246
detritus at least up to 29 days, and probably longer as the experiments had to be
terminated prematurely due to decomposition of the dialysis bags containing the
bacteria. He further pointed out that the 10
5 viable cells remaining after 29 days are
signifi cant, since from his studies it was shown that if this number of cells was
released into fresh water, their survival time would be 14 days. Michel and DuboisDarnaudpeys ( 1980 ) investigated the persistence of Aer. salmonicida in sediments
and reported that the pathogen survived and grew in sterilised river sediments for
over 10 months. However, pathogenicity of the two isolates tested was lost after 8
or 9 months. They concluded that in natural conditions such a length of time would
enable the pathogen to be released from sediment into the water, and that the behaviour of bottom-feeding fi shes would allow direct contamination of fi sh, possibly
becoming carriers. A reduction in pathogenicity, subsequent to prolonged incubation in river sediments, was also noted by Sakai ( 1986a , b ). He offered an explanation whereby avirulent cells (with a positive electrical charge), which originate from
virulent cells (negatively charged) attached to sediment, spontaneously detach from
the sediment particles (river sand in survival experiments) thus decreasing the number of virulent cells recovered. Michel and Dubois-Darnaudpeys ( 1980 ) conceded
that competition of Aer. salmonicida with large numbers of other bacteria in streams,
some with an ability to synthesise bacteriocins, may act as a regulatory mechanism
and limit the proliferation of the pathogen. However, previous work by DuboisDarnaudpeys ( 1977b ) supports the concept that Aer. salmonicida is genuinely capable of survival and multiplication in natural sediments, hence providing a reservoir
of infection, even though direct contact with diseased fi sh is likely to remain the
primary route of transmission. In addition, the regular detection of bacteriophages
specifi c for Aer. salmonicida in samples of river sediments was taken as an indirect
demonstration that the pathogen was present throughout the year (DuboisDarnaudpeys 1977b ). Sakai ( 1986b ) reported extended survival times (>15 weeks)
for virulent cultures of Aer. salmonicida if placed in the presence of dilute humic
acid (10 μg/ml), tryptone (10 μg/ml) and cleaned river sand (100 g/100 ml of
medium). Without the addition of the sand, detection of viable cells ceased within
5 weeks. However, avirulent strains of the pathogen did not survive more than
2 weeks regardless of whether or not sand was included in the experimental system.
Sakai ( 1986b ) determined that humic acid and amino acid-humic acid complexes
were absorbed onto the sand, which led to a build-up of 30–50 times the environmental concentration of amino acids on the surface of the sand particles. This, in
turn, allowed only colonisation of/attachment by bacterial cells with net negative
electrical charges (virulent cells of Aer. salmonicida in this instance), which resulted
in their enhanced survival in the presence of the sand. Thus, Sakai ( 1986b ) concluded that the electrostatic interrelationship occurring among humic acid, river
sand and the bacteria explain the ability of virulent Aer. salmonicida strains to survive for extended periods in river sediments.
McCarthy ( 1980 ) contended that during epizootics of furunculosis there existed
a strong possibility that fi sh farm implements could become contaminated with Aer.
salmonicida. In a study emphasising survival of Aer. salmonicida on fi sh nets which
would be used both to remove dead infected fi sh and to move healthy fi sh, it was
5 Aeromonadaceae Representative (Aeromonas salmonicida)
detritus at least up to 29 days, and probably longer as the experiments had to be
terminated prematurely due to decomposition of the dialysis bags containing the
bacteria. He further pointed out that the 10
5 viable cells remaining after 29 days are
signifi cant, since from his studies it was shown that if this number of cells was
released into fresh water, their survival time would be 14 days. Michel and DuboisDarnaudpeys ( 1980 ) investigated the persistence of Aer. salmonicida in sediments
and reported that the pathogen survived and grew in sterilised river sediments for
over 10 months. However, pathogenicity of the two isolates tested was lost after 8
or 9 months. They concluded that in natural conditions such a length of time would
enable the pathogen to be released from sediment into the water, and that the behaviour of bottom-feeding fi shes would allow direct contamination of fi sh, possibly
becoming carriers. A reduction in pathogenicity, subsequent to prolonged incubation in river sediments, was also noted by Sakai ( 1986a , b ). He offered an explanation whereby avirulent cells (with a positive electrical charge), which originate from
virulent cells (negatively charged) attached to sediment, spontaneously detach from
the sediment particles (river sand in survival experiments) thus decreasing the number of virulent cells recovered. Michel and Dubois-Darnaudpeys ( 1980 ) conceded
that competition of Aer. salmonicida with large numbers of other bacteria in streams,
some with an ability to synthesise bacteriocins, may act as a regulatory mechanism
and limit the proliferation of the pathogen. However, previous work by DuboisDarnaudpeys ( 1977b ) supports the concept that Aer. salmonicida is genuinely capable of survival and multiplication in natural sediments, hence providing a reservoir
of infection, even though direct contact with diseased fi sh is likely to remain the
primary route of transmission. In addition, the regular detection of bacteriophages
specifi c for Aer. salmonicida in samples of river sediments was taken as an indirect
demonstration that the pathogen was present throughout the year (DuboisDarnaudpeys 1977b ). Sakai ( 1986b ) reported extended survival times (>15 weeks)
for virulent cultures of Aer. salmonicida if placed in the presence of dilute humic
acid (10 μg/ml), tryptone (10 μg/ml) and cleaned river sand (100 g/100 ml of
medium). Without the addition of the sand, detection of viable cells ceased within
5 weeks. However, avirulent strains of the pathogen did not survive more than
2 weeks regardless of whether or not sand was included in the experimental system.
Sakai ( 1986b ) determined that humic acid and amino acid-humic acid complexes
were absorbed onto the sand, which led to a build-up of 30–50 times the environmental concentration of amino acids on the surface of the sand particles. This, in
turn, allowed only colonisation of/attachment by bacterial cells with net negative
electrical charges (virulent cells of Aer. salmonicida in this instance), which resulted
in their enhanced survival in the presence of the sand. Thus, Sakai ( 1986b ) concluded that the electrostatic interrelationship occurring among humic acid, river
sand and the bacteria explain the ability of virulent Aer. salmonicida strains to survive for extended periods in river sediments.
McCarthy ( 1980 ) contended that during epizootics of furunculosis there existed
a strong possibility that fi sh farm implements could become contaminated with Aer.
salmonicida. In a study emphasising survival of Aer. salmonicida on fi sh nets which
would be used both to remove dead infected fi sh and to move healthy fi sh, it was
5 Aeromonadaceae Representative (Aeromonas salmonicida)