriae of enteropathogenic Escherichia coli. The protein was 

described to have a molecular weight of 49 kilodaltons, which was expressed in a regularly

repeating tetragonal array beyond the bacterial cell wall (Kay et al 1981), and was present

within typical and atypical strains of the pathogen (Hamilton et al. 1981). Kay and Trust (1991) 

additionally showed that the tetragonal array is tethered to the cell surface via the O-antigen side 

chain of the bacterial lipopolysaccharide (LPS). The A-layer protein array apparently blocks

bacteriophage receptors on the outer membrane of A. salmonicida, presents a chemically

refractile and somewhat impermeant barrier (Trust et al. 1981) that buffers the underlying outer
14

membrane and its associated proteins from chemical modification involved with host defense

including elements of both the immune response and cytotoxic effects of the complement

pathway (Kay and Trust 1991). Garduno et al (2000) have also shown that A-layer positive 

strains of A. salmonicida can efficiently adhere to, enter, and survive within macrophages. 

Glycerophospholipid cholesterol acyltransferase

When injected into fish in its purified form, bacterial endotoxin or lipopolysaccharide (LPS) that

is produced by A. salmonicida is not pathogenic (Wedemeyer et al. 1969; Paterson and Fryer 

1974). Within the matrix of extracellular products produced by A. salmonicida, however, LPS 

may be aggregated with bacterial glycerophospholipid cholesterol acyltransferase (GCAT; 

molecular weight = 25 kilodaltons). Lee and Ellis (1990) have indicated that the GCAT/LPS

complex (molecular mass = 2000 kilodaton) is hemolytic for fish erythrocytes, leukocytolytic,

cytotoxic, and lethal for Atlantic salmon when injected at a concentration of 0.045 μg protein/g

of body weight. The LPS did not affect the enzymatic activity of free GCAT with egg yolk or 

phosphatidylcholine (lecithin). When complexed with LPS, GCAT was more heat stable and

both hemolytic activity and lethal toxicity was about eightfold higher in the complexed form.

Unlike earlier studies, therefore, the authors suggested that the LPS moiety of the aggregate

GCAT/LPS complex is indeed an important element in the pathogenicity of A. salmonicida. 

Bacterial proteases

Early studies indicated that as a consequence of septicemia bacterial utilization of the host's

blood sugar induced hypoglycemia and subsequent death (Field et al. 1944). At that time very

little was known about the potent action of bacterial exotoxins produced by A. salmonicida until 

Griffin (1954) suggested that this bacterium produced a leucocidin that was responsible for the

severe leukopenia observed histopathologically in lesion development. Klontz et al. (1966)

would initially show that this suppression of the inflammatory response could be produced by

injecting trout with cell-free extracts from A. salmonicida. That work would initiate additional

investigations of virulence associated with the exotoxic substances produced by A. salmonicida

that continue to this day.

Fuller et al. (1977) extracted a leukocytolytic factor from the extracellular products (ECP), which

not only was cytotoxic for leukocytes but also synergistically enhanced bacterial virulence when

injected in concert with viable cells. A protease was also extracted from the extracellular

material (Shieh and MacLean 1975) that induced the development of furuncle-like lesions in fish

(Sakai 1977). Cipriano et al. (1981) determined that the extracellular material was actually a 

composite of substances; one analogous to the leukocytolytic factor described by Fuller (1977),

another was proteolytic and induced lesion development similar to that reported by Sakai (1977), 

and yet others expressed cytotoxic activity to rainbow trout (Oncorhynchus mykiss) gonad cells 

(RTG-2) in tissue culture or were hemolytic for trout erythrocytes and lethal in brook trout

(Salvelinus fontinalis) regardless of the virulence of the strain from which they were extracted. 

Shieh (1985) found that the proteolytic activity inherent among virulent isolates was

quantitatively more toxic for Atlantic salmon than that isolated from avirulent isolates. 

Production of a protease deficient mutant which lost virulence but maintained autoagglutinative,
15

serum resistant, adhesive, hemolytic, and leukocytolytic activities provided further indication

that extracellular protease was an important element of bacterial pathogenicity (Sakai 1985). 

Based upon chymotryptic properties, inhibition by diisopropylfluorophosphate (DFP) and tosylphenylalanine-chloromethyl ketone (TPCK) and hydrolyzed N-benzoyl-L-tyrosine ethyl ester

(BTEE), Tajima et al. (1984) characterized a heat labile alkaline serine protease from the ECP of 

A. salmonicida with a molecular mass of 71 kilodaltons. Proteolytic activity was stable from pH 

5.0 to 10.0, but maximum activity was observed at pH 9.4 and 50o C. Price et al. (1989) showed 

that strains of A. salmonicida actually produced at least two types of proteases; a serine protease 

of molecular weight 70 kilodaltons (similar to that described by Tajima) which is active against

casein and gelatin and another of molecular weight 20 kilodaltons which is active against gelatin

but not casein. Because no difference was observed in the toxicity of extracellular products

produced by caseinase deficient mutant and its wild-type A. salmonicida, Drinan et al. (1989) 

inferred that the caseinase enzyme has no major role in the pathogenesis of A. salmonicida

infections. Gudmundsdottir et al. (1990) has described a 20 kilodalton protease within A. 

salmonmicida subsp. achromongenes that was lethal for Atlantic salmon and identified as a

metallo-protease based upon its inhibition by EDTA. A 35 kilodalton metalloprotease was also

isolated from A. salmonicida subsp. salmonicida with optimum acticvity at pH 7.5 and 40oC 

against gelatin and azocoll but not against casein (Arnesen et al. 1995). 

Siderophore Production and Iron Regulation

Most typical and atypical isolates of A. salmonicida can grow under conditions of ironrestriction as evidenced in vitro by multiplication in the presence of iron chelators. However, 

siderophore production was detected only among typical strains and it behaved as a 2,3-

diphenol-catechol (Hirst et al. 1991). Consequently, it was inferred that atypical and typical

isolates regulate iron-uptake by different mechanisms. Among typical strains, utilization was

siderophore-dependent and transferrin was digested by the 70 kilodalton serine protease. The

presence of the catechol siderophore and major iron-regulated outer membrane proteins

(IROMPs) were consistent and homogeneous within A. salmonicida subsp. salmonicida

(Fernandez et al. 1998). Consequently it would appear that the siderophore-independent 

utilization of transferrin within atypical isolates is a function of proteolytic digestion by the

metalloprotease. 

CONTROL

Because furunculosis infects such a wide variety of hosts in a diversity of habitats, the bacterium

is predominantly managed as a geographically ubiquitous, but obligate pathogen. The pandemic

distribution and prevalence of this bacterium, however, should never diminish the gravity of its

pathogenic ramifications in the minds of fish culturists and resource managers. Reference to the 

factoral interplay of host, pathogen, and environment is used so often that it becomes an abstract 

conceptualization of the disease process. Avoidance of A. salmonicida within populations of fish 

is critical to the prevention of furunculosis. Jarp et al. (1993) have found that the migration of

anadromous fish into hatchery water supplies, a dense concentration of other infected fish culture 

stations proximate to uncontaminated stations, and sharing personnel or equipment between

stations are among the most significant risks associated with the introduction of furunculosis
16

(Jarp. et al. 1993). Managers have some degree of control over each of these parameters. 

Ultraviolet irradiation (Bullock and Stuckey 1977) or ozonation (Wedemeyer and Nelson 1977;

Colberg and Lingg 1978) of incoming culture water, fallowing of net pen sites, and education of

personnel can alleviate significant sources of potential contamination and prevent disease. 

Regular monitoring programs that detect A. salmonicida in the water supply and provide early 

non-lethal detection on mucus can be coupled with topical disinfection or antibiotic regimens

that either preclude or minimize infection (Cipriano 1997). Furthermore, only fertilized eggs or

stocks of fish that have been certified to be free of A. salmonicida infection should be transferred 

between facilities attempting to maintain a specific pathogen free status. In practice, conduct of

the stress induced furunculosis assay and regulatory confinement of infected smolts have reduced 

the number of furunculosis outbreaks associated with early marine culture (Smith 1991; Olivier

1992).

