Introduction/Aetiology
Classification of the Causative Agent
Eubacteria, family Micrococcaceae, genus Renibacterium, species R. salmoninarum. Renibacterium salmoninarum is a Gram-positive nonsporulating, nonmotile coccobacillus that seems to act as an obligate parasite. It develops chronically in salmonid fish and results in late clinical disease.
Resistance to Physical and Chemical Action
Temperature: Optimum temperature for culture: 15oC. Preserved by refrigeration, freezing, freeze-drying.
Chemicals/
Disinfectants: Chlorine, quaternary ammonia, formalin, may be useful for disinfecting materials. However, transmission in ovo and the wide distribution of the pathogen in natural habitats limit the effectiveness of disinfection procedures.
Survival: Survival of this organism in the environment is poorly understood. It has been reported that the bacterium could remain viable in seawater for up to 1 week, and in the absence of other microflora, even longer. This duration of survival could be significant in a hatchery or netpen. May be hosted by nonsusceptible nonsalmonid species.
Epidemiology
Morbidity rate is high, due to vertical transmission.
Mortality is delayed but may become serious in highly infected populations.
Hosts
All salmonid species.
Transmission
Horizontal transmission may be direct, through contact with diseased fish and contaminated water, or indirect, through handling materials or feeding with fisheries residues.
Vertical transmission is the most frequent route of contamination. The bacteria are present in the ovarian fluids and are likely to be the source of the R. salmoninarum that have been detected in eggs from some infected female salmonids.
Sources of the Agent
Internal organs or skin tissues in cases of external lesions.
Eggs and coelomic fluid.
Inanimate vectors.
Many fish species, and even invertebrates, may be hosts of the pathogen without clinical manifestation.
Occurrence
Occurs in feral and farmed populations of salmonids in almost all areas where they are naturally distributed or have been acclimatised. No conclusive evidence has been reported for the presence of R. salmoninarum in the salmonid population of Australia, New Zealand, Russia, or some Mediterranean, countries.
For detailed information on occurrence, see recent issues of World Animal Health and the OIE Web site.
Diagnosis
Incubation period is long, and the clinical signs, often prompted by environmental causes, usually occur in fish over 1 year old.
Clinical Diagnosis
Dark coloration, exophthalmia and abdominal distension result from the destruction of interstitial kidney tissues.
Externally, haemorrhages may be observed at the base of the fins or at the vent, and the rupture of small cutaneous vesicles results in small ulcerations.
Greyish nodules or diffuse masses are generally observed in the kidney, spleen and liver. The kidney appears enlarged and the abdominal cavity is generally filled with fluid.
Lesions
Typical chronic infection characterised by granuloma scattered in the internal organs. A phagocytic reaction associated with more or less complete encapsulation may be observed. Caseous necrosis may be observed in advanced cases.
Differential Diagnosis
External manifestations are nonpathognomonic, but the course of the disease and the nature of the kidney lesions may provide presumptive indications. The disease must be differentiated from other kidney diseases of chronic progression including pseudo-kidney disease (Carnobacterium piscicola), nephrocalcinosis, and proliferative kidney disease. Confirmation must be by the observation and identification of the bacteria.
Laboratory Diagnosis
Procedures
Identification of the agent
Isolation and culture under appropriate conditions, completed by bacteriological identification or specific agglutination, require several weeks.
Antigen detection in infected tissues is more rapid.
Immunofluorescence (direct/indirect fluorescent antibody test [FAT and IFAT]).
Enzyme-linked immunosorbent assay (ELISA).
Polymerase chain reaction (PCR).
Serological tests
Not recommended. No positive correlation has been demonstrated between the antibody response and the course of the infection in fish populations.
Samples
Identification and isolation of the agent
Internal organs from diseased fish: kidney and spleen are the most convenient.
Tissue prints or smears for the detection of the antigen.
In maturing females, coelomic fluid is a reliable material and does not need to kill the fish.
Disease Prevention and Treatment
Sanitary Prophylaxis
Identification and culling of carrier broodfish.
Destruction or slaughtering of infected fish.
Disinfection of premises, materials and raceways.
Introduction of controlled pathogen-free stocks.
In infected areas, screening of asymptomatic carriers before spawning, and selection of breeders with the lowest levels of infection associated with erythromycin treatment have noticeably reduced the prevalence of the disease.
Treatment
Salmon
Trout
References
Chapter 2.2.6. in the OIE Diagnostic Manual for Aquatic Animal Diseases, OIE (World Organisation for Animal Health), Paris, France.
Chapter 2.2.6. in the OIE International Aquatic Animal Health Code, OIE (World Organisation for Animal Health), Paris, France
Cold Water Vibriosis
Introduction/Aetiology
Vibrio salmonicida, the agent of Hitra disease, a cold water vibriosis affecting Atlantic salmon (Salmo salar), is a facultatively anaerobic motile rod. This disease affects mainly fish farms with Atlantic salmon and occasionally with rainbow trout. Vibrio salmonicida has also been described as the aetiological agent of cold-water vibriosis affecting cod in Norway (Sorum et al., 1990). Hitra disease occurs mainly in late autumn, winter or early spring.
