339
parameters, namely water temperature and the quantity of organic matter in the
water, undoubtedly infl uence the severity of outbreaks. In particular, it is noteworthy that most disease outbreaks occur at high water temperature, i.e. 30 °C, when
high levels of organic matter are present. However, data showed that the incidence
of disease in catfi sh ponds rarely exceeded 5 %, except when infected fi sh were
moved to holding tanks. During these periods, edwardsiellosis became rampant
with total mortalities approaching 50 % of the population (Meyer and Bullock
1973 ).
There is some evidence that Edw. tarda occurs in sediment (Rashid et al. 1994a )
and water within the vicinity of fi sh farms (Minagawa et al. 1983 ; Park et al. 1983 ;
Rashid et al. 1994a ). It has been reported to inhabit aquatic invertebrates, such as
the freshwater aquarium snail ( Ampullaria sp.; Bartlett and Trust 1976 ) and seaurchin (Sasaki and Aita 1975 ), and has been associated with vertebrates, namely
snakes (Iverson 1971 ), frogs (Sharma et al. 1974 ), turtles (Otis and Behler 1973 ),
gulls (Berg and Anderson 1972 ) and human beings (Koshi and Lalitha 1976 ). Any
one of these hosts may serve as a reservoir for infections of fi sh. However, it is
unclear whether Edw. tarda should be regarded as a primary or opportunistic pathogen of fi sh. Indeed, it may comprise part of the normal microfl ora of fi sh surfaces,
insofar as Wyatt et al. ( 1979 ) have indicated the widespread occurrence of the
micro-organism in and around channel catfi sh. A suggestion has been made that the
organism becomes non-culturable in the aquatic environment (Sakai et al. 1994 ).
Experimentally, a VBNC state was induced following culturing in aged seawater at
4 °C when total counts remained constant over 28 days [cells became coccoid, and
decreased in size) whereas culturability declined to undetectable levels. Resuscitation
was possible in chick embryos at higher temperatures, and these cells killed turbot
following i.p. injection (Du et al. 2007 ).
The presence of sub-lethal concentrations of copper (100–250 μg/l) in water
leads to increased susceptibility of Japanese eels to infection (Mushiake et al. 1985 ).
This increased susceptibility seems likely to be attributed to a reduction in lymphocytes and granulocytes in the blood, leading to lowered phagocytosis (Mushiake
et al. 1985 ).
Pathogenicity
To date, the disease has been recorded in a diverse array of fi sh species, including
chinook salmon (Amandi et al. 1982 ), channel catfi sh (Meyer and Bullock 1973 ),
mullet (Kusuda et al. 1976 ), carp (Sae-Oui et al. 1984 ), eels (Wakabayashi and
Egusa 1973 ; Mo et al. 2015 ), tilapia (Kubota et al. 1981 ), olive fl ounder (Han et al.
2006 ) and fl ounder (Nakatsugawa 1983 ; Mekuchi et al. 1995a ; Pakingking et al.
2003 ). From laboratory-based experiments, pathogenicity has also been demonstrated in steelhead and rainbow trout (Amandi et al. 1982 ), yellowtail (Nakatsugawa
1983 ) and loach (Park et al. 1983 ). Co-infection of Edw. tarda with aquabirnavirus
has led to higher mortalities in Japanese fl ounder (Pakingking et al. 2003 ).
Edwardsiella tarda
parameters, namely water temperature and the quantity of organic matter in the
water, undoubtedly infl uence the severity of outbreaks. In particular, it is noteworthy that most disease outbreaks occur at high water temperature, i.e. 30 °C, when
high levels of organic matter are present. However, data showed that the incidence
of disease in catfi sh ponds rarely exceeded 5 %, except when infected fi sh were
moved to holding tanks. During these periods, edwardsiellosis became rampant
with total mortalities approaching 50 % of the population (Meyer and Bullock
1973 ).
There is some evidence that Edw. tarda occurs in sediment (Rashid et al. 1994a )
and water within the vicinity of fi sh farms (Minagawa et al. 1983 ; Park et al. 1983 ;
Rashid et al. 1994a ). It has been reported to inhabit aquatic invertebrates, such as
the freshwater aquarium snail ( Ampullaria sp.; Bartlett and Trust 1976 ) and seaurchin (Sasaki and Aita 1975 ), and has been associated with vertebrates, namely
snakes (Iverson 1971 ), frogs (Sharma et al. 1974 ), turtles (Otis and Behler 1973 ),
gulls (Berg and Anderson 1972 ) and human beings (Koshi and Lalitha 1976 ). Any
one of these hosts may serve as a reservoir for infections of fi sh. However, it is
unclear whether Edw. tarda should be regarded as a primary or opportunistic pathogen of fi sh. Indeed, it may comprise part of the normal microfl ora of fi sh surfaces,
insofar as Wyatt et al. ( 1979 ) have indicated the widespread occurrence of the
micro-organism in and around channel catfi sh. A suggestion has been made that the
organism becomes non-culturable in the aquatic environment (Sakai et al. 1994 ).
Experimentally, a VBNC state was induced following culturing in aged seawater at
4 °C when total counts remained constant over 28 days [cells became coccoid, and
decreased in size) whereas culturability declined to undetectable levels. Resuscitation
was possible in chick embryos at higher temperatures, and these cells killed turbot
following i.p. injection (Du et al. 2007 ).
The presence of sub-lethal concentrations of copper (100–250 μg/l) in water
leads to increased susceptibility of Japanese eels to infection (Mushiake et al. 1985 ).
This increased susceptibility seems likely to be attributed to a reduction in lymphocytes and granulocytes in the blood, leading to lowered phagocytosis (Mushiake
et al. 1985 ).
Pathogenicity
To date, the disease has been recorded in a diverse array of fi sh species, including
chinook salmon (Amandi et al. 1982 ), channel catfi sh (Meyer and Bullock 1973 ),
mullet (Kusuda et al. 1976 ), carp (Sae-Oui et al. 1984 ), eels (Wakabayashi and
Egusa 1973 ; Mo et al. 2015 ), tilapia (Kubota et al. 1981 ), olive fl ounder (Han et al.
2006 ) and fl ounder (Nakatsugawa 1983 ; Mekuchi et al. 1995a ; Pakingking et al.
2003 ). From laboratory-based experiments, pathogenicity has also been demonstrated in steelhead and rainbow trout (Amandi et al. 1982 ), yellowtail (Nakatsugawa
1983 ) and loach (Park et al. 1983 ). Co-infection of Edw. tarda with aquabirnavirus
has led to higher mortalities in Japanese fl ounder (Pakingking et al. 2003 ).
Edwardsiella tarda