1. Nature of the Disease

Furunculosis is a highly contagious, bacterial disease capable of causing high levels of morbidity and mortality in salmonid fish, particularly in unvaccinated populations. All age groups of salmonids in both fresh water and salt water are susceptible.

Furunculosis is exotic to Australia.

1.1 Aetiology

The aetiological agent of furunculosis in salmonids is the bacterium Aeromonas salmonicida subspecies salmonicida, which is commonly known as the ‘typical’ strain of A. salmonicida. This strain is exotic to Australia. For the purpose of this manual, furunculosis will be used to denote both infection and disease with A. salmonicida subspecies salmonicida (referred to as A. salmonicida subsp. salmonicida throughout this document) in salmonids and not infection or disease with other subspecies (biovars).

This is a critical distinction, as the ‘typical’ strain of the bacterium is exotic to Australia while other subspecies of the bacterium, commonly called ‘atypical’ strains, are not.  Atypical strains will not be discussed except to highlight where their presence may complicate diagnosis and surveillance of the typical strain.

A. salmonicida subsp. salmonicida is a non-motile, gram-negative rod of the family Aeromonadaceae (NCBI 2008). This was the first biovar of the species recognised and subsequently designated as a subspecies. A characteristic of this bacterium is the formation of a brown, diffusible pigment on tryptone soy agar (TSA) although this characteristic is found in some atypical strains as well. A. salmonicida subsp. salmonicida has been shown to be genetically homogeneous (O’hIci, Olivier & Powell 2000).

1.2 Susceptible species

Furunculosis may affect all species and all ages of both freshwater and marine salmonids, with brook trout (Salvelinus fontinalis) and brown trout (Salmo trutta) being particularly susceptible.

In Australia, all wild and farmed salmonid species, including Atlantic salmon (Salmo salar), rainbow trout (Oncorhynchus mykiss) and brown trout (Salmo trutta) are considered susceptible to the disease.

Non-salmonid species of fish, in both freshwater and marine environments, are also susceptible to infection with A. salmonicida subsp. salmonicida (Table 1). Some of these findings were associated with an outbreak of furunculosis in salmonids; for example, where non-salmonid ‘cleaner fish’ (fish used to ‘clean’ the salmon of external parasites) have been held in farmed salmon sea cages in which salmon have furunculosis.

The importance of this is that although it is likely that the greatest impact of the disease will be on salmonid fish, non-salmonid fish species are capable of being infected and may transfer the pathogen.

A. salmonicida subsp. salmonicida is not a human pathogen.

Table 1 - Examples of non-salmonid species susceptible to Aeromonas salmonicida subsp. salmonicida"

Scientific name	Common name	Natural or experimental infection	Genus present in Australia?	Reference
Anarhichas lupus	Wolf-fish	Natural	No	Lillehaug, Lunestad & Grave (2003)
Anguilla rostrata	Eel	Natural	Yes	Hayasaka & Sullivan (1981)ª
Gadus morhua	Atlantic cod	Natural/experimental (limited)	No	Hjeltnes et al. (1995); Lillehaug, Lunestad & Grave (2003)
Hippoglossus hippoglossus	Halibut	Natural/experimental (limited)	No	Hjeltnes et al. (1995); Lillehaug, Lunestad & Grave (2003)
Labridae spp.	Wrasse	Experimental	Yes	Hjeltnes et al. (1995)
Notropis cornutus	Common shiners and other freshwater baitfish	Natural	Yes	Ostland, Hicks & Daly (1987)
Petromyzon marinus	Sea lamprey	Natural	No	El Morabit, García-Márquez & Santos (2004)
Psetta maxima	Turbot	Natural	No	Lillehaug, Lunestad & Grave (2003)
Sander lucioperca	Pike perch	Experimental	No	Siwicki et al. (2006)
Sparus aurata	Sea bream	Natural	Yes	Real et al. (1994)
ª This paper reports eels as being infected with ‘furunculosis’, but the bacterium isolated from diseased eels was A. salmonicida with no differentiation as to subspecies.

