Global seafood security relies heavily on salmon aquaculture, a sector valued at over USD 20 billion annually, yet it faces mounting threats from infectious diseases that cause direct and indirect losses estimated at USD 1.5–2 billion each year. Bacterial pathogens such as Yersinia ruckeri (enteric redmouth disease), Aeromonas salmonicida (furunculosis), and Renibacterium salmoninarum (bacterial kidney disease) are responsible for high cumulative mortalities, with outbreaks reducing regional stock biomass by up to 30%. Viral agents, including infectious salmon anemia virus (ISAV), infectious pancreatic necrosis virus (IPNV), and piscine orthoreovirus (PRV), continue to drive trade restrictions and large-scale culling, while parasitic infestations by Lepeophtheirus salmonis (sea lice) alone incur treatment and production costs of USD 400–600 million annually. Emerging fungal pathogens, particularly Saprolegnia spp., exacerbate mortality during freshwater smoltification. Climate change, fluctuating salinity regimes, and intensive farming systems foster complex host–pathogen–environment interactions that enhance pathogen persistence, proliferation, and evolution. Despite advances in integrated pest management, vaccination, and antimicrobial stewardship, persistent challenges include antibiotic resistance, vaccine escape variants, and limited treatment options. Key research gaps involve insufficient integration of epidemiological forecasting with climate models, incomplete knowledge of pathogen life cycles and reservoirs, and limited understanding of host immune modulation. Future priorities should focus on next-generation vaccines, selective breeding for disease resistance, adoption of closed or semi-closed containment systems to reduce pathogen exchange with wild stocks, and multi-omics surveillance for early detection. Interdisciplinary research and ecosystem-based policy frameworks are critical to sustaining profitability, improving fish health, and maintaining ecological balance in salmon-producing regions.

Keywords: Disease management strategies; ecosystem based aquaculture; infectious diseases, pathogenesis; salmon aquaculture.

Aquaculture is now the fastest-growing sector of global animal food production, surpassing traditional capture fisheries. Indeed, in 2022, aquaculture accounted for nearly 51% of global aquatic animal output, underlining its critical role in meeting rising seafood demand.¹ Salmonids (family Salmonidae) are extremely essential in aquaculture for both economic and nutritional purposes. This group comprises Atlantic Salmon Salmo salar, Pacific salmon species such as Chinook Salmon Oncorhynchus tshawytscha, Coho Salmon O. kisutch, and Rainbow Trout O. mykiss, all of which are commonly cultivated in temperate and higher latitude zones (Figure 1). Farmed Atlantic salmon production reached 2.8 million tonnes in 2023, with Norway, Chile, Scotland, and Canada accounting for more than 90% of global output.¹ Rainbow trout yields are currently around 950,000 tonnes per year, with developing markets such as Australia, New Zealand, and Iceland increasing production even further.² Salmonids' market dominance stems from their efficient feed conversion, rapid development, and nutrient-rich flesh—particularly high levels of long-chain omega-3 fatty acids—which make them essential components of the global fish business.

Figure 1 Salmon producing countries in world.

However, the fast expansion of salmonid aquaculture, supported by advances in selective breeding, superior diets, and technological innovation, has hastened the emergence and spread of a variety of diseases. Farmed salmonids are exposed to a wide range of pathogens throughout their lifespan, including bacterial, viral, fungal, and parasitic infections, as well as non-infectious issues like nutritional deficiencies and environmental stress-related disorders. These conditions are caused by a complex combination of host genetics, pathogen virulence, and agricultural stresses such as temperature swings, salinity fluctuations, dissolved oxygen oscillations, and high stocking densities.³ Climate change exacerbates the problem by creating new ecological niches for illnesses and disrupting current disease patterns.

The economic burden of disease in salmonid aquaculture is staggering. Direct losses, such as mortality, slower growth, and lower carcass quality, are amplified by indirect costs associated with extended grow-out periods, increased veterinary treatments, and market interruptions. In Norway, the world's largest salmon producer, disease-related losses exceed USD 2 billion per year, with sea lice control alone accounting for over USD 700 million per year.⁴ Viral infections such as infectious salmon anaemia (ISA) and pancreas disease (PD) have traditionally resulted in large-scale culling and farm fallowing, whilst bacterial pathogens such as Piscirickettsia salmonis and Aeromonas salmonicida remain a hazard in high-density production regions.⁵ These findings emphasize the critical necessity for comprehensive disease management strategies.

Vaccines, selective breeding, stringent biosecurity measures, and chemotherapeutic treatments have all contributed to great progress. These procedures have significantly reduced the spread of diseases such as furunculosis and vibriosis.⁶ However, the struggle is far from over: antibiotic resistance, vaccine escape variants, and treatment-resistant parasite strains are all on the rise. Parasitic infections, particularly sea lice and amoebic gill disease (AGD), are notoriously difficult to control because they spread quickly in open-net pen systems and acquire treatment resistance.⁷ Furthermore, many high-impact viruses, such as piscine orthoreovirus (PRV) and infectious haematopoietic necrosis virus (IHNV), have no effective vaccines,⁸ indicating major gaps in our disease-control arsenal.

Climate change and worldwide fish commerce are further complicating salmonid health landscapes. Rising sea temperatures and changing salinity regimes encourage pathogen survival and dissemination, increasing infection risk in both farmed and wild populations.⁵ Cross-border movement of live fish and eggs raises the danger of pathogen spread, affecting regional biosecurity and disease control efforts.⁹

Despite substantial research and surveillance efforts, our understanding of salmonid disorders is still limited. The understanding of subclinical and chronic infections, mucosal immune responses, microbiome-pathogen interactions, and genetic disease resistance remains fragmented. Simultaneously, there is an urgent need for the development of cost-effective immunizations, precision medicines, and farm-level biosecurity frameworks that are in line with evolving regulatory, sustainability, and animal welfare requirements.

In this context, this review offers a critical synthesis of current information on microbiological (bacterial, viral, and fungal) and parasite diseases that endanger both farmed and wild salmonids. Their epidemiology, clinical symptoms, and pathophysiology are all thoroughly reviewed, as well as the available preventive and control strategies, including immunizations, medications, and biosecurity measures. The major purpose of this analysis is to enhance aquaculture sustainability and evidence-based fish health management by gathering key information, emphasizing recurring issues, and directing future research and policy initiatives. By embracing these perspectives, the study hopes to aid in the development of resilient, environmentally responsible salmon production methods that maintain animal welfare while meeting the growing global demand for high-quality aquatic protein.

Infectious diseases significantly hinder salmon aquaculture's productivity, profitability, and ecological sustainability; recent reviews show direct and control costs for major diseases, such as parasites and viruses, reach hundreds of millions of USD–EUR annually and with indirect market effects, damaged ecosystem and supply chain costs reach to multi-billion USD annually.^10,11 Annual control and production losses from parasitic sea lice (Lepeophtheirus and Caligus spp.) are estimated to be in the low hundreds of millions of euros (commonly quoted ≈€300M) due to repeated chemotherapeutant applications, mechanical delousing, lost growth and mortality, and the additional costs of managing evolving treatment resistance.^12,13 Viral epizootics such as infectious salmon anemia (ISAV) are epidemiologically unpredictable, and the disease can cause immediate culling and fallowing, resulting in huge economic losses in farms and regional levels (i.e., rapid economic shocks followed by prolonged recovery costs in Maine, Canada, and Chile).¹⁴ Likewise, pancreatic disease (PD) and other viral/bacterial syndromes reduce harvest weight and increase mortality. Empirical cohort studies and economic case studies show outbreak-level direct cost penalties (e.g., ~US$1.29 per kg lost in a representative Norwegian cohort, equivalent to multi-million USD farm-level impacts), prompting managerial responses (early harvest, vaccination, altered stocking) that produce further cost-benefit trade-offs.¹⁵ Regionally concentrated gill diseases, such as amoebic gill disease (AGD) in Tasmania, can erode nearly a tenth (and in some assessments up to ~9-14% of gross value of production) of affected farm revenue through mortality, recurrent freshwater or chemotherapeutant baths, and impaired growth.¹⁶ Recent CSIRO and FRDC reporting indicate annualized local losses in the order of tens of millions USD/AUD and declining treatment efficacy under warming and hydrological stress.¹⁷ Beyond direct monetary losses, the ecological externalities are increasingly quantified: robust field and modelling studies demonstrate that elevated lice loads on high-density open-net farms increase infestation pressure on wild juvenile salmon, reduce marine survival, and depress returns in impacted river systems, while chronic therapeutant application and large mortality events alter benthic community structure, scavenger dynamics, and microbial processes in farm proximity. Taken together, these lines of data suggest that disease management in salmon farming is both an enterprise-level economic and ecosystem governance issue. Mitigating the combined burden needs harmonized economic accounting, integrated farm-wild surveillance, explicit inclusion of climate-driven risk forecasts in site planning, and faster deployment of non-chemical prophylactic and structural treatments (vaccines, selective breeding for resistance, closed or semi-closed confinement) whose costs and benefits must be balanced against private losses and public ecological externalities.^18,1

Enteric redmouth disease/ yersiniosis

Etiology and epidemiology: Enteric redmouth disease (ERM), also known as Yersiniosis, is caused by the gram-negative bacterium Yersinia ruckeri,²⁰ which exists in both motile and nonmotile forms. Redmouth disease was first detected in Idaho rainbow trout in the 1950s (LSC).²¹ The illness mostly affects salmonids, notably Atlantic Salmon.

ERM is commonly associated with the freshwater and early marine stages of salmon aquaculture.²² Transmission occurs through water channels, horizontal dispersion via excrement or contaminated equipment, and carrier fish. Stress factors, including handling, temperature fluctuations (especially between 15-20°C), poor water quality, and high stocking densities, all contribute to breakouts.²³ Y. ruckeri occurs in aquatic environments and infects fish via their gills, gastrointestinal tract, or skin lesions.

Clinical signs and pathogenesis:  Clinical signs (Figure 2A) include anorexia, exophthalmia, lethargy, hemorrhage around the mouth (redmouth), gills, fins, eyes, and bloated abdomens due to ascites.²⁴ Internally, petechial hemorrhages occur in the pyloric caeca, liver, and kidney. Histopathology reveals necrosis in hematopoietic tissues (spleen and kidney), enteritis, and liver deterioration. Septicemia is frequent in the late stages. Infected fish can discharge a significant amount of bacteria in their feces. The bacterium is also found in ovarian fluid and milt. Both acute and chronic cases led to high or moderate fatality rates.²⁵

Prevention and control measures: ERM in Atlantic Salmon is mostly controlled through vaccination, biosecurity measures, and selective breeding.^26,27 Vaccination with inactivated (bacterin) vaccines remains the most effective preventative approach, notably against Yersinia ruckeri serotype O1 strains, and is generally administered via immersion or injection. Furthermore, effective biosecurity measures—such as improved farm hygiene, water disinfection, and stress reduction—are essential for disease prevention. Finally, ongoing research into the selective breeding of genetically resistant salmon stocks indicates the potential for increased long-term resilience to ERM.²⁶

Furunculosis

Etiology and epidemiology: Furunculosis is a serious bacterial disease of Atlantic Salmon caused by Aeromonas salmonicida subsp. salmonicida, a gram-negative, non-motile, facultative anaerobic rod-shaped bacterium.²⁸ The disease has been identified in salmon farms in Scotland, Norway, Canada, the Broughton Archipelago in British Columbia, and Washington State.²⁹ It was introduced into Norwegian fish farms in 1985.³⁰ Researchers revealed that furunculosis had spread to over 74 natural streams in Norway.³¹ On the contrary, the disease destroyed 1.8 million Atlantic Salmon smolts at a single commercial hatchery on Vancouver Island in early 2005.³²

Furunculosis has returned in recent years, most notably in Chile, where disease incidence in Atlantic Salmon farms—particularly in freshwater facilities with recirculation systems—has steadily increased since 2022, indicating a renewed epidemiological threat from A. salmonicida spp. Salmonicida.³³ Meanwhile, in British Columbia, Canada, A. salmonicida, including both typical and atypical strains, is still endemic in both wild and farmed salmonids in areas like the Discovery Islands, despite current risk assessments indicating a low transmission risk to wild Fraser River Sockeye under current vaccination and biosecurity practices (2002-2017 data).²⁹ Recent histological examination of Atlantic Salmon from 2022 to 2023 revealed active cases of atypical furunculosis, with clinical evaluations showing unique muscular furuncles, skin ulcers, hemorrhages, and multiorgan bacterial colonization in affected stocks.³⁴ The disease is prevalent in both freshwater and marine salmon farming, and it is commonly associated with high water temperatures (over 14°C), high stocking densities, poor water quality, and handling stress.³⁵ Transmission occurs horizontally via water, direct contact with infected fish, and contaminated equipment. Latently infected carrier fish have a critical role in disease persistence and outbreaks, particularly after stressful events or environmental changes.