Eyed eggs from sources not certified to be specific pathogen free should be disinfected upon

arrival, and must be isolated from subsequent contact with other eggs or with contaminated

packing material and containers. Povidone iodine has become the compound of choice for

disinfecting trout and salmon eggs (McFadden 1969), because it possesses greater bacteriocidal

activity than merthiolates (Gee and Sarles 1942) or acriflavine (Atkinson 1930, Blake 1930). 

The compund is available commercially as an iodophor (e.g., - Betadine and Wescodyne) that 

generally contains approximately 1.0% to 1.6% active iodine in inert organic solvents

(McFadden 1969; Amend 1974). Although Ross and Smith (1972) extended the effective use of 

povidone iodine against a number of bacterial fish pathogens including A. salmonicida, they also 

noted that disinfection was incomplete when 25 mg/L of iodophor was used for 15 to 120

minutes with certain strains of this pathogen. McCarthy (1977b) also found that a 10-minute 

treatment of artificially infected green or eyed eggs with 50 or l00 mg/L of active iodine (as

Wescodyne) may not kill all A. salmonicida cells, but that a 30-min exposure to 1,000 mg/L

acriflavine was completely efficacious. Consequently, Piper et al. (1982) recommended that

salmonid eggs should be disinfected in a solution containing 100 mg of active iodine/L for 10

minutes, but the bacteriocidal activity of iodophor may still be influenced by the concentration of 

A. salmonicida present and the degree of organic contamination in the disinfectant solution

(Sako et al. 1988). 

United States Fish and Wildlife Service regulations recommend that eggs should be disinfected

by submersion for 30 minutes in 50 mg iodine/L immediately after fertilization. If eggs are then

shipped to another facility for incubation, policy requires that those eggs undergo a secondary

disinfection in 100 mg iodine/L for 10 minutes (USFWS 1995). Disinfection should be

conducted in 10 to 15°C pathogen-free water at a pH of 7.0 (6 to 8). Soft water in which the 

normal acidity of iodophors can reduce effectiveness may be alkalized by adding 0.5 g sodium

bicarbonate per liter of water. The eggs should be rinsed immediately after treatment, unless

they are placed into a flowing-water incubator within a few minutes after disinfection.

SELECTION AND BREEDING

Selective breeding programs have been developed in salmonids to enhance experimental and field 

resistance to furunculosis. Brook trout (Salvelinus fontinalis) at the Hackettstown (NJ) state fish 

hatchery were selected on the basis of growth, coloration and the ability to survive natural

epizootics of furunculosis. Subsequent progeny were continually evaluated for acquired resistance 

to disease and furunculosis mortality was reduced from 98% to 30.8%, after four successive

generations of selection (Embody and Hayford 1925). Resistant progeny grew faster than nonselected fish, which corresponded with a rise in the average number of eggs obtained per female at 

first and second spawns but this was also accompanied by a gradual decrease in egg viability to the 

eyed-egg stage. Although the brook trout had acquired resistance to furunculosis, selection did not 
17

enhance resistance to Bacterial Gill Disease nor infestations by Gyrodactylus and Chilodonella 

(Hayford and Embody 1930). Probably the most successful selection study involves the

development of furunculosis-resistant strains of trout by the New York State Department of

Environmental Conservation (Rome, NY). Wolf (1953) collected 11 strains of brook trout and 

seven strains of brown trout (Salmo trutta) from the New England area that were inbred for a 

minimum of eight previous generations. The fish were constantly subjected to A. salmonicida via 

bath, horizontal, and dietary challenges. Mortality within strains ranged from 36% to 66% for

brook trout and from 5% to 99.7% for brown trout and Wolf concluded that enough variation

existed among the resistance of various lots to warrant further evaluation through selective breeding. 

Ehlinger (1964) continued these studies and crossbred survivors between strains with intermediate 

or low mortality. Potential brood stock was further selected on the basis of size, coloration and egg 

yield. Resistance was monitored within strains as a function of eliminating susceptible breeders

within a line and by experimental challenge on subsamples of the resultant progeny. During the 

next ten years, one resistant strain of brook trout and one strain of brown trout were produced which 

had practical application to the culture of salmonids throughout New York (Ehlinger 1977). 

Acquired resistance to furunculosis of the Rome trout is widely accepted and these fish are currently 

used throughout many hatchery programs in the New England and the Mid-Atlantic Regions

(Kincaid et al. 1997) for their survival and performance in recreational fisheries where

furunculosis is enzootic (Hulbert 1985). 

Detailed genetic studies have shown that heritability of mortality among families of Atlantic

salmon challenged by cohabitation with infected cohorts was high, h

2

 = 0.32 +/- 0.10 and 0.48 

+/- 0.17, for the sire and dam components, respectively (Gjedrem et al. 1991), suggesting that

resistance to furunculosis can be effectively improved by selective breeding (Gjedrem and Gjoen

1995). These observations were consistent with those of Bailey et al. (1993) who also indicated 

that heritabilty (h2 = 0.32 +/-6) among Atlantic salmon for resistance to furunculosis was

sufficient to warrant further selection. Langefors et al. (2001) screened MHC class IIB genotypes 

established exon 2 sequences encoding the major part of the peptide-binding region among

families of Atlantic salmon that demonstrated either high resistance (HR) or low resistance (LR)

to A. salmonicida. Three alleles were discerned from these studies, which showed some

correlation with resistance to furunculosis. One allele, e, was significantly more prevalent in HR

families than in LR families. Brood fish carrying the e allele had a 12-fold greater chance of being 

HR than cohorts without the e allele. A second allele, i, had a significantly higher frequency

among those fish that either remained uninfected or survived experimental challenges than it did

among dead individuals. A third allele, j, was prevalent in LR families and among individuals

that died from infection.

Variable degrees of resistance have also been noted among non-salmonids in response to atypical 

isolates of A. salmonicida infections. Dubois-Darnaudpeys and Tuffery (1979) have shown that 

tench are more resistant to carp erythrodermatitis than the common carp, grass carp and silver

carp, whose degree of resistance is listed in descending order. Sovenyi et al. (1988) found that 

three-month-old progeny of hybrid crosses between common carp from Hungary and Japanese

coloured carp had a body weight (43.6 +/- 22.4 g) and condition factor (8.85 +/- 1.05 g/cm3) 

were significantly higher than those of the common carp purebreds (23.5 +/- 12.3 g body weight; 

8.53 +/- 0.62 g/cm3 condition factor). Furthermore, the hybrids sustained only half the mortality

than that which was observed among the purebred carp after experimental challenge with an

atypical A. salmonicida. Houghton et al. (1991) showed that a Polish strain of carp, inbred for six 

generations) was significantly more susceptible to carp erythrodermatitis than a Hungarian strain

that had been inbred for five generations. Wiegertjes et al. (1993) further demonstrated that even 
18

within the same strain of fish, resistance to erythrodermatitis increases with age as indicated by a 

shift from subacute (85% at 3 and 5 months) to chronic (40% at 10 months) mortality.

IMMUNIZATION

Vaccines of A. salmonicida emulsified in oil adjuvants and delivered by intraperitoneal injection

provide long-lasting protection and their use is promoted in commercial aquaculture (Lillehaug

et al. 1992; Ellis 1997). Both aqueous and oil-adjuvanted vaccines are commercially produced 

and may induce immunity at water temperatures as low as 2oC. Eggset et al. (1997) noted that 

even though an antibody response for A. salmonicida was delayed or strongly suppressed by this 

temperature, protection was still satisfactory at 18 weeks after vaccination. After 18 weeks, 

these workers further noted that protection was severely reduced among those fish reared at 10oC 

and given the aqueous vaccine, but a similar reduction was not apparent among those fish that

were vaccinated with the oil-emulsion vaccine (Killie et al. 1997). Although commercial

furunculosis vaccines administered in mineral oil yield significantly higher protection than

aqueous-based vaccines, the mineral oil adjuvant may produce a higher degree of abdominal

adhesions between the internal organs and the abdominal wall near the site of injection

(Midtlyng 1993). If severe, these adhesions may decrease growth rate (Midtlyng 1994), the

severity of which is inconsistent between farms and may or may not be significant when

compared with the final growth weight of non-vaccinated fish (Midtlyng and Lillehaug 1998). 