1.3 World Distribution

Furunculosis is enzootic in northern European salmonid-producing countries, including Norway, Scotland and Ireland, as well as in North America, South Africa and Japan. It is an economically significant disease in these regions, although improved management and husbandry practices (including vaccination) have led to decreased mortality rates and outbreaks of clinical disease.

There has been no occurrence of furunculosis in Australia or New Zealand, and vaccination specific for this disease is not practiced.

1.4 Confirmation and differential diagnosis

1.4.1 Confirmation

For the purposes of this manual, confirmation of furunculosis will require the following:

• Where there are clinical signs and gross pathology in salmonids:
  
• 1. observation of clinical signs and gross pathology consistent with furunculosis
  2. presumptive identification of A. salmonicida subsp. salmonicida at the jurisdictional veterinary laboratory
  3. confirmation of A. salmonicida subsp. salmonicida by CSIRO Australian Fish Diseases Laboratory (AFDL). AFDL has evaluated and validated polymerase chain reaction (PCR) tests for detection and identification of A. salmonicida isolates (Byers, Gudkovs & Crane 2002; Byers et al. 2002).

• Where there is suspected subclinical (covert) infection in salmonids:
  
• 1. if clinical disease can be induced using a stress test, confirmation of A. salmonicida subsp. salmonicida by CSIRO AFDL using a combination of cellular and colonial morphology, and biochemical characteristics
  2. If clinical disease cannot be induced, a presumptive diagnosis of furunculosis can be made using molecular and immunological tests to detect A. salmonicida subsp. salmonicida as described above.

It is possible that A. salmonicida subsp. salmonicida may be isolated from a non-salmonid fish. In this case, CSIRO AFDL will confirm its presence, probably using PCR tests and sequence analysis. By definition, A. salmonicida subsp. salmonicida in a non-salmonid species is not called furunculosis. However, confirmation of the pathogen in this manner will still invoke the same disease response options as would the finding of furunculosis.

1.4.2 Differential diagnosis

Clinical signs observed during outbreaks of furunculosis are not specific for this disease. Therefore, differential diagnoses could include any fish disease that has the ability to cause similar, if not the same, clinical signs accompanied by high morbidity and mortality in salmonid fish. The most likely differential diagnoses are bacterial septicaemic and haemorrhagic viral conditions.

Enzootic diseases include:

• vibriosis—in particular caused by Vibrio anguillarum
• epizootic haematopoietic necrosis (EHN)—caused by EHN virus
• septicaemic conditions caused by atypical A. salmonicida.

Exotic diseases include:

• viral haemorrhagic septicaemia (VHS)—caused by VHS virus
• infectious haematopoietic necrosis (IHN)—caused by IHN virus
• vibriosis caused by a number of exotic Vibrio species.

Non-infectious conditions can cause clinical signs that resemble those observed in furunculosis. These include trauma from, for example, grading or electrocution. However, it is unlikely that these signs will be associated with high morbidity and mortality in the population.

Further information on both confirmation and differential diagnosis of furunculosis are provided in Appendix 1.

1.5 Resistance and immunity

The immune system of fish includes both innate and adaptive immunity. In comparison to mammals, the innate immune system in fish is generally more highly developed than the adaptive immune system (Watts, Munday & Burke 2001; Whyte 2007). In healthy fish, non-specific, innate defence mechanisms are immediately available to help prevent pathogenic invasion. These mechanisms include:

• physical barriers—scales, skin and associated mucous layers
• bioactive molecules—antimicrobial peptides, complement, lectins, antibodies, lysozyme, cytokines and other bacteriolytic enzymes (often found within mucous layers)
• inflammatory response cells—phagocytic cells and other leucocytes.