Clinical signs and pathogenesis: Furunculosis is clinically defined as lethargy, inappetence, skin discoloration, and hemorrhages at the base of the fins and in the musculature.³⁵ Furuncles, which are hemorrhagic boils or abscesses (Figure 2B-i) in muscular tissue, are one of the distinguishing characteristics. Internally, damaged fish may have swollen spleens, renal congestion, or peritonitis (Figure 2B-ii). Histopathological findings include necrosis in hematological tissues and inflammation in the liver, kidney, and muscle, which is frequently followed by septicemia in severe instances.³⁶

Figure 2 Pathological symptoms by bacterial diseases in salmon: A) Enteric Redmouth: i) Reddened mouth and tongue,²⁰⁰ ii) Enlarged spleen and reddened intestine (arrow);²⁰¹ B) Furunculosis: i) Hemorrhagic boils in muscular tissue,²⁰² ii) Enlarged spleen (arrow);²⁰³ C) Clod Water Vibriosis: i) Deep ulcerative lesion in abdomen area,²⁰⁴ ii) Ulcertaive lesion on base of a fin;²⁰⁴ D) Bacterial Kidney Disease: i) Swollen and discolofred kidney with granulomatous inflammation,²⁰⁵ ii) Histological image showing macrophages, lymphocytes, and tissue necrosis²⁰⁵

Prevention and control measures: Furunculosis is controlled by a mix of immunization and biosecurity policies.⁶ Inactivated whole-cell vaccinations, often paired with adjuvants, are commonly utilized and have dramatically reduced disease incidence in farmed salmon. Effective biosecurity, which includes tight hygiene measures, equipment cleaning, fish movement management, and fallowing practices, is crucial for disease prevention.

Cold water vibriosis

Etiology and epidemiology: Cold Water Vibriosis (CWV), also known as Hitra disease, is a systemic bacterial infection of Atlantic Salmon caused primarily by Aliivibrio salmonicida (formerly Vibrio salmonicida).³⁷ The sickness posed a serious threat to Norwegian aquaculture in the mid-1980s, especially affecting salmon farms in Hitra and the northern coastal areas.³⁸ Although CWV was common in the 1980s and early 1990s, causing hundreds of outbreaks across Norway, incidence has dropped significantly since the mid-1990s, when successful vaccination programs were launched. According to the,³⁹ CWV is no longer among the most prevalent notifiable diseases, while rare occurrences are still documented, particularly during the winter when water temperatures drop below 9°C.⁴⁰

CWV flourishes in low-temperature conditions, with outbreaks often occurring at seawater temperatures below 10°C, and most severely between 4 and 8°C.⁴¹ The bacterium is psychrophilic and halophilic, thrives in cold marine waters, and spreads horizontally by water or direct fish-to-fish contact.  Infections are particularly common in post-smolt and adult salmon raised in open-net pens during the cold season.  Susceptible hosts include Atlantic Salmon, Rainbow Trout, and Arctic Char.  Outbreaks frequently occur after periods of handling stress or environmental changes, particularly during the early sea-phase of growth-out,⁴² found that host and feeding parameters influence the illness outcomes.

Clinical signs and pathogenesis: The clinical appearance of CWV is predominantly defined by systemic bacterial septicemia.  Externally, infected fish frequently exhibit lethargy, inappetence, darker pigmentation, pale gills, exophthalmia (bulging eyes), deep ulcerative lesions and hemorrhages on the skin, fin bases or often on the flanks or near the head (Figure 2C).  Internal pathology includes splenomegaly, ascites, petechial hemorrhaging on internal organs, and severe congestion and inflammation in the liver, spleen, and kidney.⁴³ In severe cases, fibrinous peritonitis and significant organ necrosis may develop.  Histological abnormalities include widespread cellular degradation, inflammatory cell infiltration, and tissue necrosis, particularly in the renal tubules and hepatic parenchyma.⁴⁴ The pathogen quickly colonizes the bloodstream and internal organs, resulting in severe septicemia and significant mortality. Unvaccinated fish populations can experience mortality rates ranging from 30% to over 70%, depending on environmental factors and health state.⁴⁵ Disease development is typically rapid, with mortality happening within days of symptom start, particularly in stressful situations such as crowding, handling, or unexpected temperature changes.

Prevention and control measures: CWV is primarily controlled and prevented through vaccination, which is backed by proper husbandry and biosecurity procedures. Commercial oil-adjuvanted vaccinations, both monovalent and multivalent, have proven to be quite effective, offering over 90% protection when provided to smolts before saltwater transfer, often in doses of 30-50 grams.⁴⁶ Supportive management options include reducing stress through cautious handling, regulating stocking densities, ensuring steady water quality, and allowing infected sites to recover. Furthermore, comprehensive disinfection of equipment and transportation systems, together with regular health monitoring, is required to prevent disease recurrence.

Bacterial kidney disease (BKD)

Etiology and epidemiology

Renibacterium salmoninarum causes bacterial kidney disease, which is a chronic systemic infection that affects both wild and farmed salmonids worldwide.⁴⁷ The first BKD outbreak in wild Atlantic Salmon occurred in Scotland's rivers Dee and Spey in 1933, and in farmed salmonids in Scotland in 1976.⁴⁸ It has since been identified in salmon farms across the globe. Norway has had a revival in recent years, with the Norwegian Veterinary Institute reporting 12 outbreaks in 2023 and at least five more in 2024, mostly in agricultural areas between Nordmøre and Sør-Trøndelag.⁴⁹

The disease can spread from fish to fish⁵⁰ or from adults to their offspring through eggs.^51,52 Infection can cause high mortality in both wild and farmed salmon.⁵³ Almost all age groups of fish can be affected, although the sickness is uncommon in very young fish.  Losses are typically chronic, occurring over an extended period.

Clinical signs and pathogenesis: Infected fish exhibit a variety of clinical indications; nevertheless, some are asymptomatic, showing no evidence of disease.⁵⁴ Clinical manifestations include lethargy, darkening of the skin, bulging eyes (exophthalmia), anemia, enlarged abdomens, blood-filled blisters on the flanks, and bruising (haemorrhaging) around the vent. Internal indicators include fluid in the abdominal cavity, dilated kidneys with white/grey lesions (Figure 2D-i), and diffuse white membranes covering the internal organs.⁵⁵ Microscopic bacteria are commonly found in granulomatous kidney lesions as well as white blood cells (macrophages), where they appear to live and multiply. Histopathology symptoms include granulomatous inflammation in kidney tissue, and numerous macrophages and necrotic debris (Figure 2D-ii).⁴⁹ Mortality rates in Atlantic Salmon can exceed 40% through this disease if extensive epidemics occur.⁵⁶

Prevention and control measures: There is presently no fully effective BKD vaccine, and antibiotic therapy (e.g., erythromycin) can lower bacterial load but cannot consistently clear illnesses in dense farm populations.⁵⁷ The Renogen live Arthrobacter-based vaccination is the only somewhat effective preventive strategy, but its usage is limited and off-label.⁵⁸ As a result, control techniques prioritize strong biosecurity: early identification with qPCR, ELISA, or IFAT diagnostics, and field detection via iPCR/LAMP because of their high sensitivity.⁵⁹

Preventive approaches include culling sick broodstock, egg disinfection, lowering stocking density, site fallowing, and following tight disinfection rules for equipment and transport paths.⁶⁰ Immunomodulatory dietary therapies, such as adjusting EPA/DHA and omega-3/omega-6 fatty acid levels, have shown promise in enhancing immune responses to R. salmoninarum antigens, perhaps leading to greater resistance.⁶¹

Infectious salmon anemia (ISA)

Etiology and epidemiology: Infectious salmon anemia (ISA) is a systemic, often deadly viral disease that affects farmed Atlantic Salmon. It is caused by the infectious salmon anemia Virus (ISAV), a negative-sense, single-stranded RNA virus from the Orthomyxoviridae family.⁶² ISA was first found in Norway in the 1980s and has subsequently spread to other major salmon-producing countries such as Chile, Canada, the United States, Scotland, and the Faroe Islands.⁶³ The global epidemiology of ISA has changed dramatically during the last two decades. Data from 2022-2024 indicate that ISA continues enzootic in Norway and Chile, with developing hotspots in specific places (Møre og Romsdal, Nordland, and Troms).⁶⁴ HPR0 ISAV is endemic in Canada's Atlantic provinces, while no notable deaths have occurred in recent years.⁶⁵

ISAV spreads mostly horizontally, via saltwater, shared equipment, and direct contact between infected and vulnerable fish.⁶⁶ Vertical transmission is not completely understood; however, it is thought to occur through surface-contaminated eggs or reproductive organs. High stocking density, stressful handling, immunosuppressive co-infections (e.g., with P. salmonis or IPNV), inadequate smolt transfer protocols, and changeable environmental conditions all increase the risk of an epidemic.

Clinical signs and pathogenesis: ISA is defined by several clinical and pathological characteristics. Infected fish exhibit lethargy, anemia (as evidenced by pale gills), ascites, and exophthalmia. Internally, the diseased fish exhibit hemorrhagic liver (Figure 3A-i), splenomegaly, pericardial effusion, and peritoneal fluid accumulation.⁶⁷ Histologically, the kidney and spleen's hematopoietic tissues exhibit necrosis (Figure 3A-ii), endothelial cell death in the gills and heart, and significant vascular congestion. Thus, the disease can spread slowly in an infected farm, and in the worst-case scenario, mortality rates of up to 100% have been reported.⁶⁸

Figure 3 Pathological symptoms by viral diseases in salmon:  A) Infectious Salmon Anemia: i) Petechial haemorrhages in peripiloric fat accompanied with dark haemorrhagic liver,²⁰⁶ ii) Indirect fluorescent antibody test (IFAT) showing the presence of ISA virus in the kidney cells of an Atlantic salmon;²⁰⁶ B) Infectious Hematopoietic Necrosis: i) Skin darkening  of fish relative to lighter colored healthy fish,²⁰⁷ ii) Pale gills, exophthalmia, petechial haemorrhages, empty gut and ascitic fluid;²⁰⁸ C) Infectious pancreatic necrosis: i) Degeneration of acinar cells within the pancreas and necrotic lesions in the liver,²⁰⁹ ii) Pyloric caeca with apical hemorrhage;²¹⁰ D) Heart and Skeletal Muscle Inflammation: i) Pale heart and haemopericardium,⁹⁸ ii) Red skeletal muscle tissue, with moderate multifocal myositis;⁹⁹ E) Pancreatic Disease: i)  Post PD impact on the pancreas of fish,²¹¹ ii) White muscle lesions;²¹² F) Cardiomyopathy syndrome: i) Inflamed vent in salmon,¹¹² ii) Necrosis occured ruptured atrium¹¹⁴

Prevention and control measures: There are currently no treatments for ISA, hence prevention is the major method of control. Formalin-inactivated and DNA-based vaccinations are available and widely used in endemic countries such as Norway and Chile.⁶⁹ Instead of giving complete infection protection, these vaccines frequently reduce viral load and delay clinical development. Recent advancements in vaccination development, such as nanoparticle carriers and mucosal adjuvants, seek to improve immune protection and delivery efficiency. Selective breeding has shown promise, and genomic selection techniques now incorporate resistance loci to produce better salmon lines.⁷⁰ Furthermore, effective biosecurity practices, including area-based management, fallowing, all-in/all-out stocking, and full cleaning of equipment and vessels, are essential for reducing virus transmission. Rapid detection and culling of diseased stocks, movement control, and real-time surveillance technologies have all helped to reduce outbreaks.