It must be remembered, however, that vaccination is not an absolute barrier treatment that

guarantees further expression of furunculosis within – or transmission of furunculosis from

covertly infected vaccinated carriers (Hiney 1999).

The serologic relatedness that exists among strains of A. salmonicida (Popoff 1969; Paterson et 

al. 1980) suggests that immunization of fishes against atypical forms of this pathogen is also a

realistic possibility. However, Atlantic salmon vaccinated with a commercial vaccine against A. 

salmonicida subsp salmonicida or with this vaccine and another prepared against an autogenous 

strain of A. salmonicida subsp. achromogenes were equally protected against A. salmonicida

subsp salmonicida by cohabitation challenge. However, salmon vaccinated only with Aeromonas 

salmonicida subsp. achromogenes were not protected against classical furunculosis

(Gudmondsdottir and Gudmondsdottir 1997). Furthermore, Evenberg et al. (1988) showed only

moderate to slight protection against an atypical variant of A. salmonicida causing carp

erythrodermatitis, when carp were immunized with either cell envelope preparations, purified

LPS, purified A-layer protein, and even formalinized whole cell bacterins. When detoxified ECP 

was used as the immunogen, carp were protected against a subsequent lethal challenge.

TREATMENT

Furunculosis of salmonids was the first disease of fishes to be treated with modern drugs

including both sulfonamides and nitrofurans (Gutsell 1948). Although other drugs effectively

control this disease (Herman 1970), the U.S. Food and Drug Administration enforces stringent

requirements for drugs used on food animals in the United States, and only sulfamerazine (no

longer registered), oxytetracycline, and the potentiated sulfonamide Ro5-0037 or ROMET®

(Bullock et al. 1974) may be used. Although most sulfonamides are no longer used,

sulfamerazine American Cyanamid, Co.) has been approved to treat furunculosis in rainbow
19

trout, brook trout, and brown trout at a dose of 200 mg of drug per kilogram of fish per day (10 g 

per 45.3 kg of fish weight) for 14 days. Treatment must terminate at least 3 weeks before fish are 

to be marketed or stocked. Sulfisoxazole (Gantrisin) was preferred for treating brown trout

whose growth may be inhibited by sulfamerazine (Snieszko and Wood 1955). Oxytetracycline

(Terramycin®, Pfizer, Inc.) is cleared for use among all species of salmonids, at the rate of 50 to 

80 mg of drug per kilogram of fish per day (2.5 to 3.75 g per 45.3 kg of fish) for 10 days. Again, 

treatment must terminate at least 3 weeks before fish are released. ROMET® (HoffmanLaRoche, Inc.), which consists of five parts sulfadimethoxine and one part ormetoprim,

controlled furunculosis when fed at the rate of 50 mg per kilogram of fish per day (2.5 g per 45.3 

kg) for 14 days (Bullock et al. 1974) and has been cleared for use at the same dosage when

administered for five days with a 42 day withdrawal period. 

LITERATURE CITED

Adams, A. and K. Thompson. 1990. Development of an enzyme-linked immunosorbent assay 

(ELISA) for the detection of Aeromonas salmonicida in fish tissue. Journal of Aquatic Animal

Health. 2: 281-288.

Altman, K., M. Marshall, S. E. Nicholson, P. J. Hanna, and N. Gudkovs. 1992. Glucose 

repression of pigment production in atypical isolates of Aeromonas salmonicida responsible for 

goldfish ulcer disease. Microbios. 72: 292-293.

Amend, D. F. 1974. Comparative toxicity of two iodophors to rainbow trout eggs. Trans. Am. 

Fish. Soc. 103(1):73-78.

Arnesen, J. A., G Eggset, and T. O. Jorgensen.1995. Partial purification and characterization of 

extracellular metalloproteases from Aeromonas salmonicida spp. salmonicida. Journal of Fish 

Diseases. 18: 283 - 295.

Atkinson, N. J. 1932. A bacterial disease of trout eggs and fry and its prophylaxis with acriflavine. 

Transactions of the American Fisheries Society. 62: 152 – 155.

Austin, B. 1993. Recovery of ‘atypical’ isolates of Aeromonas salmonicida, which grow at 

37oC, from ulcerated non-salmonids in England. Journal of Fish Diseases. 16: 165 – 168.

Austin, D.A., D. McIntosh, and B. Austin. 1989. Taxonomy of fish associated Aeromonas spp. 

with the description of Aeromonas salmonicida subp. smithia subsp. nov. Systematic and

Applied Microbiology. 11: 277 – 290.

Austin, B., D. A. Austin, I. Dalsgaard, B. K. Gudmondsdottir, S. Hoie, J. M. Thornton, J. L.

Larsen, B. O’Hici, and R. Powell. 1998. Characterization of atypical Aeromonas salmonciida

by different methods. Systematic and Applied Microbiology. 21: 50 – 64. 

Bailey, J. K.; Olivier, G.; Friars, G. W. 1993. Inheritance of furunculosis resistance in Atlantic 

salmon. Bulletin of the Aquaculture Association of Canada. 4: 90-92.

Belland, R. J. and T. J. Trust. 1988. DNA-DNA reassociation analysis of Aeromonas 

salmonicida. Journal of General Microbiology. 134: 307 – 315.
20

Bjoershol, B., R. Nordmo, K. Falk, and S. Mortensen. 1999. Cohabitation of Atlantic salmon

(Salmo salar L.) and scallop (Pecten maximus) – challenge with Infectious Salmon Anemia

(ISA) Virus and Aeromonas salmonicida subsp. salmonicida. 12th International Pectinid

Workshop, Bergen (Norway), 5 – 11 May 1999.

Blake, I. 1930. The external disinfection of fish ova with reference to the prophylaxis of

furunculosis. Fisheries Board, Scotland Salmon Fisheries, 1930 No. II. is Majesty’s Stationery

Odffice, Edinburgh. 10 pp. 

Bootsma, R., and J. Blommaert. 1978. Zur Aetiologie der Erythroder- matitis beim Karpfen

Cyprinu8 ca1'pio L. Pages 20-27 in Neuere Erkenntnisse uber Fischinfektionen. Gustav Fischer 

Verlag, Stuttgart and New York.

Bootsma, R., N. Fijan, and J. Blommaert. 1977. Isolation and preliminary identification of the

causative agent of carp erythrodermatitis. Vet. Arh. 47(6):291-302.

Boyd, E. F., M. P. Hiney, J. F. Peden, P. R. Smith and D. A. Caugant. 1994. Assessment of 

genetic diversity among Aeromonas salmonicida isolates by multilocus enzyme electrophoresis. 

Journal of Fish Diseases. 17: 97 – 98.

Bruno, D. W. 1986. Furunculosis in sea-reared Atlantic salmon, Salmo salar L. Colonization of 

gill epithelium. Bulletin of the European Association of Fish Pathologists. 6: 76 - 80.

Bullock, G. L., and H. M. Stuckey. 1975. Aeromonas salmonicida: detection of

asymptomatically infected trout. Progressive Fish-Culturist. 37: 237 – 239.

Bullock, G. L., and H. M. Stuckey. 1977. Ultraviolet treatment of water for destruction of five 

gram-negative bacteria pathogenic to fishes. Journal of the Fisheries Research Board of Canada. 

34:1244 - 1249.

Bullock, G. L. and H. M. Stuckey. 1987. Studies on vertical transmission of Aeromonas 

salmonicida. The Progressive Fish Culturist. 49: 302 – 303.

Bullock, G. L., H. M. Stuckey, D. Collis, R. L. Herman, and G. Maestrone. 1974. In vitro and in 

vivo efficacy of a potentiated sulfonamide in control of furunculosis in salmonids. Journal of the

Fisheries Research Board of Canada. 31: 75 - 82.

Calabrez, M.C.T., P. Lintermans, and J. Vosjan. 1993. The polymerase chain reaction (PCR) 

technique as a specific and sensitive detection method for Aeromonas salmonicida and

Aeromonas sobria in natural ecosystems (water, sediment and fish). World Aquaculture '93 Int. 