A. salmonicida subsp. salmonicida is a facultative intracellular pathogen. This intracellular attribute may allow this bacterium to temporarily avoid the host immune system once it has successfully invaded the fish host (Dacanay et al. 2003).

The specific defence mechanisms of the adaptive immune response are delayed relative to the innate immune response. This active immune response involves both the production of specific antibodies (in fish this is immunoglobulin M only, as fish are not known to possess immunoglobulin G) and the activation of leucocytes.

Salmonid populations do not gain any long-term, specific immunity to A. salmonicida subsp. salmonicida after an outbreak of furunculosis. Thus, the adaptive immune response of fish does not protect against recurring episodes of furunculosis after natural infection.

Genetic resistance to furunculosis has been shown to have high heritability (Gjedrem 2000). Some populations of brook trout (Salvelinus fontinalis) and rainbow trout (Oncorhynchus. mykiss) have been selected for their heritable, innate resistance to furunculosis (Cipriano et al. 2002), which was linked to increased serum bactericidal activity (Hollebecq et al. 1995).

Vaccination, however, does lead to the production of antibodies against both cellular and soluble antigens of A. salmonicida. Vaccination also stimulates cellular immunity (Håstein, Gudding & Evensen 2005). Most vaccines use oil-based adjuvants because they confer superior protection and duration of protection compared to other adjuvants (Håstein, Gudding & Evensen 2005). Potent adjuvants like oil can cause intense local tissue reactions in the fish, which can be a downside of the vaccination process (see Figure 1).

Photo: P Hardy-Smith

Figure 1 - Peritoneal cavity of an Atlantic salmon showing severe local tissue reaction, including extensive melanisation in response to injection with an oil-based vaccine. Although not a typical response, it does demonstrate the severity of the reaction to the oil adjuvant.

Vaccines are included in furunculosis management strategies overseas to provide protection against clinical furunculosis. However, there are no vaccines available that prevent or eliminate covert infections of A. salmonicida subsp. salmonicida (Hiney 1999; Hiney, Smith & Bernoth 1997). Vaccination does not fully protect a population although, anecdotally, the protective effect of vaccines against furunculosis in the field has been reported to range from ‘acceptable’ to ‘very good’ (Håstein, Gudding & Evensen 2005).

Håstein, Gudding and Evensen (2005) note that both typical and atypical A. salmonicida have antigenic characters in common. Vaccination of fish against A. salmonicida subsp. salmonicida may to some extent provide protection against infection with atypical A. salmonicida. There are no furunculosis vaccines currently approved for use in Australia. However, there is a bivalent vaccine available under a minor use permit (MUP number 9793) that is currently being used in Tasmania. This vaccine contains an inactivated atypical strain of A. salmonicida. Whether Tasmanian Atlantic salmon vaccinated against an atypical strain will be protected against challenge from the typical strain is not known.

A list of furunculosis vaccines available overseas at the time of writing is provided in Appendix 2.

Leucine metabolites (e.g. β-hydroxy-β–methylbutyrate) and probiotics (e.g. Lactobacillus spp.) significantly reduced mortalities due to furunculosis when fish were challenged with A. salmonicida subsp. salmonicida, indicating a significant innate response against this pathogen (Nikoskelainen et al. 2001; Siwicki et al.2006). However, using these products in the face of a furunculosis outbreak is not recommended, as this was experimental work and the efficacy of this approach in practice has not been shown.

1.6 Epidemiology

The epidemiology of furunculosis is not fully understood, but many factors are involved in the development of the disease following infection with A. salmonicida subsp. salmonicida (Smith 1997).

A key aspect of the epidemiology of furunculosis is that covert infections are common and may persist in fish populations for months. Stressors can cause covert infections to progress to clinical disease. Covert infections in salmonids or other fishes are a major factor in managing disease, particularly in the spread of infection.