Infectious hematopoietic necrosis (IHN)                                                 

Etiology and epidemiology: Infectious hematopoietic necrosis (IHN) is a severe viral disease caused by infectious hematopoietic necrosis virus (IHNV), a bullet-shaped, enveloped, negative-sense single-stranded RNA virus from the Novirhabdovirus genus of the Rhabdoviridae family.⁷¹ It typically occurs in cooler waters (<15°C).⁷¹ The disease mostly affects juvenile salmonids, notably S. salar, resulting in significant mortality rates of more than 90% under intense aquaculture conditions.⁷² Between 2001 and 2003, a major outbreak occurred in British Columbia, Canada, affecting over 12 million farmed Atlantic salmon and resulting in an average mortality rate of 58% per farm; the virus was most likely introduced from wild fish and spread quickly between farms due to waterborne routes and inadequate biosecurity.⁷³ More recently, in 2021, Denmark lost its IHN-free status following the detection of IHNV in various freshwater trout farms, raising concerns about the virus's survival and stealthy spread in European aquaculture.⁷⁴  The virus is primarily transmitted horizontally through waterborne contact with contaminated feces, urine, mucus, or sexual fluids, but vertical transmission via infected gametes has also been described.⁷⁵

Clinical signs and pathogenesis: Clinically, infected fish show black skin (Figure 3B-i), exophthalmia, abdominal distension, pale gills, trailing fecal casts, and peculiar swimming behavior as spiraling or darting, which progresses to lethargy and death.⁷⁴ Petechial hemorrhages might arise near the fins, mouth, or vent.  Internally, typical observations include ascites and pale or hemorrhagic internal organs (Figure 3B-ii).  Histopathologically, the disease is characterized by necrosis of hematopoietic tissues in the kidney and spleen, as well as cellular degeneration, vascular injury, and tissue breakdown.  These defects impede immunological and organ functions, resulting in significant mortality, particularly in fry and smolts.⁷⁶

Prevention and control measures: There is currently no therapeutic therapy for IHN; thus, control measures rely on immunization, biosecurity, and surveillance.  The DNA vaccine APEX-IHN® (Elanco), which has been approved in Canada since 2005, has shown high efficacy in lowering mortality and inhibiting horizontal transmission in Atlantic salmon, with vaccine-induced protection lasting at least 7 months.⁷⁷ Strict biosecurity practices, including using pathogen-free water, disinfecting eggs with iodophor, sterilizing equipment, fallowing the site, and rapidly culling diseased stocks, are critical for reducing outbreaks.⁷⁸ IHN must be reported to the World Organisation for Animal Health (WOAH), and most afflicted nations have active surveillance and eradication plans in place to combat outbreaks.^74,79

Infectious pancreatic necrosis (IPN)

Etiology and epidemiology: Infectious pancreatic necrosis (IPN) is caused by an aquabirnavirus (IPNV) and is still a globally distributed disease of salmonid aquaculture, with the greatest economic impact on juvenile S. salar and S. gairdneri fry.^80,81 Vertical transmission occurs through infected broodstock and eggs, while horizontal transmission occurs by watery exposure, fomites, and carrier fish.⁸² Outbreaks are most common during the freshwater hatchery period and early seawater transfer, where naïve fry and post-smolts experience high stocking densities and handling stress.⁸³ Environmental stresses such as fast temperature fluctuations and poor water quality, together with concurrent infections, can worsen clinical manifestation and mortality.⁸⁴ Over the last two decades, widespread vaccine use and genetic selection for IPN resistance have significantly reduced large-scale fatalities,^85,86 but sporadic outbreaks continue where biosecurity is inadequate or when novel, highly virulent viral variants emerge.⁸⁷ Persistent carriers and environmental reservoirs, such as sediments and biofilms, raise the possibility of reintroduction to hatcheries and sea sites.⁸⁸

Clinical signs and pathogenesis: Clinically infected fry and post-smolts exhibit lethargy, anorexia, abdominal distention, darkening, and severe morbidity, with mortality rates varying depending on host age and strain virulence.⁸⁹ The stomach and anterior intestine may be empty, distended, and filled with a thick, clear, or whitish mucous matter. The characteristic histology is sudden necrosis of pancreatic acinar cells, with lesions extending to the exocrine pancreas, mesenteric fat, and, in extreme cases, renal tubules and hematological organs exhibiting degeneration and bleeding (Figure 3C).⁹⁰

Prevention and control measures: There is no specific antiviral therapy for IPN; thus, prevention is key. Vaccinating juveniles and broodstock with inactivated, recombinant subunit, or vectored vaccines targeting the VP2/VP3 capsid proteins lowers clinical illness and viral shedding.⁹¹ Genetic selection targeting important quantitative trait loci (QTLs) associated with resistance, particularly on chromosome 26, has significantly reduced susceptibility,^85,86 and when combined with immunization, gives synergistic protection.⁸⁵ Biosecurity procedures such as broodstock screening, egg disinfection, equipment sterilization, site fallowing, density control, and water quality optimization remain crucial.⁹² Operational techniques such as coordinated smolt transfer, proper adaptation to seawater, and quick epidemic containment all contribute to reducing spread. Molecular antivirals, RNA interference, and better adjuvants are all being researched; however, the majority of it is experimental.⁹³ To limit the danger of IPN, current best practices incorporate genetic, vaccination, and biosecurity measures.

Heart and skeletal muscle inflammation (HSMI)

Etiology and epidemiology: Heart and skeletal muscle inflammation (HSMI) is a serious condition affecting farmed Atlantic Salmon that is reliably linked to piscine orthoreovirus genotype 1 (PRV-1).⁹⁴  PRV-1 is common in salmon farming regions such as Norway, Scotland, Chile, and parts of North America,⁹⁵ but the incidence of clinical HSMI varies geographically due to differences in viral subtype virulence (e.g., PRV-1a vs PRV-1b), host genetic resistance, and environmental or management stressors.^96,97 Longitudinal surveillance demonstrates that PRV infection can be detected in freshwater smolts and persists throughout the production cycle; however, HSMI outbreaks typically occur 5-9 months after seawater transfer, when cumulative stress factors such as crowding, temperature fluctuations, and handling coincide with peak viral loads.^97,98 Recent Norwegian monitoring reports demonstrate that, while overall PRV incidence remains high (more than 80% in some places), focused biosecurity and site management have reduced the frequency and severity of clinical outbreaks compared to a decade ago.⁶⁴

Clinical signs and pathogenesis: Clinically, fish suffering from HSMI frequently exhibit lethargy, decreased feed intake, irregular swimming, pale gills, and ascites; mortality rates can range from zero to more than 20% depending on severity and co-infections.⁹⁹ Salmon can withstand substantial injury to their heart musculature without presenting obvious signs, but outbreaks of disease with increased mortality occur when a significant section of the heart becomes inflamed. HSMI induces cardiac abnormalities in almost all affected fish.¹⁰⁰ During this stage, inflammation and cell death spread to the red skeletal muscles, cell death to the liver, oedema (swelling), and interrupted blood circulation to the fish's various organs (Figure 3D-i). Histopathologically, the disease is distinguished by diffuse to multifocal lymphohistiocytic myocarditis and epicarditis encompassing both compact and spongy myocardium layers, as well as degeneration and necrosis of red skeletal muscle fibers (Figure 3D-ii).¹⁰¹ In situ hybridization and immunohistochemistry have revealed that the development of lesions coincides with the shift of PRV replication from blood cells to cardiomyocytes.¹⁰¹

Prevention and control measures: Currently, there is no licensed antiviral treatment for PRV or HSMI. Control techniques for reducing transmission risk include strict biosecurity, routine PRV surveillance of broodstock, smolts, and grow-out fish, fallowing between production cycles, and controlling the movement of equipment and workers.⁹⁷ Disease manifestation can be reduced through husbandry improvements such as improving smolt quality, gradually transferring seawater, reducing handling, and maintaining optimal stocking densities. Selective breeding strategies have shown promise in lowering susceptibility to PRV-induced HSMI, with certain strains exhibiting much decreased lesion prevalence when challenged.⁹⁷ Vaccination research continues, with experimental vaccines offering partial protection in laboratory trials, but no widely used commercial product is currently available.¹⁰¹ Future control will most likely be achieved through a mix of genetic selection, improved husbandry, and effective immunoprophylaxis integrated into regional health management systems.

Pancreatic disease (PD)

Etiology and epidemiology: Pancreas disease (PD) of Atlantic Salmon is caused by salmonid alphavirus (SAV), an enveloped single-stranded positive-sense RNA alphavirus with multiple genotypes (SAV1-SAV7) with distinct geographic and host associations;¹⁰² in recent years, SAV2 and SAV3 have dominated outbreaks in Norway, with SAV3 particularly associated with west-coast marine outbreaks.⁶⁴ PD is enzootic in many European salmon production areas (especially Norway, Ireland, and Scotland), and the WOAH/OIE has identified it as a regulatory concern because of its economic implications on growth, mortality, and product quality.⁶⁴

Epidemiological patterns are shaped by a combination of viral genotype, host genetics (breed/stock susceptibility) and farm management/connectivity: dense farm networks, timing of freshwater-to-seawater transfer, and site proximity increase transmission risk,¹⁰³ whereas genomic and quantitative genetics studies published in 2024-2025 demonstrate heritable components of resistance and identify genomic regions associated with differential responses.¹⁰⁴ Recent field and surveillance investigations (2022-2024)¹⁰⁴ highlight that, while vaccination and management have reduced clinical outbreaks in some areas, subclinical infection and low-level SAV circulation are still common, demanding continuing vigilant surveillance.

Clinical signs and pathogenesis: Inappetence, sleepiness, limited growth, and occasional mortality are common symptoms of PD, which develops 1-4 months after seawater transfer mortality.¹⁰⁵ Gross lesions include pancreatic pallor or atrophy (Figure 3E-i), pale skeletal muscle, and a flaccid heart. Histopathologically, PD exhibits a trio of lesions: severe necrosis and atrophy of pancreatic acinar cells, myocarditis, and skeletal myositis, which progresses from acute necrosis and inflammation to chronic fibrosis and tissue regeneration (Figure 3E-ii).¹⁰⁵ SAV replicates in various tissues and generates robust local immunological responses, with recent in situ investigations revealing tissue-specific viral tropism and persistent B-cell activity in afflicted organs.¹⁰⁵

Prevention and control measures: There is no specific antiviral medication for PD; rather, control is achieved by coordinated management. Vaccination with commercial inactivated oil-adjuvanted SAV vaccines decreases clinical illness, mortality, and viral shedding. Experimental DNA vaccines have shown reduced lesions and even prevented transmission in cohabitation studies.¹⁰⁶ To prevent spread, biosecurity measures such as coordinated fallowing, fish movement restrictions, equipment disinfecting, and regional coordination must be used.^107,108 report that resistance breeding based on QTLs is becoming more prevalent in control programs.

Cardiomyopathy syndrome (CMS)

Etiology and epidemiology: Cardiomyopathy syndrome (CMS) is a viral cardiac disease of farmed Atlantic Salmon caused by piscine myocarditis virus (PMCV), a non-enveloped double-stranded RNA virus from the Totiviridae family.¹⁰⁹ PMCV has been recorded in Norway, the Faroe Islands, Scotland, Ireland, and Canada during the 1980s and 2000s.¹¹⁰ PMCV is prevalent in Norwegian production, with a median latency of ~6.5 months between first identification and clinical CMS in afflicted cohorts, indicating common subclinical circulation before outbreaks.¹¹¹ Recent genetic and epidemiological research reveals PMCV sequence clusters by geography but low overall variety, and risk is raised by high farm density, site connection, and stressors (e.g., the late saltwater period), necessitating coordinated regional management.

Clinical signs and pathogenesis: CMS clinically manifests as either a rapid or gradual rise in mortality among market-sized fish with poor condition, activity intolerance, ascites, an inflamed vent (Figure 3F-i), and gross lesions centered on a flaccid, pale heart and, on occasion, pericardial effusion.¹¹² CMS is diagnosed histopathologically with severe inflammation and degradation of the spongy component of the myocardium (ventricle), as well as comparable abnormalities in the atrium (Figure 3F-ii).¹¹³ Myocyte degeneration and inflammatory alterations are uncommon in the heart's compact layer and always occur after changes to the spongy sections.¹¹⁴ Circulatory disruption, including multifocal liver necrosis, may also occur.

Prevention and control measures: There is no specific antiviral medication for CMS; thus, control is both integrated and preventive. Diagnosis and surveillance rely on sensitive qPCR screening of cardiac tissue and histology to confirm clinical illness, allowing for early site-level containment.¹¹⁵ No commercial vaccine is currently in use; however, vaccine research (subunit/plant-produced VLPs and other platforms) and experimental challenge models have been constructed and show promise in lowering viral replication and cardiac lesions in trials.¹¹⁶ Examples of risk- and impact-reducing management measures include regional coordination (zoning and synchronized fallowing), reduced site density and farm connectivity, strict biosecurity and movement controls, targeted nutritional/functional-feed strategies during outbreaks, and selective breeding for reduced susceptibility where QTLs have been identified. These measures currently make up the realistic CMS control toolset.