Conf., Torremolinos (Spain), 26-28 May 1993. Special publication. European Aquaculture 

Society. Bredene; no. 19, p. 328; 1993; (FROM DISCOVERY TO COMMERCIALIZATION; 

Carrillo, M.;Dahle, L.;Morales, J.;Sorgeloos, P.;Svennevig, N.;Wyban, J. (eds.)

Calkins, G. N. 1899. Report upon the resent epidemic among brook trout (Salvelinus fontinalis) 

on Long Island. Fourth Annual Report of the Commissioners of Fisheries, Game, and Forests. 

State of New York Fish and Game Commission. Pp. 175 – 190.

Carballo J., R. M. Seoane, and T. P. Nieto. 2000. Adhesion of Aeromonas salmonicida to 

materials used in aquaculture. Bulletin of the European Association of Fish Pathologists. 20: 77-

82.
21

Carson, J. and J. Handlinger. 1988. Virulence of the aetiological agent of goldfish ulcer disease 

in Atlantic salmon, Salmo salar L. Journal of Fish Diseases. 11: 471 – 479. 

Chapman, P. F., R. C. Cipriano, and J. D. Teska. (1991. Isolation and phenotypic

characterization of an oxidase-negative Aeromonas salmonicida causing furunculosis in coho

salmon (Oncorhynchus kisutch). Journal of Wildlife Diseaseas. 27: 61 – 67.

Cipriano, R. C. 1997. Strategies for management of furunculosis in Atlantic salmon effected by

non-lethal detection of Aeromonas salmonicida: a review. Bulletin of the European Association

of Fish Pathologists. 17: 215 – 219.

Cipriano, R. C. and J. Bertolini. 1988. Selection for virulence in the fish pathogen Aeromonas 

salmonicida using Coomassie brilliant blue agae. Journal of Wildlife Diseases. 24: 676 – 678. 

Cipriano, R. C. and A. R. Blanch. 1989. Different structural characteristics in the cell envelope 

of the fish pathogen Aeromonas salmonicida. Microbios Letters. 40: 87 – 95.

Cipriano, R. C., B. R. Griffin, and B. C. Lidgerding. 1981. Aeromonas salmonicida: relationship 

between extracellular growth products and isolate virulence. Canadian Journal of Fisheries and

Aqutic Sciences. 38: 1322 - 1326.

Cipriano, R. C., L. A. Ford, D. R. Smith, J. H. Schachte, and C. J. Petrie. 1997. Differences in 

detection of Aeromonas salmonicida in covertly infected salmonid fishes by the stress-inducible 

furunculosis test and culture-based assays. Journal of Aquatic Animal Health. 9: 108-113.

Colberg, P. J. and A. J. Lingg. 1978. Effect of ozonation on micro- bial fish pathogens,

ammonia, nitrate, nitrite, and BOD in simulated reuse hatchery water. Journal of the Fisheries

Review Board of Canada. 35: 1290 - 1296.

Collins, R. O., D. A. Ferguson, and M. A. Bonniwell. 1991. Furunculosis in wrasse. Veterinary 

Record. 128: 43

Dalsgaard, I., B. Nielsen, and J. L. Larsen. 1994. Characterization of Aeromonas salmonicida

subp. salmonicida: a comparative study of strains of different geographic origin. Journal of

Applied Bacteriology. 77: 21 – 30.

Dalsgaard, I., B. K. Gudmundsdsottir, S. Helgason, S. Hiie, O. F. Thoresen, U. P. Wichardt, and 

T. Wiklund. 1998. Identification of atypical Aeromonas salmonicida: inter-laboratory evaluation

and harmonization of methods. Journal of Applied Microbiology. 84: 999 - 1006.

Deere, D., J. Porter, R. W. Pickup, and C. Edwards. 1996. Survival of cells and DNA of

Aeromonas salmonicida released into aquatic microcosms. Journal of Applied Bacteriology. 81:

309-318.

Drinan, E. M., J. Donlon, S. Molloy, and P. R. Smith. 1989. Observations on the role of the 

caseinase enzyme in the pathogenesis of furunculosis. Journal of Fish Diseases. 12: 45 - 50.

Dubois-Darnaudpeys, A., and G. Tuffery. 1979. Etude experimentale de la Sensibilite de

differentes especes pisciaires a L'agent de L'erythrodermatite de la carpe (E.C.). Bull. Acad. Vet. 

Fr. 52(4):561-566.
22

Eggset, G., H. Mikkelsen, and J. E. A. Killie. 1997. Immunocompetence and duration of

immunity against Vibrio salmonicida and Aeromonas salmonicida after vaccination of Atlantic

salmon (Salmo salar L.) at low and high temperatures. Fish & Shellfish Immunology. 7: 247 - 

260.

Ehlinger, N. F. 1964. Selective breeding of trout for resistance to furunculosis. New York Fish

and Game Journal. 11: 78-90.

Ehlinger, N. F.1977. Selective breeding of trout for resistance to furunculosis. New York Fish and 

Game Journal. 24: 25 - 36.

Effendi, I. and B. Austin. 1994. Survival of the fish pathogen Aeromonas salmonicida in the 

marine environment. Journal of Fish Diseases. 17: 375 - 385.

Effendi, I.and B. Austin. 1995a. Dormant/unculturable cells of the fish pathogen Aeromonas 

salmonicida. Microbial Ecology. 30: 183 - 192.

Elliott, D., and E. B. Shotts, Jr. 1980a. Aetiology of an ulcerative disease in goldfish Carassius 

auratus (L.): microbiological examination of diseased fish from seven locations. Jornal of Fish

Diseases. 3: 133 - 143.

Elliott, D., and E. B. Shotts, Jr. 1980b. Aetiology of an ulcerative disease of goldfish, Carassius 

auratus (L.); experimental induction of the disease. Jornal of Fish Diseases. 3:145 - 151.

Ellis A. E. 1997. Immunization with bacterial antigens: furunculosis. Developments in

Biological Standardization. 90: 107 - 116.

Ellis, A. E., T. S. Hastings, and A. L. S. Munro. 1981. The role of Aeromonas salmonicida 

extracellular products in the pathology of furunculosis. Jornal of Fish Diseases. 4: 41 - 51.

Emmerich, R., and E. Weibel. 1890. Uber eine durch Bakterien verursachte Infektionskrankheit

der Forellen. Allg. Fisch. Ztg. 15: 85 - 92.

Enger, Ø, B. Gunnlaugsdottir, B. K. Thorsen, and B. Hjeltnes. 1992. Infectious load of

Aeromonas salmonicida subsp. salmonicida during the initial phase of cohabitant infection

experiment with Atlantic salmon, Salmo salar L. Journal of Fish Diseases. 15: 425 – 430.

Eurell, T. E., D. H. Lewis, and L. C. Grumbles. 1979. Stained bacterial antigens for use in 

microagglutination procedures. Frogressive Fish-Culturist. 41: 55 - 57.

Evenberg, D., R. Bootsma, and B. Lugtenberg. 1981. Detection, purification and

characterization of a major cell envelope protein, related to virulence, of autoagglutinating

Aeromonas salmonicida strains. Society for General Microbiology. 8: 253-254.

Evenberg, D., P. de Graaff, B. Lugtenberg, and W. B. Van Muiswinkel. 1988. Vaccine-induced 

protective immunity against Aeromonas salmonicida tested in experimental carp

erythrodermatitis. Journal of Fish Diseases. 11: 337 - 350.
23

Ezura, Y, H. Yamamoto, M. Yoshimizu, K. Tajima, H. Sannohe, K. Ikeda, H. Sako, T. Hara, and 

T. Kimura. 1984. An outbreak of furunculosis in coho salmon (Oncorhynchus kisutch) at the 

beginning of marine pen culture. Fish Pathology. 19: 75 – 80.

Ferguson, Y., L. A. Glover, D. M. McGillivray, and J. I. Prosser. 1995. Survival and activity of 

lux-marked Aeromonas salmonicida in seawater. Applied and Environmental Microbiology. 61: 

3494-3498.

Fernandez, A. I. G., A. F. Fernandez, M. J. Perez, T. P. Nieto, and A. E. Ellis. 1998. 

Siderophore production by Aeromonas salmonicida subsp. salmonicida. Lack of strain

specificity. Diseases of Aquatic Organisms. 33: 87 - 92.