There are a number of native marine and freshwater salmoniformes in Australia (e.g. Galaxiidae, Retropinnidae). Their distribution is more extensive than that of introduced salmonids. The susceptibility of native salmoniformes to furunculosis is not known, but needs epidemiological consideration as they may potentially have a profound effect on the spread of the disease.

1.6.1 Incubation period

At 14 °C, the period from exposure of naive fish to A. salmonicida subsp. salmonicida (by cohabitation with infected fish) to bacterial shedding can be as short as three days. Death can occur as soon as two days later (i.e. at five days post–exposure; Ogut & Reno 2005).

At lower temperatures, the time between infection and death may be prolonged. This may be due to the effects of temperature on pathogen multiplication and host defence mechanisms (Groberg et al. 1978).

In Australia, summer water temperatures in both fresh water and salt water where salmonids are farmed may exceed 18 °C. Hence, it is reasonable to assume that the incubation period for furunculosis could be as short as three days in many parts of Australia where salmonids are present. In winter the incubation period may be longer.

If wild salmonids in Australia are affected by furunculosis, it is possible that deaths due to the disease may not be observed, at least in the early stages. This must be considered when determining how long the disease has been present in wild populations if furunculosis is confirmed.

1.6.2 Persistence of the pathogen

General properties

A. salmonicida subsp. salmonicida is considered to be capable of surviving in a pathogenic form outside its host in marine, brackish and freshwater environments, and for prolonged periods (many months) in some waters and sediment (Hiney et al. 2002). The pathogen is also known to persist in animal reservoirs, as summarised in Table 2.

However, the period of survival reported in the scientific literature differs greatly. Reasons for the differences include:

• that cell survival is highly dependent on the composition and structure of the sediment within which survival is determined (Hiney et al. 2002)
• that A. salmonicida subsp. salmonicida is likely to survive in a non-culturable but viable state (as noted in Section 1.4.3), thus eluding common methods of detection (Pickup et al. 1996)
• the difficulties associated with isolating the pathogen from contaminated environmental samples (Hiney, Smith & Bernoth1997).

Hiney et al. (2002) note that because survival is highly dependent on many factors, no single figure for survival time in the environment should be used as an estimate for risk assessment.

Table 2 - Reservoirs and potential transport hosts of Aeromonas salmonicida subsp. salmonicida

Reservoirs and transport hosts	Marine farms	Freshwater farms and hatcheries
Breeding stock from marine farms (covert infections)	na	Yes
Farm equipment	Yes	Yes
Other infected fish (cultured or wild) in the water system	Yes	Yes
Personnel	Yes	Yes
Smolts from hatcheries (covert infections)	Yes	na
Transfer of infection between closely neighbouring farms (sediment water, birds)	Yes	Yes
Water transfer from infected hatcheries to marine farms	Yes	na

na = not applicable
Source: Smith (1997).

Live fish

overtly infected wild and farmed fish may act as reservoirs of A. salmonicida subsp. salmonicida (Bernoth 1997; Ferguson 1988). This includes both salmonid and non-salmonid fish. Continuous shedding of bacteria and re-infection can maintain the infection without additional introduction of the bacterium (Hiney, Smith & Bernoth1997).

The epidemiological relationship between wild and farmed fish is unclear, although covertly infected wild fish present in rivers supplying freshwater farms appear to influence the incidence of covert infections in hatchery fish populations (McCarthy 1977). Stress experienced by these wild fish populations during spawning and smoltification might account for seasonal fluctuations in the frequency of stress-inducible furunculosis infections in hatchery fish populations (Hiney, Smith & Bernoth 1997). Indirect evidence (Jarp et al. 1993) and epidemiological models (Johnsen & Jensen 1994) suggest that covertly infected migratory fish that escape from marine pens may transfer infection to freshwater fish or their environment by migrating upstream into rivers.