Saprolegniasis

Etiology and epidemiology: Saprolegniosis, the most troublesome oomycete infection in salmon aquaculture, is mostly caused by Saprolegnia parasitica, a common freshwater fungus that infects wild and farmed fish, amphibians, and crustaceans.¹¹⁷ The organism is an oomycete (Kingdom Stramenopila), which reproduces asexually by biflagellate zoospores and sexually via thick-walled oospores, allowing it to persist in sediments and biofilms for long periods of time. Infections are frequently opportunistic, occurring when fish are stressed, injured, or immunocompromised, allowing hyphae to infiltrate damaged epidermis, fins, or gill tissues.¹¹⁸

s.parasitica is epidemiologically widespread, with reports from all major salmon-producing locations, including Norway, Scotland, Canada, Chile, and Tasmania, as well as wild salmonid populations in North America and Europe.^118,119 The fungus is waterborne and spreads through direct contact with infected fish, motile zoospores in the water column, and adhesion to fomites such as nets, tanks, and processing equipment.^119,120 Outbreaks are more common in low-temperature freshwater phases, particularly in hatcheries, egg incubation units, and broodstock storage facilities, when fish metabolic and immunological activity is reduced and zoospores are more environmentally stable.¹¹⁸ Environmental reservoirs include sediments, organic debris, and biofilms, whereas anthropogenic risk factors include poor water quality, overpopulation, frequent handling, and the presence of dead or decaying fish.¹²⁰

Clinical signs and pathogenesis: Saprolegniosis is distinguished by cotton-wool-like hyphal development (Figure 4) on skin, fins, gills, and eggs, which causes epidermal necrosis, osmoregulatory disturbance, and severe mortality.¹²¹ Lesions might seem grayish or whitish and develop discoloration as a result of secondary microbial colonization.¹²²  Histological tests demonstrate that wide, aseptate hyphae penetrate the epidermis and superficial dermal layers, causing localized inflammation and epithelial hyperplasia.¹²³

Figure 4 Pathological symptoms by fungal disease in salmon: Saprolegniosis:  i) Saprolegina affcted salmon egg,²¹³ ii) cotton-like” tufts covering pectoral fin base²¹³

Prevention and control measures: Malachite green, an older yet effective therapy, was banned due to carcinogenic hazards.¹²⁴ Despite regulatory and safety concerns, current hatchery protocols primarily use formalin baths (37% formaldehyde solutions), as well as alternatives such as hydrogen peroxide, bronopol, iodophors, salt, boric acid, and copper sulfate, which have varying efficacy depending on concentrations and exposure durations.¹²³ UV treatment of the incubation water is also effective. Plant extracts having antifungal activities, such as garlic, onion, peppermint, chrysanthemum, Eryngium campestre, Cuminum cyminum, and Thymus linearis, are being investigated as eco-friendly treatments.¹²⁵

Ichthyophoniasis

Etiology and epidemiology: Ichthyophoniasis is a systemic disease of salmonids caused by Ichthyophonus hoferi (Figure 5A-i), a fungal-like protist from the Mesomycetozoa class.¹²⁶ It is regarded as one of the most serious chronic illnesses affecting both wild and farmed salmon populations globally, resulting in granulomatous lesions in numerous organs, reduced growth, and increased mortality.¹²⁷

Figure 5 Pathological symptoms by parasites in salmon: A) Ichthyophoniasis: i) Ichthyophonus hoferi,²¹⁴ ii) Nodules in the kidney;²¹⁵ B) Sea Lice: i) Lepeophtheirus salmonis,²¹⁶ ii) Juvenile wild salmon with sea lice;²¹⁷ C) Post mortem myoliquefaction: i) Fresh spores of K. thyrsites,²¹⁵ ii) Kudoa parasite caused soft and seperated flesh in a salmon fillets;²¹⁸ D) Gyrodactylosis: i) Gyrodactylus salaris,²¹⁹ ii) Infection on pectoral fin with Gyrodactylus;²²⁰ E) Amoebic gill disease: i) Amphizoic amoeba Neoparamoeba perurans,²²¹ ii) Thickening and fusion of the secondary lamellae, epithelial hyperplasia, mucus cell proliferation, and lamellar clubbing.²²²

I. hoferi has a worldwide range, with recorded outbreaks in important salmon-producing regions such as the North Atlantic (Norway, Scotland, Canada), North Pacific (Alaska, British Columbia), and Chile.¹²⁷ Infection prevalence varies greatly depending on geographic location and population, with wild populations frequently displaying higher prevalence than farmed fish, indicating complex transmission dynamics involving environmental reservoirs and interspecies vectors.¹²⁸ Recent molecular epidemiology investigations using PCR and sequencing techniques have discovered genetic heterogeneity among I. hoferi isolates from various locales, which may affect virulence and host susceptibility.¹²⁹ Transmission occurs through consumption of diseased tissues, direct contact with infected fish, or exposure to contaminated watery spores. The pathogen can live in fish populations asymptomatically, with clinical epidemics frequently caused by stresses including handling, poor water quality, or co-infection with other pathogens.¹²⁸

Clinical signs and pathogenesis: Clinically, infected salmon show lethargy, darker skin, decreased eating, irregular swimming, and emaciation. Necropsy showed widespread granulomatous lesions (Figure 5A-ii) primarily in the heart, kidney, liver, and skeletal muscle.¹³⁰ Histopathological examination reveals granulomas composed of dense clusters of macrophages and multinucleated giant cells surrounding thick-walled I. hoferi spherical bodies, which can be seen with specific stains such as gomori methenamine silver.¹³¹ These granulomas disrupt normal organ function, frequently leading to chronic disease progression and eventual death.

Prevention and control measures: Currently, there are no effective chemotherapeutic treatments or vaccines commercially available for Ichthyophoniasis. Control efforts focus primarily on prevention through good husbandry practices and biosecurity measures, including minimizing fish stress, avoiding overcrowding, and maintaining water quality.¹³²

Diagnostic surveillance using sensitive PCR-based assays enables early detection and management of infected populations.¹³³ Selective breeding for resistant strains has been proposed but requires further research. Experimental studies have explored the potential of immunostimulants and probiotics to enhance host resistance, though results remain preliminary.¹³⁴

Sea lice

Etiology and epidemiology: Sea lice, notably Lepeophtheirus salmonis (Figure 5B-i) and Caligus species such as C. clemensi and C. rogercresseyi, can infest both farm-grown and wild salmon, causing fatal infestations.^135,136 The parasite's life cycle is complex, including free-swimming nauplius and copepodid stages that can disperse via ocean currents, allowing transmission between various salmon populations.¹³⁷ Sea lice are ectoparasites that feed on mucus, blood, and skin. They migrate and leach onto the skin of wild salmon during the free-swimming, planktonic nauplii and copepodid larval phases, which can last several days.^135,138 These parasites can reproduce and multiply rapidly in densely packed salmon populations in net enclosures.¹³⁹ They are most prevalent in the Northern Hemisphere, affecting Atlantic and Pacific salmon species. Operators have reported infestations, particularly in Canada, Norway, Scotland, and Ireland.^140,141

Clinical signs and pathogenesis: As L. Salmonis attaches to salmon's exterior organs, physical damage such as lesions, inflammation, and erosion of the skin and underlying tissues occurs (Figure 5B-ii). Heavy infestations in Atlantic Salmon can produce serious sores on the head and dorsal areas, occasionally exposing the skull, and if sea lice populations become too large, a fish can die.¹⁴² In addition to causing direct tissue damage, sea lice infestations raise the risk of subsequent illnesses. For example, during ISA outbreaks in Scotland, locations with high sea lice density had greater connections with ISAv-positive sites and subsequent clinical illness epidemics.¹⁴³

Prevention and control measures: Management of L. salmonis infestations is difficult due to the development of resistance to chemical treatments. Historically, common parasiticides like emamectin benzoate were effective, but resistance has reduced their long-term efficacy.¹⁴⁴ Non-chemical solutions are increasingly used to reduce resistance and improve fish welfare. Mechanical removal (for example, brushing or freshwater baths), biological control with cleaner fish, and physical barriers like lice skirts are all options. A comparative research of non-medicinal delousing procedures found varying efficacy in parasite eradication and differing welfare impacts on Atlantic Salmon hosts.¹⁴⁵ Innovative treatments, such as hyposaline water, have been tested on commercial farms to reduce sea lice populations and control amoebic gill diseases. These treatments show promise as effective non-chemical alternatives.¹⁴⁶ Additionally, selective breeding programs aimed at genetic resistance to sea lice are underway. Studies on gene expression responses in Atlantic Salmon families show significant diversity, which can be used to drive breeding methods for improved parasite resistance.¹⁴⁷ Furthermore, predictive modeling of sea lice outbreaks is being conducted to optimize management. For example, a study in the Bay of Fundy, New Brunswick, Canada, evaluated infestation pressure and treatment history from 2016 to 2021 to anticipate L. salmonis abundance. The inclusion of infestation pressures enhanced these models' forecast accuracy marginally.¹⁴⁸

Post mortem myoliquefaction

Etiology and epidemiology: Kudoa thyrsites (Figure 5C-i) is a cosmopolitan myxosporean parasite infecting a wide range of salmonids, including Salmo salar and multiple Oncorhynchus spp. (chinook, coho, sockeye, chum, and pink salmon), where it is the principal etiological agent of post-mortem myoliquefaction—a “soft-flesh” syndrome causing severe quality downgrades and economic losses in aquaculture and wild fisheries.¹⁴⁹ In Pacific salmon populations, particularly Oncorhynchus tshawytscha in British Columbia, the incidence frequently exceeds 50%, with some studies predicting infection rates of 80-100% in adults, indicating substantial endemicity in ocean-reared stocks.¹⁵⁰ Sockeye Salmon, Coho Salmon, and Chum Salmon are still common in some locations, with histological surveys revealing widespread muscle plasmodia at commercial harvest levels.¹⁵¹ The parasite's life cycle is not fully understood, but it is thought to involve benthic or pelagic invertebrate hosts, and oceanographic factors have a strong influence on infection risk; salmon captured or reared in deeper offshore waters or migratory corridors have significantly higher parasite loads than fish from nearshore or surface environments.¹⁵² Age and size are important epidemiological determinants, with older, larger salmon consistently showing increased infection intensity, most likely reflecting cumulative exposure during ocean residency.¹⁵³

Clinical signs and pathogenesis: Unlike infectious diseases with overt morbidity, PMM is clinically indiscernible in live fish, with lesions appearing only after death, affecting product quality and market value. The syndrome is distinguished by the rapid softening and liquefaction of skeletal muscle within 24-48 hours after harvest, with fillets appearing flaccid, pallid, and watery, and in severe cases, muscle fibers break down to a jelly-like consistency (Figure 5C-ii).¹⁵⁴ Gross lesions include focal or diffuse white patches that correlate to parasite plasmodia, primarily in the dorsal muscle, and which frequently spread as the infection progresses.¹⁵³ Histopathological examination reveals that K. thyrsites multiplies intracellularly within myocytes, forming large plasmodia containing thousands of tetravalvulid spores, causing myofibrillar degeneration, sarcolemmal rupture, vacuolation, and loss of cross-striations, with a minimal inflammatory response due to the infection's chronic nature.¹⁵⁵ Postmortem, parasite-derived proteolytic enzymes degrade myofibrillar proteins, compromising tissue integrity and causing extensive myoliquefaction.¹⁵⁶

Prevention and control measures: There are presently no authorized treatments or vaccinations for K. thyrsites, owing to its unclear lifecycle and lack of identified intermediate hosts.¹⁵⁷ As a result, control focuses on preventive measures and post-harvest mitigation. Producers can categorize farm sites based on past infection risk to guide smolt deployment and reduce exposure; minimizing marine residence time and maximizing smolt health (nutrition, immunization) are also standard tactics.¹⁵⁷ Experimental studies investigate post-harvest therapies, such as alkaline buffer or high hydrostatic pressure treatments, to reduce flesh degradation, although these are still in the research stage.¹⁵⁸ The showing of acquired immunity in salmon provides a potential foundation for vaccine development, but practical use requires further exploration.¹⁵⁹

Gyrodactylosis

Etiology and epidemiology: Gyrodactylosis, caused mostly by Gyrodactylus salaris (Figure 5D-i), is one of the most lethal parasite illnesses of Atlantic Salmon. The parasite is a viviparous monogenean that adheres to salmonids' skin, fins, and gills (Figure 5D-ii), quickly reproducing without the requirement for an intermediary host.¹⁶⁰ The epidemiology of the parasite is directly related to water temperature, host density, and salmon life cycle. Warmer temperatures (12-18 °C) hasten parasite reproduction, causing epidemics in hatcheries and wild populations.¹⁶¹ In 1972, the parasite migrated from Norwegian hatcheries to wild salmon, affecting some populations.¹⁶² While historically limited to Scandinavia and portions of Russia, the parasite strains have migrated to other regions due to host species and geographical patterns.¹⁶³ According to recent data, over 50 rivers in Norway have been confirmed as infected, resulting in catastrophic population losses in wild salmon, with juvenile mortality rates exceeding 90%.¹⁶² G. salaris' tenacity in hatchery systems and capacity to spread via fish translocation make it a constant biosecurity threat in aquaculture.

