624
Piscirickettsiaceae Representative
Piscirickettsia salmonis
Characteristics of the Disease
Degenerate or obligately parasitic bacteria, i.e. chlamydias and rickettsias, have
been long established as pathogens of invertebrates, and sporadically mentioned in
connection with fi sh diseases (Wolf 1981 ). Yet, fi rm evidence of their role in fi sh
pathology has not been forthcoming until an upsurge of interest in Chile. Thus since
1989, a disease coined “coho salmon syndrome”, Huito disease (Schäfer et al. 1990 )
or salmonid rickettsial septicaemia (Cvitanich et al. 1991 ) has been observed in
coho salmon, chinook salmon, Atlantic salmon and rainbow trout, with a spread to
Atlantic salmon in Norway (Olsen et al. 1997 ) and white sea bass in California,
USA (Arkush et al. 2005 ). Losses fl uctuated between 3 and 7 % of stock per week;
the cumulative mortalities reaching 90 %. The organism was formally recognised as
a new taxon, for which the name of Piscirickettsia salmonis was proposed (Fryer
et al. 1992 ), and is a representative of the Gammaproteobacteria . Although the
pathogen was initially associated with salmon, there has been a spread to other
groups, including sea bass (McCarthy et al. 2005 ; Arkush et al. 2005 ). Also, the
geographical range has spread from Chile to North America and Europe, including
Greece (McCarthy et al. 2005 ) and Scotland (Birkbeck et al. 2004 ). Infected fi sh
gathered at the surface of cages, became sluggish and were inappetant. External
signs included melanosis, epidermal indurations, and paleness of the gills, which
was indicative of anaemia. The haemacrits fell to ≤27 %. Internally, haemorrhages
were evident on the abdominal walls, visceral fat and on the air bladder. A mottled
liver and swollen spleen was apparent in heavily infected animals. The kidney was
infl ammed and swollen. The intestine was full of yellowish mucoid material
(Schäfer et al. 1990 ; Branson and Diaz-Munoz 1991 ). Initially, the disease was not
considered to occur during the freshwater stage of fi sh culture, Instead, mortalities
have been noted to begin 6–12 weeks after transfer of fi sh from fresh to seawater
(Fryer et al. 1992 ). However in a later development, the pathogen was recovered
from the freshwater stage of coho salmon and rainbow trout (Bravo 1994 ; Gaggero
et al. 1995 ).
Isolation
Isolation of the pathogen from the kidney of infected fi sh was possible in the cytoplasm of salmon cell lines (including CH5E-214) with incubation at 12–21 °C (optimally at 15–18 °C), whereupon a cytopathic effect was demonstrated in 5–6 days
(Fryer et al. 1990 ). The cell sheet was completely lysed in 14 days. Originally,
growth did not occur on bacteriological media, including BHIA, blood agar, mycoplasma medium, charcoal yeast extract agar, Loeffl er medium (Appendix in
11 Miscellaneous Pathogens
Piscirickettsiaceae Representative
Piscirickettsia salmonis
Characteristics of the Disease
Degenerate or obligately parasitic bacteria, i.e. chlamydias and rickettsias, have
been long established as pathogens of invertebrates, and sporadically mentioned in
connection with fi sh diseases (Wolf 1981 ). Yet, fi rm evidence of their role in fi sh
pathology has not been forthcoming until an upsurge of interest in Chile. Thus since
1989, a disease coined “coho salmon syndrome”, Huito disease (Schäfer et al. 1990 )
or salmonid rickettsial septicaemia (Cvitanich et al. 1991 ) has been observed in
coho salmon, chinook salmon, Atlantic salmon and rainbow trout, with a spread to
Atlantic salmon in Norway (Olsen et al. 1997 ) and white sea bass in California,
USA (Arkush et al. 2005 ). Losses fl uctuated between 3 and 7 % of stock per week;
the cumulative mortalities reaching 90 %. The organism was formally recognised as
a new taxon, for which the name of Piscirickettsia salmonis was proposed (Fryer
et al. 1992 ), and is a representative of the Gammaproteobacteria . Although the
pathogen was initially associated with salmon, there has been a spread to other
groups, including sea bass (McCarthy et al. 2005 ; Arkush et al. 2005 ). Also, the
geographical range has spread from Chile to North America and Europe, including
Greece (McCarthy et al. 2005 ) and Scotland (Birkbeck et al. 2004 ). Infected fi sh
gathered at the surface of cages, became sluggish and were inappetant. External
signs included melanosis, epidermal indurations, and paleness of the gills, which
was indicative of anaemia. The haemacrits fell to ≤27 %. Internally, haemorrhages
were evident on the abdominal walls, visceral fat and on the air bladder. A mottled
liver and swollen spleen was apparent in heavily infected animals. The kidney was
infl ammed and swollen. The intestine was full of yellowish mucoid material
(Schäfer et al. 1990 ; Branson and Diaz-Munoz 1991 ). Initially, the disease was not
considered to occur during the freshwater stage of fi sh culture, Instead, mortalities
have been noted to begin 6–12 weeks after transfer of fi sh from fresh to seawater
(Fryer et al. 1992 ). However in a later development, the pathogen was recovered
from the freshwater stage of coho salmon and rainbow trout (Bravo 1994 ; Gaggero
et al. 1995 ).
Isolation
Isolation of the pathogen from the kidney of infected fi sh was possible in the cytoplasm of salmon cell lines (including CH5E-214) with incubation at 12–21 °C (optimally at 15–18 °C), whereupon a cytopathic effect was demonstrated in 5–6 days
(Fryer et al. 1990 ). The cell sheet was completely lysed in 14 days. Originally,
growth did not occur on bacteriological media, including BHIA, blood agar, mycoplasma medium, charcoal yeast extract agar, Loeffl er medium (Appendix in
11 Miscellaneous Pathogens