99
indigenous water-borne organisms, i.e. using fi lter-sterilised river water, renibacterial cells survived for 28 days, after which there was a rapid decline in numbers.
Essentially, these data show that renibacteria have the potential to survive outside of
fi sh for limited periods, although in water it is probably unable to compete with
members of the normal aquatic microfl ora (Austin and Rayment 1985 ). In one
study, the pathogen was found only in association with asymptomatic and clinically
diseased fi sh (Austin and Rayment 1985 ). In another investigation, it was determined that the blue mussel (Mytilus edulis) cleared and killed most Ren. salmoninarum cells from seawater (Paclibare et al. 1994 ). However, some renibacterial cells
could be found in mussel faeces during settling. Yet, it was conceded that mussels
were unlikely to pose a realistic threat to fi sh farms regarding the survival and spread
of renibacterium. But what if infected mussels are transferred to clean seawater?
The answer according to Paclibare et al. ( 1994 ) was that the mussel cleared Ren.
salmoninarum from within them upon transfer to clean sites. Clearly, early studies
may have been hampered by lack of a suitable selective medium. Nevertheless, the
use of SKDM has not, as yet, produced any defi nite evidence to suggest a non-fi sh
reservoir for the organism (Austin et al. 1983 ; Embley 1983 ; Austin and Rayment
1985 ). The precise source of infection is unclear, but may include clinically or
asymptomatically diseased fi sh (Wood and Wallis 1955 ; Wolf 1966 ; Bucke 1978 ;
Mitchum et al. 1979 ; Paterson et al. 1979 ; Fryer and Sanders 1981 ). The organism
has been recovered from faeces of both cultured and wild salmonid stocks.
According to Balfry et al. ( 1996 ), renibacterium is shed from faeces, and may survive in seawater for a week. Attention has also been focused on the role of eggs in
the transmission of BKD (‘vertical’ transmission) (Allison 1958 ; Wolf 1966 ;
MacLean and Yoder 1970 ; Mitchum et al. 1979 ; Lee and Evelyn 1989 ). Allison
( 1958 ) indicated the involvement of eggs when BKD occurred following transfer of
ova from an infected site. Similarly, Bullock et al. ( 1978 )) implicated disinfected
eggs of chinook salmon in the spread of the disease. Moreover, the preliminary data
of Paterson et al. ( 1981 ) pointed to the presence of Renibacterium within fertilised
eggs. Evelyn et al. ( 1984 ) demonstrated the presence of renibacteria in 11.6–15.1 %
of eggs from a coho salmon which was infected with BKD, such that the coelomic
fl uid was cloudy because of high numbers of the organism. These authors suggested
that Ren. salmoninarum was present in the yolk of the eggs, even after treatment
with erythromycin (Evelyn et al. 1986a ). Artifi cial contamination experiments led
to the observation that infection occurred by entry of renibacterial cells from the egg
surface to the perivitelline space through the micropyle during water-hardening
(Kohara et al. 2012 ). Of greater signifi cance was the fi nding that iodophors were
ineffective at preventing intra-ovum infections. However, using rainbow trout and
amago salmon ( Oncorhynchus masou ), the pathogen was not isolated from egg contents suggesting that there was minimal risk of intra-ovum infection of salmonid
eggs in the coelomic cavity (Kohara et al. 2013 ).
The manifestation of the disease is complicated by certain environmental factors,
including water hardness (Warren 1963 ), temperature, salinity and diet. Belding and
Merrill ( 1935 ) were the fi rst workers to describe the seasonal nature of BKD, with
a correlation between water temperature and level of mortality. Earp et al. ( 1953 )
Renibacterium salmoninarum
indigenous water-borne organisms, i.e. using fi lter-sterilised river water, renibacterial cells survived for 28 days, after which there was a rapid decline in numbers.
Essentially, these data show that renibacteria have the potential to survive outside of
fi sh for limited periods, although in water it is probably unable to compete with
members of the normal aquatic microfl ora (Austin and Rayment 1985 ). In one
study, the pathogen was found only in association with asymptomatic and clinically
diseased fi sh (Austin and Rayment 1985 ). In another investigation, it was determined that the blue mussel (Mytilus edulis) cleared and killed most Ren. salmoninarum cells from seawater (Paclibare et al. 1994 ). However, some renibacterial cells
could be found in mussel faeces during settling. Yet, it was conceded that mussels
were unlikely to pose a realistic threat to fi sh farms regarding the survival and spread
of renibacterium. But what if infected mussels are transferred to clean seawater?
The answer according to Paclibare et al. ( 1994 ) was that the mussel cleared Ren.
salmoninarum from within them upon transfer to clean sites. Clearly, early studies
may have been hampered by lack of a suitable selective medium. Nevertheless, the
use of SKDM has not, as yet, produced any defi nite evidence to suggest a non-fi sh
reservoir for the organism (Austin et al. 1983 ; Embley 1983 ; Austin and Rayment
1985 ). The precise source of infection is unclear, but may include clinically or
asymptomatically diseased fi sh (Wood and Wallis 1955 ; Wolf 1966 ; Bucke 1978 ;
Mitchum et al. 1979 ; Paterson et al. 1979 ; Fryer and Sanders 1981 ). The organism
has been recovered from faeces of both cultured and wild salmonid stocks.
According to Balfry et al. ( 1996 ), renibacterium is shed from faeces, and may survive in seawater for a week. Attention has also been focused on the role of eggs in
the transmission of BKD (‘vertical’ transmission) (Allison 1958 ; Wolf 1966 ;
MacLean and Yoder 1970 ; Mitchum et al. 1979 ; Lee and Evelyn 1989 ). Allison
( 1958 ) indicated the involvement of eggs when BKD occurred following transfer of
ova from an infected site. Similarly, Bullock et al. ( 1978 )) implicated disinfected
eggs of chinook salmon in the spread of the disease. Moreover, the preliminary data
of Paterson et al. ( 1981 ) pointed to the presence of Renibacterium within fertilised
eggs. Evelyn et al. ( 1984 ) demonstrated the presence of renibacteria in 11.6–15.1 %
of eggs from a coho salmon which was infected with BKD, such that the coelomic
fl uid was cloudy because of high numbers of the organism. These authors suggested
that Ren. salmoninarum was present in the yolk of the eggs, even after treatment
with erythromycin (Evelyn et al. 1986a ). Artifi cial contamination experiments led
to the observation that infection occurred by entry of renibacterial cells from the egg
surface to the perivitelline space through the micropyle during water-hardening
(Kohara et al. 2012 ). Of greater signifi cance was the fi nding that iodophors were
ineffective at preventing intra-ovum infections. However, using rainbow trout and
amago salmon ( Oncorhynchus masou ), the pathogen was not isolated from egg contents suggesting that there was minimal risk of intra-ovum infection of salmonid
eggs in the coelomic cavity (Kohara et al. 2013 ).
The manifestation of the disease is complicated by certain environmental factors,
including water hardness (Warren 1963 ), temperature, salinity and diet. Belding and
Merrill ( 1935 ) were the fi rst workers to describe the seasonal nature of BKD, with
a correlation between water temperature and level of mortality. Earp et al. ( 1953 )
Renibacterium salmoninarum