Clinical signs and pathogenesis: Gyrodactylosis causes both mechanical and immunological harm. G. salaris binds to the host epithelium via its opisthaptor and feeds on epidermal cells, resulting in epithelial hyperplasia, hemorrhages, and secondary bacterial and fungal infections.¹⁶⁴ High parasite burdens cause severe epidermal erosion, osmoregulatory dysfunction, and increased mucus production, which eventually leads to stress and death.¹⁶⁵ Epidermal weakening, necrosis, and inflammatory cell infiltration are among the histopathological alterations observed in extensively infested tissues. Juvenile salmon are especially vulnerable because they have little acquired immune response, resulting in uncontrolled parasite multiplication.¹⁶⁶ In contrast, some salmonid hosts (O. mykiss) exhibit partial resistance, implying that the parasite modulates immune responses according to the species.¹⁶⁷

Prevention and control measures: Control of G. salaris remains difficult due to the parasite's direct life cycle and rapid replication. Historically, chemical treatments such as rotenone and aluminum sulfate have been used to eliminate parasites from contaminated rivers, but these methods are environmentally hazardous and necessitate significant restocking operations.¹⁶⁸ Hydrogen peroxide and formalin baths have been used in aquaculture, but their efficacy has been varied, raising concerns about fish welfare.¹⁶⁹ Biological techniques, such as selective breeding for resistant salmon strains and immunological research, are gaining popularity.¹⁰⁸ Research into host-parasite interactions has discovered candidate immune genes that could be used to build vaccines, while no commercial vaccines are currently available. Biosecurity remains the foundation of prevention, with rigorous regulations on fish movement and cleaning measures required to restrict transmission.¹⁷⁰

Amoebic gill disease (AGD)

Etiology and epidemiology: Amoebic gill disease (AGD) is a major gill illness affecting marine-farmed S. salar caused by the amphizoic amoeba Neoparamoeba perurans (Figure 5E-i)..¹⁷¹ AGD was initially characterized in Tasmania in the mid-1980s and is now seen in most major Atlantic salmon-producing locations, including Ireland, Scotland, Norway, and Chile.¹⁷² It has become a recurring health and economic issue in Norway since its initial discovery in 2006, with major losses observed since 2012.¹⁷³ Contemporary reviews in 2024 emphasize the parasite's global prevalence and aquaculture significance.¹⁷⁴ Disease emergence and recurrence are seasonal and temperature-related, with outbreaks typically occurring within ~7-20°C during marine grow-out, and risk amplified by high biomass and net-pen husbandry.^175,176

Clinical signs and pathogenesis

Symptoms often emerge two months after the fish are moved from freshwater hatcheries to open net sea cages.¹⁷⁷ AGD appears as white, elevated mucoid patches on gill surfaces, indicating increased mucus and epithelial growth.¹⁷⁶ Multifocal lamellar epithelial hyperplasia and hypertrophy, inter-lamellar cell mass formation, lamellar fusion (Figure 5E-ii), and variable inflammation characterize the histopathology; these changes impair gas exchange and ion regulation, predisposing to hypoxia and osmoregulatory failure.^178,179 Molecular and morphometric investigations show that lesion burden and mucous-cell dynamics are associated with disease severity and may be regulated by some therapies (e.g., peracetic acid).¹⁸⁰ Host size and condition also influence disease expression, with bigger cohorts exhibiting lower parasite loads and gross pathology in controlled exposure experiments.¹⁸¹

Prevention and control measures

Freshwater bathing (usually 2-3 hours in low-salinity water via wellboats or tarpaulins) remains the most effective commercial intervention, with lesions visibly regressing within days.¹⁸² Hydrogen peroxide (H₂O₂) baths are commonly used when freshwater access is limited. Proper dosing and temperature are crucial for efficacy and safety. H₂O₂ can affect hypoxia tolerance and mucosal responses, necessitating careful welfare management.^183,184 Peracetic acid (PAA) is being actively investigated as an alternative/adjunct, with experimental and project data indicating immunomucosal effects that could improve management, while field standards are still evolving.¹⁸⁵ Integrated management involves optimizing biomass and oxygenation, reducing net fouling, minimizing handling stress, scheduling freshwater/H₂O₂/PAA interventions based on early detection, and incorporating fallowing and site rotation when possible.^173,176 There is no commercial vaccine available; current research focuses on host-parasite treatment immunology and microbiome interactions to improve prophylactic and treatment.^180,186

Current disease management measures in salmonid aquaculture have made significant progress; however, they are only partially effective, depending on the disease and production system. Vaccination, biosecurity, selective breeding, and improved husbandry have significantly reduced the impact of several bacterial and viral diseases, particularly Aeromonas salmonicida (furunculosis) and Yersinia ruckeri (enteric redmouth disease), for which vaccines have proven highly effective.^6,27 Similarly, selective breeding operations have produced salmon strains that are resistant to infectious pancreatic necrosis (IPN), resulting in much lower mortality rates.¹⁸⁷ However, other infections, such as Renibacterium salmoninarum (bacterial kidney disease) and Flavobacterium psychrophilum (coldwater disease), are more difficult to control due to a lack of effective vaccines and their ability to survive in the environment or within human tissues.⁶⁴ Parasitic infestations, notably sea lice (Lepeophtheirus salmonis), remain one of the most costly and chronic issues, as parasites have evolved resistance to many chemical treatments, and biological or mechanical approaches are inconsistently effective.¹⁴⁵ Biosecurity and fallowing programs, particularly when coordinated across farms, have been shown to reduce the spread of viral diseases such as infectious salmon anemia (ISA) and infectious hematopoietic necrosis (IHN), but open-water systems still allow transmission between farms and wild populations.¹⁸⁸ Furthermore, misuse of antibiotics has resulted in rising antimicrobial resistance in aquaculture environments.¹⁸⁹ In general, current strategies work moderately to very well against a wide range of bacterial and viral infections. However, they don't work as well against chronic and parasitic diseases. This means that future management will need to use a combination of genomics, next-generation vaccines, environmental monitoring, and ecosystem-level collaboration.

Despite significant breakthroughs in diagnoses, treatments, and management, salmon aquaculture still faces ongoing disease issues as a result of changing pathogens, environmental stressors, and intensification, showing significant research gaps. Viral pathogens such as ISAV and SAV continue to be regionally significant, but there are still knowledge gaps in understanding host-pathogen genotype interactions, latency, and viral persistence in wild reservoirs, which limit predictive disease modeling and early detection.^190,191 PRV is already common in many areas, but the mechanisms underpinning strain-specific pathogenicity and subclinical infections that cause HSMI remain unknown.⁹⁶ Poor vaccination efficiency and dependency on antibiotics highlight critical gaps in understanding immune evasion, field-level vaccine performance, and genetic resistance in bacterial pathogens such as P. salmonis.¹⁹² Parasitic challenges, particularly sea lice (L. salmonis, Caligus spp.), have developed resistance to delousing chemicals, highlighting the need for genomic surveillance, resistance evolution modeling, and non-chemical strategies.^193,194 Gill health syndromes, such as AGD, are increasingly involving multifactorial stressors such as harmful algal blooms, low oxygen, and co-infections, but the cumulative effects on growth, welfare, and treatment windows are difficult to quantify.^186,195 Moreover, climate-driven changes in temperature, salinity, and hydrodynamics exacerbate disease dynamics, but mechanistic research on pathogen ecology under future scenarios is sparse.¹⁹⁶ Therefore, research priorities include: (i) enhancing molecular epidemiology and biomarker identification for early pathogen detection; (ii) improving SRS vaccine design using systems immunology, phage therapy, and selective breeding. (iii) implementing genomic monitoring to track lice resistance alleles; (iv) creating precision health management systems that combine hydrodynamic and agent-based epidemiological models for farm zoning and fallowing methods;^197-199 and (v) adding welfare and resilience measures to climate adaptation frameworks. To enable sustainable salmon aquaculture, these deficiencies must be addressed through interdisciplinary, ecosystem-based approaches that incorporate host genetics, microbiome science, oceanography, and regulatory harmonization.

Infectious diseases continue to be a defining constraint on the sustainability, profitability, and resilience of global salmon aquaculture, with impacts that extend beyond farm-level losses to encompass significant ecological and socio-economic dimensions. Epidemiological research underscores the complexity of pathogen dynamics in intensive farming systems, where high host densities, anthropogenic stressors, and environmental variability create conditions for pathogen amplification and emergence. Key viral, bacterial, and parasitic agents—such as ISAV, P. salmonis, and L. salmonis—continue to impose heavy burdens despite advances in diagnostics, vaccination, and biosecurity, highlighting persistent gaps in early detection, transmission modelling, and cross-species infection risks. Although pathological findings have improved our understanding of host-pathogen interactions, there is still a lack of knowledge about the complex effects of genetic diversity, microbial community alterations, and stress caused by climate change.

Effective biosecurity measures (pathogen-free stock, disinfecting eggs and equipment, controlling water sources, enforcing farm zoning and fallowing, monitoring fish health, and coordinating area-based management) must be followed properly to reduce disease transmission in salmonids. Besides, a paradigm change toward integrated disease management is necessary, integrating ecosystem-based methods, precision treatments, data-driven epidemiological modeling, enhanced surveillance systems, and selective breeding for disease resistance. To reduce the transmission of pathogens between production zones, stronger regulatory frameworks, standardized reporting requirements, and international collaboration are essential. In order to predict new risks and guide adaptive management techniques, it is also essential to invest in multidisciplinary research, such as host immunological investigations and omics-based pathogen profiling. In order to secure salmon aquaculture's future, proactive health management must replace reactive disease control. Innovation, environmental stewardship, and cooperative governance must be used to achieve sustainable growth while preserving ecosystem integrity and animal welfare.

This review is based exclusively on previously published literature, and all figures and information have been appropriately cited. The author gratefully acknowledges the contributions of the scientific community whose work (findings, data, and figures) informed this manuscript.

The author acknowledges to AI in language improving, and proofreading of the essay.

The authors declare no conflicts of interest.

No original data were created, generated, or analyzed for this review. All information discussed is available in the cited publications.

Ethical approval was not required for this review as it does not include any studies with human participants or animals conducted by the author.

Not Applicable

No funding was received for this work.

1. FAO Report: Global fisheries and aquaculture production reaches a new record high. 2024.
2. Zahoor S, Jan A, & Husain, N. Current status of rainbow trout (Oncorhynchus mykiss) production in India and global world. International Journal of Creative Research Thoughts (IJCRT). 2024; 12(2):1884–1894.
3. Miller KM, Teffer A, Tucker S, et al. Infectious disease, shifting climates, and opportunistic predators: cumulative factors potentially impacting wild salmon declines. Evol Appl. 2014; 7(7):812–55.
4. Norway’s salmon industry taking heat for high premature death rates at sea farms. 2024.
5. Ruth BM, Pincinato FA, Hogne B, et al. Factors influencing production loss in salmonid farming. Aquaculture. 2021;532:736034.
6. Shefat SHT. Vaccines for infectious bacterial and viral diseases of fish. Journal of Bacteriology and Infectious Diseases. 2018;2(2):1–5.
7. Mark DP, Pat R, Torstein K. Freshwater treatment of amoebic gill disease and sea–lice in seawater salmon production: Considerations of water chemistry and fish welfare in Norway. Aquaculture, 2015; 448:18–28.
8. Mordecai G, Bass AL, Routledge R, et al. Assessing the role of Piscine orthoreovirus in disease and the associated risk for wild Pacific salmon. BMC Biol. 2023;21(1):114.
9. Rodgers C, Mohan C, Peeler E. The spread of pathogens through trade in aquatic animals and their products. Revue scientifique et technique (International Office of Epizootics). 2011; 30(1):241–56.
10. Rodger H. Fish Disease Causing Economic Impact in Global Aquaculture. In: Fish Vaccines, 2016;1–34.
11. Maezono M, Nielsen R, Buchmann K, et al. The Current State of Knowledge of the Economic Impact of Diseases in Global Aquaculture. Reviews in Aquaculture. 2025;17(3).
12. Costello MJ. The global economic cost of sea lice to the salmonid farming industry. Journal of Fish Diseases. 2009;32:115–118. 

13. Jevne LS, Guttu M, Båtnes AS. Planktonic and Parasitic Sea Lice Abundance on Three Commercial Salmon Farms in Norway Throughout a Production Cycle. Frontiers in Marine Science. 2021;8.
14. Animal and Plant Health Inspection Service, USDA. Infectious Salmon Anemia: Payment of Indemnity (Interim rule and request for comments) (Docket No. 01–126–1). Federal Register. 2002; 67(70):17605–17611.
15. Pettersen JM, Osmundsen T, Aunsmo A, et al. Controlling emerging infectious diseases in salmon aquaculture. Revue Scientifique et Technique de l'OIE. 2015a;34(3):923–938.
16. Oldham T, Rodger H, Nowak BF. Incidence and distribution of amoebic gill disease (AGD) – An epidemiological review. Aquaculture. 2016;457.
17. CSIRO. Reducing impact of Atlantic salmon gill disease. 2021.