Other vertebrate animals

Animals that may come in contact with infected fish should be considered potential transport hosts capable of spreading viable A. salmonicida subsp. salmonicida. For example, sea birds and rodents around land-based farms could carry the lipophilic aggregates of free A. salmonicida subsp. salmonicida cells (Enger 1997) and transfer the bacteria to the fish.

Aquatic invertebrates

Marine plankton, protozoa and other ectoparasites such as copepods (e.g. salmon louse) and branchiurans may act as reservoirs of A. salmonicida subsp. salmonicida (Nese & Enger 1993). Bivalve molluscs can acquire A. salmonicida subsp. salmonicida via filter feeding and then act as a source either directly or via translocation (Starliper 2001).

Water

The bacterium is considered to be capable of surviving in a pathogenic form outside its host in marine, brackish and freshwater environments (Hiney et al. 2002).

Survival times for A. salmonicida subsp. salmonicida in fresh water and sea water vary greatly, being from 2 to 63 days and 2 to 24 days respectively (Hiney 1994). Other studies have shown a 90% reduction in the number of colony-forming cells after 1.4–2.2 days in sea water and 3.4 days in brackish water or fresh water (Enger 1997; McCarthy 1977; Rose, Ellis & Munro 1990). Survival time is dependent on many factors including temperature, salinity and the presence of organic matter.

Biofilms

A. salmonicida subsp. salmonicida is capable of adhering to solid surfaces (Carballo, Seoane & Nieto 2000), and hence may be present in the biofilm but not detectable in the water column. Biofilms are microenvironments that can be important in protecting bacteria from lethal factors.

Sediment

Sediment is an important environmental reservoir of A. salmonicida subsp. salmonicida as the pathogen can survive and retain its pathogenicity in faecal and food waste sediment at the bottom of sea cages, freshwater tanks or in pond mud (Hiney 1994; Munro & Hastings 1993). For example, A. salmonicida subsp. salmonicida was detectable in non-sterile pond mud for at least 29 days (McCarthy 1977), retaining its pathogenicity in such mud for 6–9 months (Plumb 1999). Viable A. salmonicida subsp. salmonicida cells were detected for more than 105 days when the pathogen was exposed to organic particulate matter (Sakai 1986).

In the absence of overt disease, A. salmonicida subsp. salmonicida can persist in marine salmon farms for periods of up to six months (Smith et al. 1982).

Hiney et al. (2002) showed that A. salmonicida subsp. salmonicida in a sediment–water mix remains viable for as long as 276 days.

Farm equipment

During an outbreak of furunculosis, it is likely that farm equipment will become contaminated with A. salmonicida subsp. salmonicida.

A. salmonicida subsp. salmonicida can survive for up to six days on both wet and dry contaminated fish nets (McCarthy 1977). In Sweden, contaminated equipment has been implicated in the spread of furunculosis to uninfected sites on at least two occasions (Wichard, Johansson & Ljungberg 1989). The surface of the equipment may be important; one study indicated that A. salmonicida subsp. salmonicida attached to plastics in much higher numbers than to stainless steel (Carballo, Seoane & Nieto 2000).

1.6.3 Modes of transmission

Horizontal spread

A. salmonicida subsp. salmonicida is shed into the environment primarily by clinically diseased and dead fish, which are the main environmental source of this pathogen. Shedding from live, clinically affected fish is primarily via faeces and urine, and from furuncular lesions (Enger et al. 1992; McCarthy 1977; Novotny 1978). It may also be shed from reservoirs of infection, such as resuspended infected sediment.

There are three potential portals of entry of A. salmonicida subsp. salmonicida into the fish: gills, skin and gastrointestinal tract.

Branchial (i.e. gill) colonisation with A. salmonicida subsp. salmonicida is frequently observed in infected fish (Ferguson 1988; Hiney 1994).The pathogen is often present on the external surfaces of infected fish and can readily invade via any form of skin lesion. A. salmonicida subsp. salmonicida is also able to colonise the intestinal lumen and cross the intestinal wall (Jutfelt et al. 2006; Ringø et al. 2004).