Field, J. B., L. L. Gee, C. A. Elvehjem, and C. Juday. 1944. The blood picture in furunculosis 

induced by Bacterium salmonicida in fish. Arch. Biochem. 3: 277 - 284.

Fijan, N. N. 1972. Infectious dropsy of carp, a disease complex. Pages 39-51 in L. E.

Mawdesley-Thomas, ed. Symposia of the Zoological Society of London. Academic Press, New

York.

Fish, F. F. 1934. Ulcer disease of trout. Transactions of the American Fisheries Society. 64: 252 -

258.

Ford, L. A. 1994. Detection of Aeromonas salmonicida from water using a filtration method. 

Aquaculture. 122: 1-7.

Fuller, D. W., K. S. Pilcker, and J. L. Fryer. 1977. A leukocyto- lytic factor isolated from

cultures of Aeromonas salmonicida. Journal of the Fisheries Research Board of Canada. 34:

1118 - 1125.

Garcia, J. A., J. L. Larsen, I. Dalsgaard, and K. Pedersen. 2000. Pulsed field gel elctrophoresis 

analysis of Aeromonas salmonicida subsp. salmonicida. FEMS Microbiology Letters. 190: 163 

– 166.

Garduno, R. A., A. R. Moore, G. Olivier, A. L. Lizama, E.Garduno, and W. W. Kay. 2000. 

Host cell invasion and intracellular residence by Aeromonas salmonicida: role of the S-layer. 

Canadian Journal of Microbiology. 46: 660-668.

Gayer, E. K., L. Bekesi, and G. Csaba. 1980. Some aspects of the histopathology of carp

erythrodermatitis (CE). Pages 127-136 in w. Ahne, ed. Fish diseases. Third COPRAQ-Session. 

Springer- Verlag, Berlin, Heidelberg, New York.

Gee, L. I. And W. B. Sarles. 1942. The disinfection of trout eggs contaminated with Bacterium 

salmonicida. Journal of Bacteriology. 44: 111 - 126.

Gjedrem, T.and H. M. Gjoen. 1995. Genetic variation in susceptibility of Atlantic 

salmon, Salmo salar L., furunculosis, BKD and cold water vibriosis. Aquaculture 

Research. 26: 129 - 134.

Gjedrem, T., R. Salte, and H. M. Gjoen. 1991. Genetic variation in susceptibility of Atlantic 

salmon to furunculosis. Aquaculture. 97: 1 - 6.
24

Griffin, P. J. 1953. Pigment formation by Bacterium salmonicida Journal of Bacteriology. 65:

652 – 659.

Griffin, P. J. 1954. The nature of bacteria pathogenic to fish. Transaction of the American

Fisheries Society. 83: 241 - 253.

Griffin, P. J., S. F. Snieszko, and S. B. Friddle. 1953. A more comprehensive description of

Bacterium salmonicida. Transactions of the American Fisheries Society. 82: 129 - 138.

Gudmundsdottir, B. K. and S. Gudmundsdottir. 1997. Evaluation of cross protection by

vaccines against atypical and typical furunculosis in Atlantic salmon, Salmo salar L. Journal of

Fish Diseases. 20: 343 - 350.

Gudmundsdottir, B. K., T. S. Hastings, and A. E. Ellis. 1990. Isolation of a new toxic protease 

from a strain of Aeromonas salmonicida subspecies achromogenes. Diseases of Aquatic

Organisms. 9: 199-208

Gustafson, C. E., C. J. Thomas, and T. J. Trust. 1992. Detection of Aeromonas salmonicida

from fish by using polymerase chain reaction amplification of the virulence surface array protein

gene. Applied and Environmental Microbiology.. 58: 3816 -3825.

Gutsell, J. S. 1948. The value of certain drugs, especially sulfa drugs, in the treatment of

furunculosis in brook trout, Salve- linus fontinalis. Transactions of the American Fisheries

Society. 75: 186 - 199.

Hamilton, R.C., H. Kalnins, N. R. Ackland, and L. D. Ashburner. 1981. An extra layer in the 

surface layers of an atypical Aeromonas salmonicida isolated from Australian goldfish. Journal

of General Microbiology. 122: 363 - 366.

Hamilton-Miller, J, M, T. 1975. Possible misidentification of the fish pathogen Aeromonas

salmonicida. British Veterinary Journal. 131: 663 - 664.

Hammel, K. L. 1995. An overview of furunculosis in Atlantic Canada. Bulletin of the

Aquaculture Association of Canada. 95: 8 – 11.

Hanninen, M. L., J. Ridell, and V. Hirvela-Koski. 1995. Phenotypic and molecular

characteristics of Aeromonas salmonicida subsp. salmonicida isolated in Southern and Northern 

Finland. Journal of Apllied Bacteriology. 79: 12 – 21.

Hayford, C. O., Embody, G. C. 1930. Further progress in the selective breeding of brook trout 

at the New Jersey State Hatchery. Transactions of the American Fisheries Society. 60: 109 -

113.

Herman, R. L. 1970. Prevention and control of fish diseases in hatcheries. Pages 3-15 in S. F. 

Snieszko, ed. A symposium on diseases of fishes and shellfishes. American Fisheries Society, 

Special Publication No.5.

Hiney, M. 1999. Field observation of clinical furunculosis in Atlantic salmon smolts vaccinated 

with an oil-based furunculosis vaccine. Bulletin of the European Association of Fish

Pathologists. 19: 66 - 69.
25

Hiney, M. P. and P. R. Smith 1998. Validation of polymerase chain reaction-based techniques 

for proxy detection of bacterial fish pathogens: Framework, problems and possible solutions for

environmental applications; review. Aquaculture 162: 41 – 68.

Hiney, M., M. T. Dawson, D. M. Heery, P. R. Smith, F. Gannon, and R. Powell. 1992. DNA 

probe for Aeromonas salmonicida. Applied and Environmental Microbiology. 58: 1039 - 1042.

Hiney, M. P. J. J. Kilmartin, and P. R. Smith. 1994. Detection of Aeromonas salmonicidia in

Atlantic salmon with asymptomatic furunculosis infections. Diseases of Aquatic Organisms. 19:

161 – 167.

Hiney, M. P., P. R. Smith, and E. M. Bernoth. 1997. Covert Aeromonas salmonicida infections, 

pp. 54 – 97, in: Bernoth, E. -M., A. E. Ellis, P. J. Midtlyng, G. Olivier, and P. Smith, eds. 

Furunculosis Multidisciplinary Fish Disease Research. Academic Press. San Diego, California. 

529 pp.

Hirst, I. D., T. S. Hastings, and A. E. Ellis. 1991. Siderophore production by Aeromonas 

salmonicida. Journal of General Microbiology. 137: 1185 – 1192

Holt, J. G., N. R. Krieg, P. H. A. Sneath, J. T. Staley, S. T. Williams. 1994. Bergey’s Manual of 

Determinative Bacteriology, Ninth Edition. Williams and Wilkins, Baltimore, Maryland. 787 pp.

Houghton, G., G. F. Wiergertjes, A. Groenveld, and W. B. van Muiswinkel. 1991. Differences 

in resistance of carp, Cyprinus carpio L., to atypical Aeromonas salmonicida. Journal of Fish 

Diseases. 14: 333 - 341.

Horne, J. H. 1928. Furunculosis in trout and the importance of carriers in the spread of the

disease. Journal of Hygiene. 28: 67 – 78. 

Humphrey, J. D. and L. D. Ashburner. 1993. Spread of the bacterial fish pathogen Aeromonas 

salmonicida after importation of infected goldfish, Carrasius auratus, into Australia. Australian

Veterinary Journal. 70: 453 – 454.

Hulbert, P. J. 1985. Post-stocking performance of hatchery-reared yearling brown trout. New 

York Fish and Game Journal. 32: 1 – 8.

Husevåg, B. 1995. Starvation survival of the fish pathogen Aeromonas salmonicida in seawater. 

FEMS Microbiology Ecology. 16: 25 - 32.

Høie, S., M. Heum, and O. F. Thoresen. 1997. Evaluation of a polymerase chain reaction-based 

assay for the detection of Aeromonas salmonicida ss salmonicida in Atlantic salmon Salmo 

salar. Diseases of Aquatic Organisms. 30: 27-35. 