18. Hall SJ, Delaporte A, Phillips M, et al. Blue Frontiers: Managing the Environmental Costs of Aquaculture. Penang, Malaysia. The WorldFish Center. 2011.
19. Troell M, Costa–Pierce B, Stead S, et al. Perspectives on aquaculture's contribution to the Sustainable Development Goals for improved human and planetary health. Journal of the World Aquaculture Society. 2023; 54(2);251–342.
20. Kumar G, Menanteau S, Saleh M, et al. Yersinia ruckeri, the causative agent of enteric redmouth disease in fish. Vet Res., 2015; 46(1):103.
21. Wikipedia Contributors. Enteric redmouth disease. In: Wikipedia. 2025.
22. Zorriehzahra MJ, Adel M, Torabi DS. Enteric redmouth disease: Past, present and future: A review. Iranian Journal of Fisheries Science, 2017; 16(4):1135–1156.
23. Zorriehzahra M, Mohd DH, Nazari A, et al. Assessment of environmental factors effects on enteric redmouth disease occurrence in rainbow trout (Oncorhynchus mykiss) farms in Hamedan province, Journal of Comparative Clinical Pathology Research. 2012;13:79–85.
24. Barnes A, Barnes AC. Enteric redmouth disease. CABI Compendium. 2019.
25. Guijarro JA, García–Torrico AI, Cascales D, et al. The Infection Process of Yersinia ruckeri: Reviewing the Pieces of the Jigsaw Puzzle. Front Cell Infect Microbiol. 2018;8:218.
26. Henryon M, Berg P, kjær T, et al. Selective breeding provides an approach to increase resistance of rainbow trout (Onchorhynchus mykiss) to the diseases, enteric redmouth disease, rainbow trout fry syndrome, and viral haemorrhagic septicaemia. Aquaculture. 2005; 250(3): 621–636.
27. Yang H, Zhujin D, Marana MH, et al. Immersion vaccines against Yersinia ruckeri infection in rainbow trout: Comparative effects of strain differences. J Fish Dis., 2021; 44(12):1937–1950.
28. Cipriano R, Bullock G. Furunculosis and Other Diseases Caused by Aeromonas salmonicida. Fish Disease Leaflet No. 66, U.S. Fish and Wildlife Service. 2001.
29. Boily F, Malcolm G, Johnson SC. Characterization of Aeromonas salmonicidaand Furunculosis to inform pathogen transfer risk assessments in British Columbia. Fisheries and Ocean Canada. 
30. Johnsen BO, Jensen AJ. The spread of furunculosis in salmonids in Norwegian rivers. Journal of Fish Biology. 1994;45:47–55.
31. Bakke T, Harris PD. Diseases and parasites in wild Atlantic salmon (Salmo salar) populations. Canadian Journal of Fisheries and Aquatic Sciences. 1998; 55:247–266.
32. Dublin DR. Detection methods for the epizootiological survey of aeromonas salmonicida, the causative agent of furunculosis. MS Thsis, Hokkaido University, Japan. 2012; 110 pp.
33. Marcos M, Adriana O, Yassef Y, et al. Major antigenic differences in Aeromonas salmonicida isolates correlate with the emergence of a new strain causing Furunculosis in Chilean salmon farms. Frontiers in Cellular and Infection Microbiology. 2025;15.
34. Godoy M, Montes de Oca M, Suarez R, et al. Genomics of Re–Emergent Aeromonas salmonicidain Atlantic Salmon Outbreaks. 2023;12(1):64.
35. Hamdi O & Reno P. Prevalence of Furunculosis in Chinook Salmon Depends on Density of the Host Exposed by Cohabitation. North American Journal of Aquaculture. 2004; 66(3):191–197.
36. The Scottish Government. Furunculosis in salmon. Marine Directorate, Diseases of Finfish, Molluscs and Crustaceans. The Scottish Government. 2023.
37. Kashulin A, Seredkina N, Sørum H. Cold–water vibriosis. The current status of knowledge. J Fish Dis. 2017;40(1):119–126.
38. Egidius E, Andersen K, Clausen E, et al. Cold–water vibriosis or 'Hitra disease' in Norwegian salmonid farming. Journal of Fish Diseases. 1981;4(4):353–354.
39. Norwegian Veterinary Institute. Fish Health Report 2023. 2023.
40. Fish Farming Expert. Norway’s fish mortality figures highlight ongoing health challenges. 2024.
41. S. Fish and Wildlife Service. Atlantic Salmon: 7.3 - Predation, Disease, and Competition. National Conservation Training Center. 2025.
42. Damsgård B, Sørum U, Ugelstad I, et al. Effects of feeding regime on susceptibility of Atlantic salmon (Salmo salar) to cold water vibriosis. 2004;239(1–4):37–46.
43. Tilusha M, Annas S, Mohammad NAA, et al. Pathology and pathogenesis of Vibrio infection in fish: A review. Aquaculture Reports. 2023;28:101459.
44. Sharaby SMA, Abd–Elgaber M, Tarabees R, et al. Bacteriological and histopathological studies on Vibrio species isolated from naturally infected freshwater fish in Delta region, Egypt. Advances in Animal and Veterinary Sciences. 2018;6(1):17–26.
45. Hossain KZ. Fillet quality and health of vaccinated or unvaccinated Atlantic salmon (Salmo salar L). MS thesis, Norwegian University of Life Sciences, Norway, 2016; 79 pp.
46. Lillehaug A. Vaccination strategies in seawater cage culture of salmonids. Developments in biological standardization. 1997; 90:401– 408.
47. Delghandi MR, El–Matbouli M, Menanteau–Ledouble S. Renibacterium salmoninarum–The Causative Agent of Bacterial Kidney Disease in Salmonid Fish. 2020;9(10):845.
48. Government of Scotland. Bacterial Kidney Disease in wild and farmed finfish. 2023.
49. Norwegian Veterinary Institute. Health of farmed salmon in Norway: resurgence of BKD. WeAreaAquaculture. 2024a.
50. Mitchum D & Sherman L. Transmission of Bacterial Kidney Disease from Wild to Stocked Hatchery Trout. Canadian Journal of Fisheries and Aquatic Sciences. 2011;38:547–551.
51. Bullock GL. Bacterial kidney disease of salmonid fishes caused by Corynebacterium salmonis. Fish Disease Leaflet 89,S. Fish and Wildlife Service. 1980: 10 pp.
52. Jónsdóttir H, Malmquist H, Snorrason S, et al. Epidemiology of Renibacterium salmoninarum in wild Arctic charr and brown trout in Iceland. Journal of Fish Biology. 1998;53:322–339.
53. European Commission, Health and Consumer Protection Directorate–General. Welfare of farmed fish: opinion of the Scientific Committee on Animal Health and Animal Welfare [Internet]. Brussels: European Commission. 1999.
54. European Commission. Bacterial Kidney Disease: Report of the Scientific Committee on Animal Health and Animal Welfare (Document No. Sanco/B3/AH/R14/1999) [PDF]. Directorate–General for Health & Consumer Protection. 1999.
55. Ferguson H & Sandoval C. Bacterial Kidney Disease (BKD) in Salmonids – Gross Pathology. Fish Pathology.
56. Kong H, Gong H, Jung J, et al. First Report of Bacterial Kidney Disease (BKD) Caused by Renibacterium salmoninarum in Chum Salmon (Oncorhynchus keta) Farmed in South Korea. Microorganisms. 2024;12(11):2329.
57. Weber ES. Renal Disease in Teleost Patients. Veterinary Clinics of North America. Exotic Animal Practice. 2020;23(1):231–247.
58. Manol Aqua Fish Disease Library. Bacterial kidney disease (BKD). In: Manol Aqua Fish Diseases. 2025.
59. EFSA Panel on Animal Health and Welfare (AHAW), Nielsen SS, Alvarez J, et al. Assessment of listing and categorisation of animal diseases within the framework of the Animal Health Law (Regulation (EU) 2016/429): Bacterial kidney disease (BKD). EFSA J. 2023; 1(10):e08326.
60. Hall M, Soje J, Kilburn R, et al. Cost–effectiveness of alternative disease management policies for Bacterial kidney disease in Atlantic salmon aquaculture. Aquaculture. 2014;434:88–92.
61. Emam M, Eslamloo K, Caballero–Solares A, et al. Nutritional immunomodulation of Atlantic salmon response to Renibacterium salmoninarum Front Mol Biosci. 2022;9:931548.
62. Mjaaland S, Rimstad E, Falk K, et al. Genomic characterization of the virus causing infectious salmon anemia in Atlantic salmon (Salmo salar): an orthomyxo–like virus in a teleost. J Virol. 1997;71(10):7681–7686.
63. Plarre H, Devold M, Snow M, et al. Prevalence of infectious salmon anaemia virus (ISAV) in wild salmonids in western Norway. Dis Aquat Org. 2005;66:71–79.
64. Norwegian Veterinary Institute (NVI). Fish Health Report 2023.
65. Gagné N & LeBlanc F. Overview of infectious salmon anaemia virus (ISAV) in Atlantic Canada and first report of an ISAV North American–HPR0 subtype. J Fish Dis. 2018;41(3):421–430.
66. Nylund A, Plarre H, Karlsen M, et al. Transmission of infectious salmon anaemia virus (ISAV) in farmed populations of Atlantic salmon (Salmo salar). Archives of virology. 2007;152:151–79.
67. Simon W., Bernhardt L, Qviller L, et al. Infectious Salmon Anemia Virus Shedding from Infected Atlantic Salmon (Salmo salar L.)–Application of a Droplet Digital PCR Assay for Virus Quantification in Seawater. Viruses. 2021;13:1770.
68. Dannevig BH, Mjaaland S, Rimstad E. Infectious Salmon Anemia Virus, Editor(s): Brian WJM, Marc HV Van Regenmortel, Encyclopedia of Virology (Third Edition). Academic Press. 2008;89–95.
69. Tobar J, Contreras F, Betz Y, et al. Oral Vaccination Against Infectious Salmon Anemia in Atlantic Salmon (Salmo salar) Induces Specific Immunity and Provides Protection Against Infectious Salmon Anemia Virus Challenge. World Aquaculture Congress. San Diego, EEUU.
70. Ross DH, Chris SH, Alastair H, et al. Major Quantitative Trait Loci Affect Resistance to Infectious Pancreatic Necrosis in Atlantic Salmon (Salmo salar). Genetics, 2008;178(2):1109–1115.
71. Leong J. Infectious haematopoietic necrosis. CABI Compendium. 2024.
72. Sophie S, Carl R, Garth T, et al. Evidence for a carrier state of infectious hematopoietic necrosis virus in chinook salmon Oncorhynchus tshawytscha. Dis Aquat Org.. 2001; 46:173–179.
73. Saksida SM. Infectious haematopoietic necrosis epidemic (2001 to 2003) in farmed Atlantic salmon Salmo salar in British Columbia. Dis Aquat Organ. 2006;72(3):213–23.
74. Norwegian Veterinary Institute. Infectious Hematopoietic Necrosis (IHN).
75. Wolf K. Fish Viruses and Fish Viral Diseases. Cornell University Press.
76. Kim HJ, Olesen NJ, Dale OB, et al. Pathogenicity of two lineages of infectious hematopoietic necrosis virus (IHNV) to farmed rainbow trout (Oncorhynchus mykiss) in South Korea. Virus Res. 2023;332:199133.
77. Long A, Richard J, Hawley L, et al. Transmission potential of infectious hematopoietic necrosis virus in APEX–IHN®–vaccinated Atlantic salmon. Dis Aquat Orga. 2023;122(3):213–221.
78. Murray AG & Peeler EJ. A framework for understanding the potential for emerging diseases in aquaculture. Preventive Veterinary Medicine. 2005;67(2–3):223–235.
79. World Organisation for Animal Health (WOAH). Infectious hematopoietic necrosis (Chapter 2.3.5). In: Manual of Diagnostic Tests for Aquatic Animals. WOAH. 2023.
80. Dopazo CP. The Infectious Pancreatic Necrosis Virus (IPNV) and its Virulence Determinants: What is Known and What Should be Known. Pathogens. 2020;9(2):94.
81. Hillestad B, Johannessen S, Melingen GO, et al. Identification of a New Infectious Pancreatic Necrosis Virus (IPNV) Variant in Atlantic Salmon (Salmo salar) that can Cause High Mortality Even in Genetically Resistant Fish. Front Genet. 2021;12:635185.
82. Rimsta E. Infectious Pancreatic Necrosis. 79273, CABI Compendium. 2022.
83. Layman C, Kadar J, Lyall B, et al. A Review of Factors Affecting Farmed Atlantic Salmon (Salmo salar) Welfare in Australia and Beyond. 2024.
84. Sanaa AM, Abdulmotalib J, Noor MS. Effect of environmental pollutants on fish health: An overview. Egyptian Journal of Aquatic Research. 2024;50(2):225–233.
85. Houston RD, Haley CS, Hamilton A, et al. Major Quantitative Trait Loci Affect Resistance to Infectious Pancreatic Necrosis in Atlantic Salmon (Salmo salar). Genetics. 2008;178(2):1109–1115.
86. Moen T, Baranski M, Sonesson AK. Confirmation and fine–mapping of a major QTL for resistance to infectious pancreatic necrosis in Atlantic salmon (Salmo salar): population–level associations between markers and trait. BMC Genomics. 2009;10:368 (2009).
87. Tapia D, Eissler Y, Reyes–Lopez FE, et al. Infectious pancreatic necrosis virus in salmonids: Molecular epidemiology and host response to infection.Rev Aquac. 2022;14:751–769. 
88. Murray AG. Persistence of infectious pancreatic necrosis virus (IPNV) in Scottish salmon (Salmo salar) farms. Prev Vet Med. 2006; 76(1–2):97–108.
