532
It has been well documented that epizootics occur in the warm summer months
when water temperatures exceed 10 °C, the water is depleted of dissolved oxygen,
and the fi sh stressed by overcrowding and poor hygiene (Anderson and Conroy
1970 ). There are exceptions to the norm insofar as outbreaks have been documented
in fresh water (e.g. Rucker 1959 ) and at low temperature, i.e. 1–4 °C (Olafsen et al.
1981 ). It is perhaps ironic that isolates recovered from rainbow trout in fresh water
have an obvious salt requirement for growth (Rucker 1959 ). Perhaps, the organisms
were contained in a protected ecological niche such as within the fi sh body, prior to
the manifestation of the disease. However, it should be remembered that the pathogen has been recovered sporadically from fresh water (West and Lee 1982 ). The
determination of plasmid profi les may have value for epizootiological investigations (Wiik et al. 1989 ).
The presence of heavy metals, notably copper and iron, contributes to an exacerbation of vibriosis. Yet sublethal concentrations of chlorine do not appear to promote the development of infections (Hetrick et al. 1984 ). Levels of only 30–60 μg
copper/ml and 10 μg of iron/ml have caused severe problems (Rødsaether et al.
1977 ; Nakai et al. 1987 ). Further investigation demonstrated the susceptibility to
vibriosis was dependent upon concentration and time of exposure to copper (Baker
et al. 1983 ). The debilitating effect has been attributed to coagulation in the mucus
layer of the gills, and thus the inhibition of oxygen transport leading to respiratory
stress (Westfall 1945 ). The practical outcome from this information is that fi sh holding facilities should not be coated with copper-containing anti-fouling compounds,
which could trigger vibriosis.
Pathogenicity
AHL signal molecules, which have been recognized in V. anguillarum, may well
have a role in the expression of virulence factors, e.g. biofi lm formation and protease production (Buchholtz et al. 2006 ). Cultures produced two dominant molecules,
i.e. N -(2-oxodecanoyl)-L-homoserine lactone and N -(3-hydroxy-hexanoyl)-Lhomoserine lactone. Smaller amounts of other molecules were also present. Apart
from production associated in vitro with laboratory cultures, there was evidence that
infected fi sh produce the two dominant AHLs, although there may be some overall
differences in balance between the molecules in in vitro and in vivo conditions
(Buchholtz et al. 2006 ).
The exact mode of infection undoubtedly involves colonisation of (attachment
to) the host starting with the skin (Spanggaard et al. 2000 ) and/or gills (Avci et al.
2012 ), and thence penetration of the tissues. It is regarded that chemotactic motility
is necessary for virulence (O’Toole et al. 1999 ; Larsen et al. 2004 ), particularly
invasion of the host. The pathogen is attracted to amino acids and carbohydrates
particularly in intestinal and to a lesser extent to skin mucus (O’Toole et al. 1999 ).
Chemotaxis to serine, more so at higher, i.e. 25 °C, than lower, namely 5 and 15 °C,
temperatures has been documented (Larsen et al. 2004 ). Also, chemotaxis was
10 Vibrios
It has been well documented that epizootics occur in the warm summer months
when water temperatures exceed 10 °C, the water is depleted of dissolved oxygen,
and the fi sh stressed by overcrowding and poor hygiene (Anderson and Conroy
1970 ). There are exceptions to the norm insofar as outbreaks have been documented
in fresh water (e.g. Rucker 1959 ) and at low temperature, i.e. 1–4 °C (Olafsen et al.
1981 ). It is perhaps ironic that isolates recovered from rainbow trout in fresh water
have an obvious salt requirement for growth (Rucker 1959 ). Perhaps, the organisms
were contained in a protected ecological niche such as within the fi sh body, prior to
the manifestation of the disease. However, it should be remembered that the pathogen has been recovered sporadically from fresh water (West and Lee 1982 ). The
determination of plasmid profi les may have value for epizootiological investigations (Wiik et al. 1989 ).
The presence of heavy metals, notably copper and iron, contributes to an exacerbation of vibriosis. Yet sublethal concentrations of chlorine do not appear to promote the development of infections (Hetrick et al. 1984 ). Levels of only 30–60 μg
copper/ml and 10 μg of iron/ml have caused severe problems (Rødsaether et al.
1977 ; Nakai et al. 1987 ). Further investigation demonstrated the susceptibility to
vibriosis was dependent upon concentration and time of exposure to copper (Baker
et al. 1983 ). The debilitating effect has been attributed to coagulation in the mucus
layer of the gills, and thus the inhibition of oxygen transport leading to respiratory
stress (Westfall 1945 ). The practical outcome from this information is that fi sh holding facilities should not be coated with copper-containing anti-fouling compounds,
which could trigger vibriosis.
Pathogenicity
AHL signal molecules, which have been recognized in V. anguillarum, may well
have a role in the expression of virulence factors, e.g. biofi lm formation and protease production (Buchholtz et al. 2006 ). Cultures produced two dominant molecules,
i.e. N -(2-oxodecanoyl)-L-homoserine lactone and N -(3-hydroxy-hexanoyl)-Lhomoserine lactone. Smaller amounts of other molecules were also present. Apart
from production associated in vitro with laboratory cultures, there was evidence that
infected fi sh produce the two dominant AHLs, although there may be some overall
differences in balance between the molecules in in vitro and in vivo conditions
(Buchholtz et al. 2006 ).
The exact mode of infection undoubtedly involves colonisation of (attachment
to) the host starting with the skin (Spanggaard et al. 2000 ) and/or gills (Avci et al.
2012 ), and thence penetration of the tissues. It is regarded that chemotactic motility
is necessary for virulence (O’Toole et al. 1999 ; Larsen et al. 2004 ), particularly
invasion of the host. The pathogen is attracted to amino acids and carbohydrates
particularly in intestinal and to a lesser extent to skin mucus (O’Toole et al. 1999 ).
Chemotaxis to serine, more so at higher, i.e. 25 °C, than lower, namely 5 and 15 °C,
temperatures has been documented (Larsen et al. 2004 ). Also, chemotaxis was
10 Vibrios