Epidemiology
Hitra disease appeared in 1977 and occurred for the first time on a large scale in 1979 in fish farms in the Norwegian island of Hitra. Since then, it has devastated fish farms located along the western and northern Norwegian coast (Egidius et al., 1981). However, single outbreaks have also been reported in Scotland (Bruno et al., 1985, 1986), on the Faroe Islands (Dalsgaard et al., 1988) and in New Brunswick and Nova Scotia, Canada (reference in Sorum et al., 1992).
Epidemiological studies based on plasmid profiles suggest that V. salmonicida was transmitted from cod to Atlantic salmon and vice versa in fish farms in northern Norway (Sorum et al., 1990).
Diagnosis
The characteristics of this disease, also known as haemorrhagic syndrome, are anaemia and haemorrhages with a generalized septicaemia, presenting large amounts of bacterial cells in the blood of moribund or recently dead fish. The haemorrhages are mainly found in the integument surrounding the internal organs of the fish ( Poppe et al., : Egidius et al.,)
Treatment
Salmon
Trout
References
© CAB INTERNATIONAL 1999. Fish Diseases and Disorders, Volume 3: Viral, Bacterial and Fungal Infections (eds P.T.K. Woo and D.W. Bruno)
Enteric Redmouth Disease [ERM]
Introduction
Enteric Redmouth Disease (ERM) is caused by the bacterial pathogen Yersinia ruckeri. The first instances of the disease were reported in Rainbow trout (Oncorhynchus mykiss) in the USA in the 1950s. Subsequent clinical outbreaks occurred in the UK in 1982 and in most other parts of Europe over the following few years. It is now endemic in all trout producing countries where it can cause severe economic losses. It is also becoming a more significant pathogen of farmed salmon, primarily in freshwater but it has been reported to cause losses in the sea as well.
According to estimates from within the British Trout Association in 1998, the cost of ERM in the UK trout industry alone was approximately 1.3-1.5 million per year. This figure is based on the costs of mortality, growth penalties and subsequent reduction in feed conversion rate, grading problems, withdrawal periods due to antibiotic treatments and subsequent harvesting delays as a result of the disease. This can be calculated as 10% of the production cost of the industry. Extrapolating these figures to the European trout industry producing 200,000 tons per year indicates ERM causes a potential economic loss of 20 million each year.
Aetiology
ERM is characteristically a disease of rising and falling water temperatures. The highest risk of disease occurs between 8o and 16oC although mortality can occur at temperatures as low as 4oC. At the higher temperatures mortality can rise quickly. Levels of 15 – 20 % have been reported even with antibiotic treatments. Fish of all sizes are affected, however, fish of 50 – 200g are the most susceptible. Stressful conditions such as high stocking densities and poor water quality will increase the level of susceptibility and mortality.
Species Common name
Salmonids
Oncorhynchus kisutch Coho salmon
Oncorhynchus mykiss Rainbow trout
Oncorhynchus nerka Sockeye salmon
Oncorhynchus tschawytscha Chinook salmon
Salmo clarkii Cutthroat
Salmo salar Atlantic salmon
Salmo trutta Brown trout
Salvelinus alpinus Arctic char
Salvelinus fontinalis Brook trout
Non-salmonids
Acipenser baeri Sturgeon
Anguilla anguilla Eel
Aristichthys nobilis Bighead carp
Carassius auratus Goldfish
Coregonus artedii Cisco
Coregonus peled Whitefish
Coregonus muksun Whitefish
Cyprinus carpio Common carp
Hypophthalmichthys molitrix Silver carp
Ictalurus punctatus Channel catfish
Lota lota Burbot
Notemigonus atherinoides Emerald shiner
Pimephales promelas Minnow
Scophthalmus maximus Turbot
Solea solea Sole
Symptoms
The most distinctive external and internal signs and symptoms of the disease are:
Black, lethargic fish “hanging” in areas of low flow at the edges of ponds and raceways or against outlet screens.
Bilateral exophthalmia
Abdominal distension as a result of fluid accumulation
Haemorrhages of the mouth and gills. The so-called “Redmouth” is rarely seen in acute infections but may be present in chronic infections.
General septicaemia with inflammation of the gut
Petechial haemorrhage of the pyloric caecae
Diffuse haemorrhages within the swim bladder. These are the most diagnostic symptoms of ERM
The spleen is often enlarged and can be almost black in colour
The external symptoms mentioned above are also seen with other bacterial and parasitic infections so some further diagnosis must be carried out. Yersinia ruckeri is easily isolated from diseased fish on TSA plates or preferably upon a semi-selective media designed for the purpose.
Following an incubation period of 24-48 hours shiny off-white colonies develop. Identity can be rapidly confirmed using specific antisera such as Mono YR test kits
Epidemiology
Known to be present over large areas of the USA and Europe (Denmark, France, Germany, Italy, Norway and UK). It is also present in Australia, South Africa and Chile, all of which received imported salmonid eggs and fry from these areas. However, there is some variation in the strains and serotypes within the genus associated with geographical areas and it cannot be ruled out that it is of a more widespread occurrence in a natural manner than was at first thought.
Treatment
Good husbandry can play an important part in limiting the level of mortality caused by ERM. Reducing stocking densities at times of high risk and avoiding stressful procedures such as grading will help.
Salmon
Trout
References
© CAB INTERNATIONAL 1999. Fish Diseases and Disorders, Volume 3:
Viral, Bacterial and Fungal Infections (eds P.T.K. Woo and D.W. Bruno)