89. Evensen Ø, Santi N. Infectious Pancreatic Necrosis Virus. Editor(s): Brian WJ, Mahy Marc HV. Van Regenmortel, Encyclopedia of Virology (Third Edition), Academic Press, 2008;83–89.
90. Ellis AE, Cavaco A, Petrie A, et al. Histology, immunocytochemistry and qRT–PCR analysis of Atlantic salmon, Salmo salar, post–smolts following infection with infectious pancreatic necrosis virus (IPNV). J Fish Dis. 2010;33(10):803–18.
91. Rivas AA, Cortez–San MM, Galaz J, et al. Evaluation of the immune response against immature viral particles of infectious pancreatic necrosis virus (IPNV): A new model to develop an attenuated vaccine. 2012;30(34):5110–5117.
92. Ahmadivand S, Savage ACNP, Palic D. Biosecurity and Vaccines for Emerging Aquatic Animal RNA Viruses.  2025;17(6):768.
93. Maria KD, Jorunn BJ. Antiviral defense in salmonids – Mission made possible?, Fish & Shellfish Immunology. 2019;87:421–437.
94. Dhamotharan K, Bjørgen H, Malik MS, et al. Dissemination of Piscine orthoreovirus-1(PRV–1) in Atlantic Salmon (Salmo salar) during the Early and Regenerating Phases of Infection. 2020;9(2):143.
95. Polinski M, Vendramin N, Cuenca A, et al. Piscine orthoreovirus: Biology and distribution in farmed and wild fish. Journal of Fish Diseases. 2020;43(11).
96. Wessel Ø, Braaen S, Alarcon M, et al. Infection with purified Piscine orthoreovirus demonstrates a causal relationship with heart and skeletal muscle inflammation in Atlantic salmon. PLOS ONE. 2017;12(8):e0183781.
97. Kongtorp R, Taksdal T. Studies with experimental transmission of heart and skeletal muscle inflammation in Atlantic salmon, Salmo salar Journal of Fish Diseases. 2009;32:253–62.
98. Kongtorp RT, Kjerstad A, Taksdal T, et al. Heart and skeletal muscle inflammation in Atlantic salmon, Salmo salar L.: Clinical, pathological, and epidemiological aspects. Diseases of Aquatic Organisms, 2004a;59(3):217–224.
99. Kongtorp R, Taksdal T, Lyngøy A. Pathology of heart and skeletal muscle inflammation (HSMI) in farmed Atlantic salmon Salmo salar Diseases of Aquatic Organisms, 2004b; 59(3):217–224.
100. Sandoval C. Heart and Skeletal Muscle Inflammation (HSMI) – Histopathology. Fish Pathology.
101. Haatveit HM, Wessel Ø, Markussen T, et al. Viral Protein Kinetics of Piscine Orthoreovirus Infection in Atlantic Salmon Blood Cells. 2017;9(3):49.
102. Taksdal T, Olsen AB, Bjerkås I, et al. Pancreas disease in farmed Atlantic salmon, Salmo salar, and rainbow trout, Oncorhynchus mykiss (Walbaum), in Norway. Journal of Fish Diseases. 2007;30(9):545–558.
103. McLoughlin MF & Graham DA. Alphavirus infections in salmonids––a review. J Fish Dis. 2007; 30(9):511–531.
104. Manousi D, Jaskula DM, Grammes F, et al. Dissecting the genetic basis of response to salmonid alphavirus in Atlantic salmon. BMC Genomics. 2025;26:657(2025).
105. Herath T, Ashby A, Jayasuriya N, et al. Impact of Salmonid alphavirus infection in diploid and triploid Atlantic salmon (Salmo salar) fry. PLOS ONE. 2017;12:e0179192.
106. Røsæg M, Thorarinsson R, Aunsmo A. Effect of vaccines against pancreas disease in farmed Atlantic salmon. Journal of Fish Diseases. 2021;44.
107. Pettersen JM, Rich KM, Jensen BB, et al. The economic benefits of disease triggered early harvest: A case study of pancreas disease in farmed Atlantic salmon from Norway. Prev Vet Med. 2015;121(3–4):314–24.
108. Yáñez JM, Houston RD, Newman S. Genetics and genomics of disease resistance in salmonid species. Front Genet. 2014;5:415.
109. Garseth ÅH, Fritsvold C, Svendsen JC, et al. Cardiomyopathy syndrome in Atlantic salmon Salmo salar: A review of the current state of knowledge. J Fish Dis. 2018;41:11–26. 
110. Fritsvold C, Mikalsen A, Poppe T, et al. Characterization of an outbreak of cardiomyopathy syndrome (CMS) in young Atlantic salmon, Salmo salar Journal of Fish Diseases. 2021;44(2).
111. Mikalsen AB, Haugland O, Rode M, et al. Atlantic Salmon Reovirus Infection Causes a CD8 T Cell Myocarditis in Atlantic Salmon (Salmo salar L.). PLoS ONE. 2012;7:e37269.
112. Scottish Government. Cardiomyopathy syndrome. Diseases of wild and farmed finfish. 2023.
113. Rodger H, Mccleary S, Ruane N. Clinical cardiomyopathy syndrome in Atlantic salmon, Salmo salar Journal of fish diseases. 2013; 37(10).
114. Ferguson H. Cardiomyopathy syndrome in Atlantic salmon (CMS) – Histopathology. Fish Histopathology.
115. Svendsen JC, Nylund S, Kristoffersen AB, et al. Monitoring infection with Piscine myocarditis virus and development of cardiomyopathy syndrome in farmed Atlantic salmon (Salmo salar) in Norway. J Fish Dis. 2019;42(4):511–518.
116. Su H, Eerde A, Steen H, et al. Establishment of a piscine myocarditis virus (PMCV) challenge model and testing of a plant–produced subunit vaccine candidate against cardiomyopathy syndrome (CMS) in Atlantic salmon Salmo salar. 2021;541:736806.
117. Sandoval SJ, Latif F, Martín M, et al. Saprolegnia species affecting the salmonid aquaculture in Chile and their associations with fish developmental stage. 2014;434.
118. Pieter W. Saprolegnia parasitica, an oomycete pathogen with a fishy appetite: new challenges for an old problem. 2006;20(3):99–104.
119. Bruno DW, Pieter W, Beakes GW. Saprolegnia and other Oomycetes. In: Fish Diseases and Disorders, Volume 3: Viral, Bacterial and Fungal Infections, CAB International. 2011;669–720.
120. Yang S, Chen D, Ou Y, et al. A Review: Factors Affecting Outbreaks of Saprolegniosis on Aquatic Animals. Israeli Journal of Aquaculture-Bamidgeh. 2018;70.
121. Norwegian Veterinary Institute (NVI). Saprolegniosis.
122. Korkea–aho T, Wiklund T, Engblom C, et al. Detection and Quantification of the Oomycete Saprolegnia parasiticain Aquaculture Environments. Microorganisms. 2022;10:2186.
123. Misk E, Gonen S, Garber AF. Resistance to Saprolegnia parasitica infection: A heritable trait in Atlantic salmon. Journal of Fish Diseases. 2022;45(9):1333–1342.
124. Lindholm–Lehto PC & Pylkkö P. Saprolegniosis in aquaculture and how to control it? Aquaculture, Fish and Fisheries. 2024;4(4):e2200. 
125. Pavić D, Grbin D, Hudina S, et al. Tracing the oomycete pathogen Saprolegnia parasitica in aquaculture and the environment. Sci Rep. 2022;12(1):16646.
126. Refai MK., Sherif M, Nermeen A et al. Monograph on Fungal Diseases of Fish. A guide for postgraduate students. 2016.
127. Hershberger PK. Ichthyophonus disease (Ichthyophoniasis). In: AFS Fish Health Section Blue Book (Chapter 3.2.18). American Fisheries Society. 2014.
128. Yokota M, Watanabe S, Hatai K, et al. Transmission of the Parasite Ichthyophonus hoferi in Cultured Rainbow Trout and Comparison of Epidemic Models. Journal of aquatic animal health. 2009;20(4):207–214.
129. Teffer AK, Jonathan C, Amy T, et al. A molecular assessment of infectious agents carried by Atlantic salmon at sea and in three eastern Canadian rivers, including aquaculture escapees and North American and European origin wild stocks. 2020;5(1):234–263.
130. Meyers TR, Burton T, Evans W, et al. Detection of viruses and virus–like particles in four species of wild and farmed bivalve molluscs in Alaska, U.S.A., from 1987 to 2009. Dis Aquat Organ. 2009;88(1):1–12.
131. Sekhawat V. A histopathological approach to diagnosis and classification of invasive fungal infections. Diagnostic Histopathology. 2024;30(10):554–563.
132. Subasinghe R, Alday–Sanz V, Bondad–Reantaso M, et al. Biosecurity: Reducing the burden of disease. Journal of the World Aquaculture Society. 2023;54(2):397–426.
133. Hamazaki T, Kahler E, Borba B, et al. PCR testing can be as accurate as culture for diagnosis of Ichthyophonus hoferi in Yukon River Chinook salmon Oncorhynchus tshawytscha. Diseases of aquatic organisms. 2013;105:21–25.
134. Ganguly SP & Mukhopadhay S. Immunostimulant, probiotic and prebiotic – their applications and effectiveness in aquaculture: A Review. The Israeli journal of aquaculture –Bamidgeh. 2010;62(3):130–138.
135. Krkosek M, Lewis MA, Morton A, et al. Epizootics of wild fish induced by farm fish. Proc Natl Acad Sci U S A. 2006;103(42):15506–10.
136. Okechukwu I, John B. Lepeophtheirus salmonis: a persisting challenge for salmon aquaculture. Animal Frontiers. 2013;4(1):22–32.
137. Emily N, Shawn R, Feindel N, et al. Horizontal and vertical distribution of sea lice larvae (Lepeophtheirus salmonis) in and around salmon farms in the Bay of Fundy, Canada. Journal of Fish Diseases. 2017;41(6).
138. Morton A, Routledge R, Krkosek M. Sea Louse Infestation in Wild Juvenile Salmon and Pacific Herring Associated with Fish Farms off the East‐Central Coast of Vancouver Island, British Columbia. North American Journal of Fisheries Management. 2008;28(2):523–532.
139. Sussie D, Frode O, Minnie H. Salmon lice detached during aquaculture practices survive and can reinfest other hosts. Aquaculture. 2025;598:742065.
140. SeafoodSource. Ireland expands sea lice cover-up inquiry. 2013.
141. Jeong J, Arriagada G, Revie CW. Targets and measures: Challenges associated with reporting low sea lice levels on Atlantic salmon farms. 2023;563(1):738865.
142. Grimnes A & Jakobsen P. The physiological effects of salmon lice (Lepeophtheirus salmonis Krøyer) infection on post smolt of Atlantic salmon (Salmo salar). Journal of Fish Biology. 2005;48(6):1179–1194.
143. Barker SE, Bricknell IR, Covello J, et al. Sea lice, Lepeophtheirus salmonis (Krøyer 1837), infected Atlantic salmon (Salmo salar) are more susceptible to infectious salmon anemia virus. PLoS ONE. 2019;4(1):0209178.
144. Jones SRM, Revie CW, Stewardson L. Trends in abundance of sea lice Lepeophtheirus salmonis and Caligus clemensi on juvenile wild Pacific salmon unchanged following cessation of salmon aquaculture in coastal British Columbia. Journal of Fish Diseases. 2025;e14136.
145. Thompson CRS, Madaro A, Nilsson J. Comparison of non–medicinal delousing strategies for parasite (Lepeophtheirus salmonis) removal efficacy and welfare impact on Atlantic salmon (Salmo salar) hosts. Aquacult Int. 2024;32:383–411.
146. McDermott T, D'Arcy J, Kelly S, et al. Novel use of nanofiltered hyposaline water to control sea lice (Lepeophtheirus salmonis and Caligus elongatus) and amoebic gill disease, on a commercial Atlantic salmon (Salmo salar) farm. Aquaculture Reports. 2021;20(1–4).
147. Krasnov A, Skugor S, Todorcevic M, et al. Gene expression in Atlantic salmon skin in response to infection with the parasitic copepod Lepeophtheirus salmonis, cortisol implant, and their combination. BMC Genomics. 2012;13:130.
148. Marianne IP, Henrik S, Hammell KL, et al. Predicting the abundance of Lepeophtheirus salmonis in the Bay of Fundy, New Brunswick. Journal of Aquatic Animal Health. 2024;36(4):355–373.
149. Kristmundsson Á & Freeman, M. Negative effects of Kudoa islandica sp. (Myxosporea: Kudoidae) on aquaculture and wild fisheries in Iceland. International Journal for Parasitology, Parasites and Wildlife. 2014;3:135–146.
150. Marty GD, Ferguson JA, Meyers TR, et al. Pathogens from salmon aquaculture in relation to conservation of wild Pacific salmon in Canada: An alternative perspective. Aquaculture, Fish and Fisheries. 2025;5:e70079.
151. Ferguson J, St–Hilaire S, Peterson T, et al. Survey of Parasites In Threatened Stocks of Coho Salmon (Oncorhynchus kisutch) In Oregon By Examination of Wet Tissues and Histology. The Journal of parasitology. 2011;97:1085–98.
152. Arthur B, Anderson SC, Bateman AW, et al. Intrinsic and extrinsic factors associated with the spatio–temporal distribution of infectious agents in early marine Chinook and Coho salmon. Marine Ecology Progress Series. 2024;736.
153. Lucilla G, Egil K, Paolo C, et al. Long–term investigation of the ‘soft flesh’ condition in Northeast Atlantic mackerel induced by the myxosporean parasite Kudoa thyrsites (Cnidaria, Myxozoa): Temporal trends and new molecular epidemiological observations. Fisheries Research. 2022;248:106221.