Høie, S., I. Dalsgaard, I. L. Aase, M. Heum, J. M. Thornton, and R. Powell. 1999. Polymerase 

chain reaction (PCR)-based typing analysis of atypical isolates of the fish pathogen Aeromonas 

salmonicida. Systematic and Applied Microbiology. 22: 403 – 411.

Jarp, J., K. Tangen, F. V. Willumsen, H. O. Djupvik, and A. M. Tveit. 1993. Risk factors for 

infection with Aeromonas salmonicida in Norwewgian freshwater hatcheries. Diseases of

Aquatic Organisms. 17: 81 – 86.
26

Johnsen, B. O.and A. J. Jensen. 1994. The spread of furunculosis in salmonids in Norwegian

rivers. Journal of Fish Biology. 45: 47 - 55.

Kay, W. W. and T. J. Trust. 1991. Form and functions of the regular surface array (S-layer) of 

Aeromonas salmonicida. Experientia. 47: 412 – 414.

Kay, W. W., J. T. Bulkley, E. E. Ishiguro, B. M. Phipps, J. D. L. Monette, and T. J. Trust. 1981. 

Purification and disposition of a surface protein associated with virulence of Aeromonas salmonicida. Journal of Bacteriology. 147: 1077 - 1084.

Killie, J. E. A., G. Eggset, and H. Mikkelsen. 1997. Immunocompetence and duration of

immunity against Vibrio salmonicida and Aeromonas salmonicida after vaccination of Atlantic

salmon (Salmo salar L.) at low and high temperatures. Developmental and Comparative 

Immunology. 21: 181.

Kincaid, H. L., Gray, M. J., Mengel, L. J., Brimm, S. 1997. National Fish Strain Registry –

Trout species tables of reported strains and broodstocks. U.S. Fish and Wildlife Service / U.S. 

Geological Survey. Washington, D.C. 165 pp.

King, C. H. and E. B. Shotts. 1988. Enhancement of Edwardsiella tarda and Aeromonas

salmonicida through ingestion by the ciliated protozoan Tetrahymena pyriformis. FEMS

Microbiology Letters. 51: 95 – 100.

Klontz, G. W., and J. W. Wood. 1973. Observations on the epidemiology of furunculosis disease 

in juvenile coho salmon (Oncorhynchus kisutch). Pages 1-8 in W. A. Dill, ed. Symposium on the 

major communicable fish diseases in Europe and their control. European Inland Fisheries

Advisory Commission. Technical Paper Number 17: Supplement 2.

Klontz, G. W., W. T. Yasutake, and A. J. Ross. 1966. Bacterial diseases of the Salmonidae in the 

Western United States: pathogenesis of furunculosis in rainbow trout. American Journal of

Veterinary Research. 27: 1455 - 1460.

Krantz, G. E., J. M. Reddecliff, and C. E. Heist. 1964. Immune response of trout to Aeromonas 

salmonicida. Part I. Development of agglutinating antibodies and protective immunity.

Progressive Fish-Culturist. 26: 3 - 10.

Laidler, L. A., J. W. Treasurer, A. N. Grant, and D. I. Cox. 1999. Atypical Aeromonas

salmonicida infection in wrasse (Labridae) used as cleaner fish of farmed Atlantic salmon, Salmo 

salar L., in Scotland. Journal of Fish Diseases. 22: 209 – 213.

Langefors A. Lohm J. Grahn M. Andersen O. von Schantz T. 2001. Association between 

major histocompatibility complex class IIB alleles and resistance to Aeromonas salmonicida in 

Atlantic salmon. Proceedings of the Royal Society of London. 268: 479 – 485. 

Lee, K. K.and A. E. Ellis. 1990. Glycerophospholipid: cholesterol acyltransferase complexed

with lipopolysaccharide (LPS) is a major lethal exotoxin and cytolysin of Aeromonas 

salmonicida: LPS stabilizes and enhances toxicity of the enzyme. Journal of Bacteriology. 172: 

5382 - 5393.
27

Lillehaug, A., T. Lunder, and T. T. Poppe. 1992. Field testing of adjuvanted furunculosis

vaccines in Atlantic salmon, Salmo salar L. Journal of Fish Diseases. 15: 485 - 496.

Mackie, T. J., J. A. Arkwright, T. E. Pryce-Tannatt, J. C. Mot tram, W. D. Johnston, and and w. 

J. M. Menzies. 1930. Furunculosis Committee interim report. H. M. Stationery Office,

Edinburgh. 65 pp.

Mackie, T. J., J. A. Arkwright, T. E. Pryce-Tannatt, J. C. Mot tram, . w. D. Johnston, and w. J. 

M. Menzies. 1933. Second interim report of the Furunculosis Committee. H. M. Stationery

Office, Edinburgh. 81 pp.

Maheshkumar, S. M., S. M. Goyal, and P. P. Economon. 1990. Concentration and detection of 

Aeromonas salmonicida from hatcehery water. Journal of Fish Diseases. 13: 513 – 518.

Marsh, M. C. 1905. The Cold Spring Harbor epidemic among trout. Tenth Annual Report of 

the Commissioners of Fisheries, Game, and Forests. State of New York Fish and Game

Commission. Pp. 125 – 139.

Mawdesley-Thomas, L. E. 1969. Furunculosis in the goldfish, Carassius auratus (L.). Journal of 

Fish Biology. 1:19 - 23.

McArdle, J. F., C. Dooley-Martyn, and F. McKierman. 1986. Histological examination of the 

gills as a method of detecting asymptomatic carriers of A. salmonicida in Atlantic salmon (Salmo 

salar). Bulletin of the European Association of Fish Pathologists. 6: 80 – 84. 

McCarthy, D. H. 1975. Detection of Aeromonas salmonicida antigen in diseased fish tissue.

Journal of General Microbiology. 88: 384 - 386.

McCarthy, D. H. 1977a. The identification and significance of atypical strains of Aepomonas 

salnonicida. Bull. Off. Int. Epizoot. 87: 459 - 463.

McCarthy, D. H. 1977b. Some ecological aspects of the bacterial fish pathogen Aepomonas 

salmonicida. Aquatic Microbiology. 6: 299 - 324.

McCarthy, D. H. and C. T. Rawle. 1975. The rapid serological diagnosis of fish furunculosis

caused by rough and smooth strains of Aepomonas salmonicida. Journal of General

Microbiology. 86: 185 - 187.

McCarthy, D. H. and P. Whitehead. 1977. An immuno-India ink tech- nique for rapid laboratory 

diagnosis of fish furunculosis. Journal of Applied Bacteriology. 42: 429 - 431

McCarthy, D. H. and R. J. Roberts. 1980. Furunculosis of fish--the present state of our

knowledge. Pages 293-341 in M. R. Droop and H. W. Jannasch, eds. Advances in Aquatic

Microbiology, Vol. 2. Academic Press, London.

Midtlyng, P.J. 1993. Efficacy and side-effects in Atlantic salmon (Salmo salar L.) of injectable 

furunculosis vaccines. Special publication. European Aquaculture Society. Bredene; 19: 414; 

1993; In: From Discovery To Commercialization, Carrillo, M.;Dahle, L.;Morales, J.;Sorgeloos,

P.;Svennevig, N.;Wyban, J. (eds.)
28

Midtlyng, P.J. 1994. Growth of Atlantic salmon after intraperitoneal injection of oil-adjuvanted 

furunculosis vaccines. International Symposium on Aquatic Animal Health, Seattle, WA (USA),

4-8 Sep 1994. Univ. Of California, School Of Veterinary Medicine: Davis, Ca (Usa), Pp. P. W24.4; 1994; (International Symposium On Aquatic Animal Health: Program And Abstracts)

Midtlyng, P. J. and A. Lillehaug. 1998. Growth of Atlantic salmon Salmo salar after

intraperitoneal administration of vaccines containing adjuvants. Diseases of Aquatic Organisms.

32: 91 - 97.

Miyata, M., V. Inglis, and T. Aoki. 1996. Rapid identification of Aeromonas salmonicida

subspecies salmonicida by the polymerase chain reaction. Aquaculture. 141: 13 - 24.