Horizontal transmission of furunculosis may occur if fish are exposed to:

• other fish (direct fish-to-fish contact); the risk of transmission occurring via this route increases with:
  - increased stocking densities (Ogut & Reno 2004)
  - fish crowding in one area of the enclosure
  - handling procedures
  - the presence of small, wild fish
  - introduced or naturally present ‘cleaner’ fish
• fresh water infected with A. salmonicida subsp. salmonicida (McCarthy 1977). Hatcheries can minimise outbreaks of furunculosis if their intake water is free from A. salmonicida subsp. salmonicida (Needham & Rymes 1992; P Hardy-Smith, pers. obs.)
• sea water infected with A. salmonicida subsp. salmonicida (Hiney 1994). The pathogen can potentially spread through the water column to neighbouring marine farms (Turrell & Munro 1988); this is dependent on water currents, density of fish in farms and pathogen load in the water
• lipid-rich bacterial aggregates found at the water surface; these adhere to birds or to food pellets dropped into the water and form aerosols in high winds (Enger 1997; Enger & Thorsen 1991)
• invertebrates such as sea lice (e.g. Lepeophtheirus salmonis) (Nese & Enger 1993) and bivalve molluscs (Starliper 2001). L. salmonis is not present in Australia but it is possible that ectoparasites found in Australia, such as branchiurans (e.g. Argulus spp.) and copepods (e.g. Caligus and Ergasilus) could become vectors for the transmission of A. salmonicida subsp. salmonicida.

Vertical spread

There is evidence that the pathogen is associated with surface contamination of fertilised eggs (Cipriano et al. 2001).

It is standard practice in farming areas where furunculosis is endemic to perform surface disinfection on all fertilised eggs using an iodine preparation. Cipriano et al. (2001) reported that an effective regime to prevent transmission of egg associated A. salmonicida subsp. salmonicida is to disinfect eggs twice; once using 50 mg/L active iodine for 30 minutes and then using 100 mg/L active iodine for 10 minutes.

1.6.4 Factors influencing transmission and expression of disease

Predisposing factors that lead to the development of clinical furunculosis are primarily those that cause the fish to be stressed, leading to elevated plasma cortisol levels and consequent leukocytopenia and immunosuppression. This makes the fish more susceptible both to primary infection and to the progression of clinical disease from covert infection with A. salmonicida subsp. salmonicida.

Endogenous factors

• Smoltification. Atlantic salmon (Salmo salar) are anadromous and ‘smolt’ at any time from one to three years of age. Smoltification is a process of extensive physiological change in preparation for the marine environment and can cause a prolonged period of stress.
• Spawning. The stress of spawning can also increase a salmonid’s susceptibility to furunculosis.

