There are predisposing factors, other than age and inherent susceptibility, that are associated with the precipitation of clinical furunculosis in hatchery stocks throughout the year. These include physical damage, poor water quality, presence of ectoparasites and other diseases, diet and physical and psychological stresses, such as grading, tagging, injection and netting (Olivier, 1997; Pickering, 1997). However, a marked seasonality in the incidence of both clinical and covert furunculosis infections has been observed in hatchery stocks and wild populations. In hatchery stocks, both smolting and high water temperatures have been implicated in this apparent seasonality. The period of smolting is associated with major physiological changes, including chronic cortisol elevation, which can bring about severe depression of the fish's defence system and increased susceptibility to bacterial infections (Maule et al., 1986; Pickering, 1997). In addition, high water temperatures (12-15°C) in late spring-early summer increase the likelihood of furunculosis outbreaks in both fresh water and sea water (Klontz and Wood, 1972; Johansson, 1977; Novotny, 1978). In fact, Malnar et al. (1988) would contend that high temperature is the major factor influencing the development of furunculosis. High water temperature not only influences the stress response of fish but may act at the level of the pathogen (Groberg et al., 1978), and it has been demonstrated that the growth of
A. salmonicida in the blood of cherry salmon (Oncorhynchus masou) correlated positively with water temperatures in the range 5-20°C (Sako and Hara, 1981). Not surprisingly, the seasonal nature of clinical infection by A. salmonicida is not confined to hatchery stocks. As early as 1926, Horne observed that the incidence of furunculosis in a riverine population of brown trout first appeared towards the end of May and declined in October (Horne, 1928). Blake and Clarke (1931) observed that spawning in salmon rendered them susceptible to furunculosis. There is no reason to suspect that the temperature effects observed in hatchery reared stocks will not also apply to wild stocks. The influence of spawning on increased susceptibility to furunculosis would appear to be similar in a wide range of salmonids (Nomura et al., 1993) and includes chronic cortisol elevation and associated lymphocytopaenia (Pickering, 1986), decline in antibody production (Yamaguchi et al., 1980) and immunosupression associated with gonadal steroids (Slater and Schreck, 1993). The presence of wild spawning fish in the vicinity of freshwater hatcheries may also have an impact on the seasonality of furunculosis in stocks contained within those hatcheries.
The occurrence of covert A. salmonicida infections in hatchery populations has also been observed to be seasonal (Jensen and Larsen, 1980; Scallan and Smith, 1984, 1993; Hiney, 1994). However, neither smolting, spawning nor high water temperatures can explain other peaks in the incidence of clinical and covert infections observed by these authors at a number of freshwater hatcheries and supported by anecdotal evidence from the industry. Scallan (1983) suggested that these peaks may result from the stress induced in fish by both high water temperatures and rapidly changing water temperature.
As a general rule, both clinical and covert furunculosis are more likely to occur in smolting and spawning fish with the onset of higher water temperatures in spring or during periods of rapid temperature change. However, it is important to keep in mind that furunculosis outbreaks can also occur in very young fish (alevin and fry) and at temperatures as low as 2-4°C (Drinan, 1985).
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