Miyazaki, T. and S. S. Kubota. 1975a. Histopathological studies on the furunculosis of the

Amago. – II. Perbranchial infection. Fish Pathology. 9: 203 – 212.

Miyazaki, T. and S. S. Kubota. 1975b. Histopathological studies on the furunculosis of the

Amago. – III.. Perbcutaneous infection. Fish Pathology. 9: 213 – 218. 

Mooney, J., E. Powell, C. Clabby, and R. Powell. 1995. Detection of Aeromonas salmonicida in 

wild Atlantic salmon using a specific DNA probe test. Diseases of Aquatic Organisms. 21: 131 -

135.

Morgan, J. A. W, G. Rhodes, and R. W. Pickup. 1993. Survival of nonculturable Aeromonas 

salmonicida in lake water. Applied and Environmental Microbiology. 59: 874 - 880.

Nese, L. and ? . Enger. 1993. Isolation of Aeromonas salmnicida from salmon lice

Lepeophtheirus salmonis and marine plankton. Diseases of Aquatic Organisms. 19: 79 – 81.

Nielsen, B., J. E. Olsen, and J. L. Larsen. 1994. Ribotyping of Aeromonas salmonicida subsp. 

salmonicida. Diseases of Aquatic Organisms. 18: 155 – 158.

Nomura, T. 1993. The epidemiological study of furunculosis in salmon propagation. Scientific 

Reports of the Hokaido Salmon Hatchery (Japan). 47: 1 – 99.

Nordmo, R., A. Ramstad, and J. M. H. Riseth. 1998. Induction of experimental furunculosis in 

heterogeneous test populations of Atlantic salmon (Salmo salar) by use of a cohabitation

method. Aquaculture. 162: 11 – 21.

Oakey, H. J., J. T. Ellis, and L. F. Gibson. 1998. The development of random DNA probes 

specific for Aeromonas salmonicida. Journal of Applied Microbiology. 84: 37 - 46.

O'Brien, D., J. Mooney, D. Ryan, E. Powell, M. Hiney, P. R. Smith, and R. Powell. 1994. 

Detection of Aeromonas salmonicida, causal agent of furunculosis in salmonid fish, from the

tank effluent of hatchery-reared Atlantic salmon smolts. Applied and Environmental

Microbiology. 60: 3874 - 3877.
29

O’Hici, B., G. Olivier, and R. Powell. 2000. Genetic diversity of the fish pathogen Aeromonas 

salmonicida demonstrated by random amplified polymorphic DNA and pulse-field gel

electrophoresis analyses. Diseases of Aquatic Organisms. 39: 109 – 119.

Olivier, G. 1990. Virulence of Aeromonas salmonicida: lack of relationship with phenotypic

characteristics. Journal of Aquatic Animal Health. 2:119 - 127. 

Olivier, G. 1992. Furunculosis in the Atlantic Provinces: An overview. Bulletin of the

Aquaculture Association of Canada. 92: 4 – 10.

Paterson, W. D. and J. L. Fryer. 1974. Immune response of juvenile coho salmon

(Oncorhynchus kisutch) to Aeromonas salmonicida cells administered intraperitoneally in

Freund’s complete adjuvant. Journal of the Fisheries Research Board of Canada. 31: 1751 –

1755.

Paterson, W. D., D. Douey, and D. Desautels. 1980. Relationships between selected strains of

typical and atypical Aeromonas sa~onicidaJ Aeromonas hydrophila, and Hemophilus piscium. 

Canadian Journal of Microbiology. 26: 588 - 598.

Pavan, M. E., S. L. Abbott, J. Zorzopulos, and J. M. Janda. 2000. Aeromonas salmonicida

subsp. pectinolytica subsp. nov., a new pectinase-positive subspecies isolated from a heavily

polluted river. International Journal of Systematic and Evolutionary Microbiology. 50: 1119 –

1124.

Pedersen, K., H. Kofod, I. Dalsgaard, and J. L. Larsen. 1994. Isolation of oxidase-negative 

Aeromonas salmonicida from diseased turbot Scopthalmus maximus. Diseases of Aquatic

Organisms. 18: 149 – 154.

Perez, M. J., A. I. G. Fernandez, L. A. Rodriguez, and T. P. Nieto. 1995. Importance of the 

sample size to determine the survival time of Aeromonas salmonicida. Bulletin of the European 

Association of Fish Pathologists.15: 45 - 48.

Piper, R. G., I. B. McElwain, L. E. Orme, J. P. McCraren, L. G. Fowler, and J. R. Leonard. 1982. 

Fish Hatchery Management. United States Department of the Interior, Fish and Wildlife Service, 

Washington DC. 517 pp.

Pol, J. M. A., R. Bootsma, and J. M. Berg-Blommaert. 1980. Pathogenesis of carp

erythrodermatitis (CE): role of bacterial endo- and exotoxin. Pages 120 - 125 in w. Ahne, ed. 

Fish diseases. Third COPRAQ-Session. Springer-Verlag, Berlin, Heidelberg, New York.

Popoff, M. 1969. A study of Aeromonas salmonicida. I. Biochemical and antigenic

characteristics. Ann. Rech. Vet. 3: 49 -57.

Powell, R., J. L. Larsen, S. Hoie, I. Dalsgaard, B. Gudmundsdottir, and B. Austin. 1998. 

Improved identification and taxonomy of atypical isolates of the fish pathogen Aeromonas 

salmonicida. European Commission DG 12 Science, Research and Devevelopment:

Luxembourg. Pp. 110 – 113; Third European Marine Science and Technology Conference. 

Lisbon 23 – 27 May 1998. Volume 5. Fisheries and Aquaculture (AIR: 1990-94).
30

Price, N. C., L. Stevens, D. Duncan, and M. Snodgrass. 1989. Proteases secreted by strains of 

Aeromonas salmonicida. Journal of Fish Diseases. 12: 223 - 232.

Rabb, L., J. W. Cornick, and L. A. McDermott. 1964. A macroscopic slide agglutination test for 

presumptive diagnosis of furun- culosis in fish. Progressive Fish-Culturist. 26: 118 - 120.

Rose, A. S., A. E. Ellis, and A. L. S. Munro. 1990a. The survival of Aeromonas salmonicida

subsp. salmonicida in sea water. Journal of Fish Diseases. 13: 205 - 214.

Rose, A. S., A. E. Ellis, and A. L. S. Munro. 1990b. Evidence against dormancy in the bacterial 

fish pathogen Aeromonas salmonicida subsp. salmonicida. FEMS Microbiology Letters. 68: 

105 - 108. 

Ross, A. J. 1962. Isolation of a pigment-producing strain of Aeromonas liquefaciens from silver 

salmon (Oncorhynchus kisutch). Journal of Bacteriology. 84: 590 – 591.

Ross, A. J., and C. A. Smith. 1972. Effect of two iodophors on bacterial and fungal fish pathogens. 

Journal of the Fisheries Research Bopard of Canada. 29: 1359 – 1361.

Sakai, D. K. 1977. Causative factor of Aeromonas salmonicida in salmonid furunculosis: 

extracellular protease. Scientific Reports of the Hokaido Salmon Hatchery. 32: 61 - 89.

Sakai, D. K. 1978. Colliquative activity of purified protease for muscular tissue in Aeromonas 

salmonicida subsp. salmonicida. Scientific Reports of the Hokaido Salmon Hatchery. 33: 55 –

73. 

Sakai, D. K. 1985. Loss of virulence in a protease-deficient mutant of Aeromonas salmonicida. 

Infection and Immunity. 48: 146 - 152.

Sakai, D. K. 1986. Electrostatic mechanism of survival of virulent Aeromonas salmonicida

strains in river water. Applied and Environmental Microbiology. 51: 1343 – 1349.

Sako, H., N. Ishida, Y. Maeno, and M. Sorimachi. 1988. Bactericidal activities of five

disinfectants on Aeromonas salmonicida, Vibrio anguillarum and V. ordalii. Fish Pathology. 

23: 219 – 229.

Scallan, A. and P. Smith. 1993. Importance of sampling time in detecting stress inducible

furunculosis in Atlantic salmon smolts. Bulletin of the European Association of Fish

Pathologists. 13: 77 - 78.