Exogenous factors

• Elevated temperature. This is considered a primary factor influencing the onset of clinical furunculosis. Water temperatures of 15–20 °C (as experienced in late spring, summer and early autumn in southern Australia) correlate with increased clinical signs of furunculosis as a direct result of temperature stress (Lillehaug, Lunestad & Grave 2003; Sako & Hara 1981), and also with more rapid growth of A. salmonicida subsp. salmonicida (Malnar, Teskeredzic & Coz-Racovac 1988; Pickering 1997). Groberg et al. (1978) showed that at 3.9 °C and 6.7 °C, mortality in fish infected with A. salmonicida varied from 2% to 26% among three salmonid species (Oncorhynchus mykiss, O. kisutch and O. tshawytscha), whereas at 20.5 °C, 93–100% of these fish died within 2–3 days. This paper did not specify a subspecies of A. salmonicida but the disease was reported as being furunculosis.
• Low levels of dissolved oxygen. Low dissolved oxygen can cause respiratory distress and may induce a classical stress response leading to infection and clinical furunculosis. Likewise, oxygen supersaturation can also predispose fish to infection, clinical disease and death.
• Poor water quality. This is closely associated with the onset of bacterial infections in fish. Exposure of fish to high ammonia levels, chlorine, pesticides, metal pollution, sewage sludge and other organic matter or respiratory waste can result in suppression of the immune system and greater susceptibility to infection.
• Physical damage to the skin and gills. Physical damage resulting from, for example, rough handling, predator attack, algal blooms and ectoparasites can lead to infection with A. salmonicida subsp. salmonicida (Morgan, Rhodes & Pickup 1993; Pickering 1997).
• Improper timing of transfer of fish from fresh water to sea water. In Atlantic salmon, the ‘smolt window’ (i.e. time during which fish are physiologically prepared for the transition from fresh water to salt water) is relatively narrow and does not necessarily occur at the same time for all fish within a population. It can be difficult to judge when a population of anadromous salmonids is capable of surviving the transfer from fresh water to seawater. ‘Pre-smolts’ who are not yet ready for transfer can suffer osmotic shock and severe immunosuppression if transferred into a full marine environment. Likewise, ‘post-smolts’ will also suffer osmotic stress before reverting back to a freshwater physiological state.
• Management practices. Management practices that may trigger a transient stress response in fish (Pickering & Pottinger 1989) include:
  - high stocking densities
  - grading
  - handling and hauling (transporting)
  - netting
  - injection and smolt transfer
  - lighting
  - inadequate predator protection
  - poor or inadequate nutrition, especially vitamin C deficiency.

Fish exposed to these transient stresses are less susceptible to bacterial infection than those exposed to chronic stresses, such as poor water quality (Pickering 1997).

Transmission of furunculosis is directly related to stocking density (Ogut & Reno 2004). Reducing stocking density (and hence stress) has reduced mortalities during a furunculosis outbreak (Glenn & Taylor 2006).

Stopping feeding can also reduce mortalities, although the reduction in mortality is often transitory (P Hardy-Smith, pers. obs.).

Psychological stress associated with social domination is one of the most potent forms of chronic stress in subordinate fish.

1.7 Impact of the disease

The Australian salmonid industry includes commercial farming, hatcheries, tourism and recreational fishing.

Salmonids are not native to the southern hemisphere, but have been introduced into Australia over the last 150 years. Salmonid imports have been prohibited under quarantine regulations since 1975. There are five species of exotic salmonids in Australia:

• Atlantic salmon (Salmo salar)
• brook trout (Salvelinus fontinalis)
• brown trout (Salmo trutta)
• chinook (quinnat) salmon (Oncorhynchus tshawytscha)
• rainbow trout (O. mykiss).

Of these species, brown, brook and rainbow trout have established self-sustaining populations where suitable conditions exist (Kahn et al. 1999). Wild populations of Atlantic and chinook salmon are supported by regular release of hatchery-bred fish.

Farmed salmonid production in Australia for the financial year 2007–08 was $299.3 million (ABARE 2009). This was produced by over 80 farms across Australia. Most production was in Tasmania ($290.9 million), which was predominantly Atlantic salmon.

In 1999, the recreational salmonid fishing sector was estimated to be worth approximately $234 million. In Tasmania, New South Wales and Victoria, salmonid fishing activity is significant. Trout fishing is important in Western Australia and South Australia (McIlgorm & Pepperell 1999). McIlgorm and Pepperell (1999) estimated a value of $1 025 million (highest estimate) arising from the total collapse of expenditure nationally due to disease over a five-year period, assuming a 6% discount rate. These estimates are ‘worst case scenarios’.

Therefore, there is considerable value in these industries, particularly in Tasmania where salmon farming is one of the most important animal production industries. If furunculosis was to become endemic in Australia, the value of these industries will decrease. The extent of the reduction would depend on the extent of the establishment of the disease. For example, if the disease became established in Tasmania, the reduction in value could conceivably be in the millions of dollars.

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