154. Kristmundsson Á & Freeman MA. Negative effects of Kudoa islandica sp. (Myxosporea: Kudoidae) on aquaculture and wild fisheries in Iceland, International Journal for Parasitology: Parasites and Wildlife. 2014;3(2):135–146.
155. Sophie S, Hill M, Kent M, et al. A comparative study of muscle texture and intensity of Kudoa thyrsites infection in farm–reared Atlantic salmon Salmo salar on the Pacific coast of Canada. Diseases of Aquatic Organisms. 1997;31:221–225.
156. Natacha LS, Kurt B. The ‘jellied’ or ‘mushy’ condition of fish in the North Atlantic and North Pacific fisheries: Characteristics, causes and consequences. Heliyon. 2024;10(6):e27130.
157. The Fish Site. Resistance to Kudoa thyrsites in Atlantic Salmon.
158. Henning SS, Hoffman LC, Manley M. A review of Kudoa-induced myoliquefaction of marine fish species in South Africa and other countries. South African Journal of Science. 2013;109(11–12):1–5.
159. Braden LM, Rasmussen KJ, Purcell SL, et al. Acquired Protective Immunity in Atlantic Salmon Salmo salar against the Myxozoan Kudoa thyrsites Involves Induction of MHIIβ+ CD83+ Antigen–Presenting Cells. Infection and Immunity. 2017;86(1):e00556–17.
160. Bakke TA, Cable J, Harris PD. The biology of gyrodactylid monogeneans: the "Russian–doll killers". Adv Parasitol. 2007;64:161–376.
161. Jansen PA, Bakke TA. Temperature–dependent reproduction and survival of Gyrodactylus salaris Malmberg, 1957 (Platyhelminthes: Monogenea) on Atlantic salmon (Salmo salar). Parasitology. 1991;102 Pt 1:105–12.
162. Paladini G, Shinn AP, Taylor NGH, et al. Geographical distribution of Gyrodactylus salaris Malmberg, 1957 (Monogenea, Gyrodactylidae). Parasites and Vectors. 2021;14:34.
163. Hansen H, Bachmann L, Bakke TA. Mitochondrial DNA variation of Gyrodactylus spp. (Monogenea, Gyrodactylidae) populations infecting Atlantic salmon, grayling, and rainbow trout in Norway and Sweden. International Journal for Parasitology. 2003;33(13):1471–1478.
164. David C, Odense P. Pathology of five species of Gyrodactylus Nordmann, 1832 (Monogenea). Canadian Journal of Zoology. 2011; 62(6):1084–1088.
165. Chong R. Infection with Gyrodactylus salaris. Chapter 42 – Editor(s): Frederick SB, Bernardo B, Roger SMC, Aquaculture Pathophysiology. Academic Press. 2022;513–515.
166. Harris P, Soleng A, Bakke T. Increased susceptibility of salmonids to the monogenean Gyrodactylus salaris following administration of hydrocortisone acetate. Parasitology. 2000;120 (Pt 1)(01):57–64.
167. Lindenstrom T & Buchmann K. Acquired resistance in rainbow trout against Gyrodactylus derjavini. J Helminthol. 2000; 74(2):155–60.
168. Schelkle B, Shinn AP, Peeler E, et al. Treatment of gyrodactylid infections in fish. Diseases of Aquatic Organisms.2009; 86(1);65–75.
169. Burridge L, Weis JS, Cabello F, et al. Chemical use in salmon aquaculture: A review of current practices and possible environmental effects. Aquaculture. 2010;306(1–4):7–23.
170. Mazzucato M, Dorotea T, Franzago E, et al. Overview on the Biosecurity Measures of Salmonid Fish Farms: A Case Study in Italy. Fishes. 2023;8(11):554.
171. Crosbie PB, Bridle AR, Cadoret K, et al. In vitro cultured Neoparamoeba perurans causes amoebic gill disease in Atlantic salmon and fulfils Koch's postulates. Int J Parasitol. 2012;42(5):511–5.
172. Talbot A, Gargan L, Moran G. Investigation of the transcriptomic response in Atlantic salmon (Salmo salar) gill exposed to Paramoeba perurans during early onset of disease. Sci Rep. 2021;11:20682.
173. Norwegian Veterinary Institute. Amoebic Gill Disease (AGD). 2025.
174. Young N, Dyková I, Snekvik K, et al. Neoparamoeba perurans is a cosmopolitan aetiological agent of amoebic gill disease. Diseases of Aquatic Organisms, 2008;78(3):217–23.
175. Douglas HM, Saksida S, Raverty S, et al. Temperature as a risk factor for outbreaks of Amoebic Gill Disease in farmed Atlantic salmon (Salmo solar). Bulletin- European Association of Fish Pathologists. 2001 21(3):114–116.
176. Talbot A, Gargan L, Moran G, et al. Investigation of the transcriptomic response in Atlantic salmon (Salmo salar) gill exposed to Paramoeba perurans during early onset of disease. Sci Rep. 2021;11(1):20682.
177. Padrós F & Constenla M. Diseases Caused by Amoebae in Fish: An Overview. Animals (Basel). 2021;11(4):991.
178. Marcos–López M, Calduch–Giner JA, Mirimin L, et al. Gene expression analysis of Atlantic salmon gills reveals mucin 5 and interleukin 4/13 as key molecules during amoebic gill disease. Sci Rep. 2018;8(1):13689.
179. Gjessing MC, Steinum T, Olsen AB, et al. Histopathological investigation of complex gill disease in sea farmed Atlantic. salmon. PLOS ONE. 2019;14(10):e0222926.
180. Lazado CC, Strand DA, Breiland MW, et al. Mucosal immune and stress responses of Neoparamoeba perurans–infected Atlantic salmon (Salmo salar) treated with peracetic acid shed light on the host–parasite–oxidant interactions. Front Immunol. 2022;13:948897.
181. Smith AJ, Mark BA, Philip BBC, et al. Size–dependent resistance to amoebic gill disease in naïve Atlantic salmon (Salmo salar). Fish & Shellfish Immunology. 2022;122:437–445.
182. Taylor RS, Slinger J, Stratford C, et al. Evaluation of the Infectious Potential of Neoparamoeba peruransFollowing Freshwater Bathing Treatments. 2021;9(5):967.
183. Gonzalez R. Study Reveals Ideal Condition for Most Effective Treatment for Amoebic Gill Disease. Aquaculture North America.
184. Veltman CV, Whyte SK, Purcell SL, et al. Exposures to hydrogen peroxide impact healing, redox and oxygen transport differentially from immune mechanisms in the gill of Atlantic Salmon (Salmo salar). Aquaculture. 2025;598:742007.
185. Lazado CC, Timmerhaus G, Pedersen LF, et al. Peracetic acid as a potential treatment for amoebic gill disease (AGD) in Atlantic salmon – Stage 1. Nofima, Nofima Marked. Rapport No. 21/2019. 2019.
186. Vallarino MC, Dagen SL, Costelloe E, et al. Dynamics of Gill Responses to a Natural Infection with Neoparamoeba peruransin Farmed Tasmanian Atlantic Salmon. Animals (Basel). 2024;14(16):2356.
187. Ahmad A, Aslam ML, Evensen Ø, et al. The genetics of resistance to infectious pancreatic necrosis virus in rainbow trout unveiled through survival and virus load data. Front Genet. 2024;15:1484287.
188. Aly SM, Fathi M. Advancing aquaculture biosecurity: a scientometric analysis and future outlook for disease prevention and environmental sustainability. Aquacult Int. 2024;32:8763–8789.
189. Mohammed EAH, Kovács B, Kuunya R, et al. Antibiotic Resistance in Aquaculture: Challenges, Trends Analysis, and Alternative Approaches. Antibiotics (Basel). 2025;14(6):598.
190. World Organisation for Animal Health (WOAH). Chapter 2.3.5. Infection with HPR–deleted or HPR0 infectious salmon anaemia virus. In: Manual of Diagnostic Tests for Aquatic Animals, 8th ed. Paris, WOAH, 2019;1–16.
191. Thapa PC, Raquib A, Mears K, et al. Global genetic diversity of Infectious Salmon Anemia Virus (ISAV) a scoping review protocol. PLOS ONE, 2025;20(6):e0325115.
192. Rozas–Serri M, Peña A, Gardner I, et al. Co-infection by LF-89-like and EM-90-like genogroups of Piscirickettsia salmonis in farmed Atlantic salmon in Chile: Implications for surveillance and control of piscirickettsiosis. Pathogens. 2023;12:450.
193. Kjetså MH, Ødegård J, Meuwissen THE. Accuracy of genomic prediction of host resistance to salmon lice in Atlantic salmon (Salmo salar) using imputed high–density genotypes. Aquaculture. 2020;526:735415.
194. Cáceres P, López P, Araya C, et al. Uncovering Allele–Specific Expression Patterns Associated with Sea Lice (Caligus rogercresseyi) Burden in Atlantic Salmon. Genes, 2025;16(7):841.
195. Johnson MJ, Oldham T, Nowak BF. Amoebic gill disease: a growing threat. Microbiology Australia. 2016;37(3):140–142.
196. Crozier LG & Siegel J. Impacts of climate change on salmon of the Pacific Northwest: A review of the scientific literature published in 2017. Fish Ecology Division, Northwest Fisheries Science Center, National Marine Fisheries Service, NOAA, Seattle, WA. 2018.
197. Salama NK, Collins CM, Fraser JG, et al. Development and assessment of a biophysical dispersal model for sea lice. J Fish Dis. 2013;36(3):323–37.
198. Martin F, Kevin F, Tomas N, et al. Precision fish farming: A new framework to improve production in aquaculture. Biosystems Engineering. 2018;173:176–193.
199. Urke HA, Daae K, Viljugrein H, et al. Improvement of aquaculture management practice by integration of hydrodynamic modelling. Ocean & Coastal Management. 2021;213:105849.
200. Department of Agriculture, Water and the Environment. Enteric red mouth disease (ERMD): Also known as infection with Yersinia ruckeri. In: Aquatic animal diseases significant to Australia: Identification field guide (5th ed.). Commonwealth of Australia. 2020.
201. Kumar G, Hummel K, Razzazi–Fazeli E, et al. Modulation of posterior intestinal mucosal proteome in rainbow trout (Oncorhynchus mykiss) after Yersinia ruckeri Veterinary Research. 2019;50(54).
202. Godoy M. Atypical Furunculosis in Atlantic salmon (Salmo salar): gross pathology. Flickr. 2022a.
203. Chong RS. Chapter 30 – Furunculosis. Editor(s): Frederick SBK, Bernardo B, Roger SC. Aquaculture Pathophysiology. Academic Press. 2022;395–406.
204. Tilusha M, Annas S, Noor AA, et al. Pathology and pathogenesis of Vibrio infection in fish: A review, Aquaculture Reports. 2023;28:101459.
205. Wiens G, Kaattari SL. Bacterial kidney disease [Datasheet]. CABI Compendium. 2019.
206. Ferguson H. Infectious Salmon Anaemia (ISA) – Gross Pathology. Fish Pathology. 2022.
207. Kurath G. An Online Database for IHN Virus in Pacific Salmonid Fish: MEAP-IHNV (U.S. Geological Survey Fact Sheet 2012–3027). 2012.
208. Dixon P, Paley R, Alegria–Moran R, et al. Epidemiological characteristics of infectious hematopoietic necrosis virus (IHNV): a review. Veterinary Research. 2016;47:63.
209. Godoy M. Infectious pancreatic necrosis [Flickr album]. Flickr. 2022b.
210. Mileva E. Infectious pancreatic necrosis of salmonid fish – Distribution and laboratory methods for diagnosis. Trakia Journal of Sciences. 2019;17(4):401–412.
211. Graham D, Rodger H. Pancreas disease in farmed salmon: health management and investigations at Irish farm sites 2005–2008. Marine Environment & Health Series No. 34, Marine Institute,
212. McLoughlin M. How would you recognise Pancreas Disease (PD) on your farm? The Fish Site. 2006.
213. Norwegian School of Veterinary Science. New findings about Saprolegnia infections in Norwegian salmon hatcheries. org. 2011.
214. Sitjà BA. "Schizonts of Ichthyophonus hoferi." Photograph. Flickr. 2017.
215. The University of Tokyo. (n.d.). Kudoa thyrsites. Fish Parasite Database, Department of Aquatic Bioscience, Graduate School of Agricultural and Life Sciences, The University of Tokyo,.
216. Salmon louse. 2025b.
217. Meadows R. Salmon farms create deadly clouds of sea lice. Conservation Magazine (now Anthropocene Magazine).
218. Why does farmed salmon flesh sometimes go soft? Study offers new insights. Salmon Farm Science blog. 2014.
219. Science Photo Library. Gyrodactylus salaries. SEM [Scanning electron micrograph], Science Photo Library, 2016.
220. Network of Aquaculture Centres in Asia–Pacific (NACA), & Australian Government Department of Agriculture, Fisheries and Forestry. Parasitic diseases—Gyrodactylosis. In: Aquatic Animal Diseases Significant to Asia–Pacific: Identification Field Guide.
221. Bron JE, Cano I, Fernández C, et al. Neoparamoeba perurans. In: Fish Parasites. A Handbook of Protocols for their Isolation, Culture. European Association of Fish Pathologists Book Series. 2021;78–94.
222. Downes J, Collins E, Morrissey T, et al. Confirmation of Neoparamoeba perurans on the gills of Atlantic salmon during the earliest outbreaks of amoebic gill disease in Ireland. Bulletin of the European Association of Fish Pathologists. 2018; 38(1):42–48.