Scallan, A., C. Hickey, and P. Smith. 1994. Evidence for the transient nature of strees

indiucible asymptomatic Aeromonas salmonicida infections of Atlantic salmon. Bulletin of the

European Association of Fish Pathologists. 13: 210 – 212.

Schultz, D. 1980. Erythrodermatitis of carp: studies of the mode of infection. Pages 137 - 144 in 

W. Ahne, ed. Fish diseases. Third COPRAQ-Session. Springer-verlag, Berlin, Heidelberg, New

York.
31

Scott, M. 1968. The pathogenicity of Aeromonas salmonicida in sea and brackish waters. Journal 

of General Microbiology. 50: 321 - 327.

Shieh, H. S. 1985. Correlation between cell virulence and protease toxicity of Aeromonas 

salmonicida isolates. Microbios Letters. 28: 69 - 72.

Shieh, H. S. and J. R. MacLean. 1975. Purification and proper- ties of an extracellular protease 

of Aeromonas salmonicida, the causative agent of furunculosis. International Journal of

Biochemistry. 6: 653 - 656.

Shimura, S., K. Innoue, M. Kudo, and S. Egusa. 1983. Studies on effects of parasitism of

Argulus corregoni (Crustacea: Branchiura)on furunculosis of Oncorhynchus masou

(Salmonidae). Fish Pathology. 18: 37 – 40.

Smith, P. R. 1991. Stress test picks up furunculosis carriers. Fish Farmer. 14: 18.

Snieszko, S. F. 1952. Ulcer disease in brook trout (Salvelinus fontinalis): its economic

importance, diagnosis, treatment and prevention. Progressive Fish-Culturist. 14: 43 - 49.

Snieszko, S. F., and S. B. Friddle. 1948. A contribution to the etiology of ulcer disease of trout. 

Transactions of the American Fisheries Society. 78: 56 - 63.

Snieszko, S. F., and E. M. Wood. 1955. The effect of some sulfonamides on the growth of brook 

trout, brown trout, and rainbow trout. Transactions of the American Fisheries Society. 84: 86 -

92.

Snieszko, S. F., P. J. Griffin, and S. B. Friddle. 1950. A new bacterium (Hemophilus piscium n. 

sp.) from ulcer disease of trout. Journal of Bacteriology. 59: 699 - 710.

Sovenyi, J. F., M.Bercsenyi, and J.Bakos. 1988. Comparative examination of susceptibility of

two genotypes of carp (Cyprinus carpio L.) to infection with Aeromonas salmonicida. 

Aquaculture. 70: 301 - 308.

Starliper, C. E. 2001. The effect of depuration on transmission of Aeromonas salmonicida

between the bivalve Amplema plicata and Arctic char. Journal of Aquatic Animal Health. 13: 56 

– 62.

Tajima, K., T. Takahashi, Y. Ezura, and T. Kimura. 1984. Enzymatic properties of the purified 

extracellular protease of Aeromonas salmonicida , Ar-4 (EFDL) Bulletin of the Japanese Society 

of Scientific Fisheries. 50: 145 - 150.

Takahashi, K., T. Kawana, and T. Nakamura. 1975. Studies on ulcer disease of goldfish – III. 

Infection experiments. Fish Pathology. 9: 187 – 192.

Teska, J. D. and R. C. Cipriano. 1993. Nonselective nature of Coomassie brilliant blue agar for 

the presumptive identification of Aeromonas salmonicida in clinical specimens. Diseases of

Aquatic Organisms. 16: 239 – 242.
32

Thornton, J. M., D. A. Austin, B. Austin, and R. Powell. 1999. Small subunit rRNA gene

sequences of Aeromonas salmonicida subsp. smithia and Hemophilus piscium reveal pronounced 

similarities to A. salmonicida subsp. salmonicida. Diseases of Aquatic Organisms. 35: 155 –

158.

Treasurer, J. W. and L. A. Laidler. 1994. Aeromonas salmonicida infection in wrasse

(Labridae) used as cleaner fish on an Atlantic salmon, Salmo salar L., farm. Journal of Fish

Diseases. 17: 155 – 161. 

Trust, T. J. A. G. Khouri, R. A. Austen, and L. D. Ashburner. 1980. First isolation in Australia 

of atypical Aeromonas salmonicida. FEMS Microbiology Letters. 9: 39 – 42.

Trust, T.J., W. W. Kay, E. E. Ishiguro, J. T. Buckley, and T. W. Pearson. 1981. Properties of a 

protein, a virulence factor on the surface of Aeromonas salmonicida. “Conference on

Immunology and Immunization of Fish,” van Muiswinkel, W.B.;Cooper, E.L. (eds.)

Wageningen (Netherlands), 22 - 24 Jun 1981. Developmental and Comparative Immunology. 

Suppl. 2: 175 - 180.

Tuffery, G., and C. Dehand. 1979. Experimental study of the conditions for isolation of the agent 

of carp erythrodermatitis. Bull. Fr. Piscic. 275: 83 - 89. 

Udey, L. R. 1978. An additional cell wall layer associated with virulence of the fish pathogen,

Aeromonas salmonicida. Abstracts of the Annual Meeting of the American Society for

Microbiology. 78. (Abstract B-66)

Umelo, E. and T. J. Trust. 1998. Physical map of the chromosome of Aeromonas salmonicida

and genomic comparison between Aeromonas strains. Microbiology. 144: 2141 – 2149.

USFWS. 1995. U.S. Fish and Wildlife Service, Fisheries: Fish Health Operations. U. S.

Department of the Interior. Washington DC. FWM 170, Part 713 FW, pp. 1 - 4.

Wedemeyer, G. A., and N. C. Nelson. 1977. Survival of two bacterial fish pathogens

(Aeromonas salmonicida and the enteric redmouth bacterium) in ozonated, chlorinated, and

untreated water. Journal of the Fisheries Research Board of Canada. 34: 429 - 432.

Wedemeyer, G., A. J. Ross, and L. Smith. 1969. Some metabolic effects of bacterial endotoxins 

in salmonid fishes. Journal of the Fisheries Research Board of Canada. 26: 115 - 122.

Whittington, R. J., N. Gudkovs, M. J. Carrigan, L. D. Ashburner, and S. J. Thurstan. 1987. 

Clinical, microbiological and epidemiological findings in recent outbreaks of goldfish ulcer

disease due to atypical Aeromonas salmonicida in southeastern Australia. Journal of Fish

Diseases.10: 353 - 362.

Wiegertjes, G. F., J. G. Daly, and W. B. van Muiswinkel. 1993. Disease resistance of carp, 

Cyprinus carpio L.: identification of individual genetic differences by bath challenge with

atypical Aeromonas salmonicida. Journal of Fish Diseases. 16: 569 - 576.
33

Wiklund, T. 1995. Virulence of 'atypical' Aeromonas salmonicida isolated from ulcerated

flounder Platichthys flesus. Diseases of Aquatic Organisms. 21: 145 - 150.

Wiklund, T. and I. Dalsgaard. 1998. Occurrence and significance of atypical Aeromonas 

salmonicida in non-salmonid and salmonid fish species: a review. Diseases of Aquatic

Organisms. 32: 49 - 69.

Wiklund, T., I. Dalsgaard, E. Eerola, and G. Olivier. 1994. Characteristis of ‘atypical’

cytochrome oxidase-negative Aeromonas salmonicida isolated from ulcerated flounders

(Platichthys flesusL.). Journal of Applied Bacteriology. 76: 511 – 520.

Wolf, L. E. 1938. Observations on ulcer disease of trout. Transactions of the American Fisheries 

Society. 68: 136 - 151.

Wolf, L. E. 1953. Development of disease-resistant strains of fish. Transactions of the American

Fisheries Society. 83: 342 - 349.

Wooster, G. A.and P. R. Bowser. 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 World Aquaculture Society. 27: 7 - 14.

Yamada, Y., Y. Kaku, and H. Wakabayashi. 2000. Phylogenetic intra-relationships of atypical 

Aeromonas salmonicida isolated in Japan as determined by 16S rDNA sequencing. Gyobyo

Kenkyu/Fish Pathology. 35: 35 – 40.