In one study the patho gen was found only in association with asymptomatic and

In one study the patho gen was found only in

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Rayment, 1985). In one study, the patho- gen was found only in association with asymptomatic and clinically diseased fish (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 settHng. Yet, it was conceded that mussels were unHkely to pose a realistic threat to fish 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 definite evidence to suggest a non-fish reservoir for the organism (Austin et al., 1983a; Embley, 1983; Austin and Rayment, 1985). The precise source of infection is unclear, but may include clinically or asymptomatically diseased fish (Wood and WalHs, 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), Renibac- terium 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) (AlHson, 1958; Wolf, 1966; MacLean and Yoder, 1970; Mitchum et al, 1979; Lee and Evelyn, 1989). AlHson (1958) indicated the involvement of eggs when BKD occurred following transfer of ova from an infected site. Similarly, Bullock et al. (1978b) 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 o^ Renibacter- ium within fertilised eggs. Evelyn et al. (1984) demonstrated the presence of renibac- teria in 11.6-15.1% of eggs from a coho salmon which was infected with BKD, such that the coelomic fluid 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). Of greater significance was
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Epizootiology: Gram-positive bacteria 241 the finding that iodophors were ineffective at preventing intra-ovum infections. Clearly, this has profound implications for control of the disease. The manifestation of the disease is complicated by certain environmental factors, including water hardness (Warren, 1963), temperature, saHnity and diet. Belding and Merrill (1935) were the first workers to describe the seasonal nature of BKD, with a correlation between water temperature and level of mortality. Earp et al. (1953) found that BKD occurred over a wide range of water temperatures from 8 to 18°C. Most epizootics occurred in the autumn and winter, i.e. during periods of declining water temperatures. However, most mortalities occurred at higher tempera- tures, a conclusion which has been echoed by Austin (1985), although the reverse has
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