546
Tor’ biotype, i.e. production of ornithine decarboxylase and utilisation of mannose
(these were reported as negative for the fi sh pathogenic isolates). However, the fi sh
isolates did not react, by slide agglutination, with antisera to V. cholerae . Therefore,
the conclusion was that the fi sh pathogenic isolates comprised V. cholerae non-O1.
It should be emphasised, however, that the fi sh isolates demonstrated 86 %
DNA:DNA homology with a reference strain of V. cholerae . This coincided well
with the intraspecifi c homology values of V. cholerae (Citarella and Colwell 1970 ).
Again, there was reasonably close agreement between V. cholerae and the isolates
studied by Reddacliff et al. ( 1993 ). Yet, a detailed taxonomic study by Austin et al.
1997 ) reported heterogeneity among 6 isolates received as V. cholerae, insofar as
they were recovered as single member ribotype clusters, and displayed diverse
BIOLOG-GN fi ngerprints and API 20E profi les. However, 5 cultures corresponded
with V. cholerae serogroups, namely O8, O9, O23, O32 and O63.
Epizootiology
V. cholerae survives in the aquatic environment. For example at 25 °C, strain
PS-7701 survived for 32 days in fresh water, saline Ringers buffer, and normal
strength and diluted seawater. Survival was considerably reduced at 2 °C (Yamanoi
et al. 1980 ); an observation which coincides with the fi ndings of Singleton et al.
( 1982a , b ). It is likely that infection occurs via the water borne route, insofar as V.
cholerae appears to inhabit the aquatic environment (Lee et al. 1982 ; West and Lee
1982 ).
Pathogenicity
The evidence suggests that V. cholerae is a highly virulent fi sh pathogen, insofar as
ayu and eels may be infected following immersion in only 1.26 × 10
4 cells/ml and
1.26 × 10
2 cells/ml, respectively. Yamanoi’s team noted that with ayu, mortalities
began in 2 to 7 days at water temperatures of 21 and 26 °C, but no deaths occurred
if the water temperature was at 16 °C. In comparison, an eel population suffered
10 % mortalities within 5 days at a water temperature of 21 °C, and 30 % deaths in
3–7 days at 26 °C. Clearly, this information suggests that V. cholerae is likely to be
troublesome only in higher water temperatures.
Vibrio furnissii
There has been an indication that V. furnissii may be associated with eel disease in
Spain (Esteve 1995 ). However, isolates were recovered from water rather than diseased eels. Therefore, the association with fi sh pathology is dubious.
10 Vibrios
Tor’ biotype, i.e. production of ornithine decarboxylase and utilisation of mannose
(these were reported as negative for the fi sh pathogenic isolates). However, the fi sh
isolates did not react, by slide agglutination, with antisera to V. cholerae . Therefore,
the conclusion was that the fi sh pathogenic isolates comprised V. cholerae non-O1.
It should be emphasised, however, that the fi sh isolates demonstrated 86 %
DNA:DNA homology with a reference strain of V. cholerae . This coincided well
with the intraspecifi c homology values of V. cholerae (Citarella and Colwell 1970 ).
Again, there was reasonably close agreement between V. cholerae and the isolates
studied by Reddacliff et al. ( 1993 ). Yet, a detailed taxonomic study by Austin et al.
1997 ) reported heterogeneity among 6 isolates received as V. cholerae, insofar as
they were recovered as single member ribotype clusters, and displayed diverse
BIOLOG-GN fi ngerprints and API 20E profi les. However, 5 cultures corresponded
with V. cholerae serogroups, namely O8, O9, O23, O32 and O63.
Epizootiology
V. cholerae survives in the aquatic environment. For example at 25 °C, strain
PS-7701 survived for 32 days in fresh water, saline Ringers buffer, and normal
strength and diluted seawater. Survival was considerably reduced at 2 °C (Yamanoi
et al. 1980 ); an observation which coincides with the fi ndings of Singleton et al.
( 1982a , b ). It is likely that infection occurs via the water borne route, insofar as V.
cholerae appears to inhabit the aquatic environment (Lee et al. 1982 ; West and Lee
1982 ).
Pathogenicity
The evidence suggests that V. cholerae is a highly virulent fi sh pathogen, insofar as
ayu and eels may be infected following immersion in only 1.26 × 10
4 cells/ml and
1.26 × 10
2 cells/ml, respectively. Yamanoi’s team noted that with ayu, mortalities
began in 2 to 7 days at water temperatures of 21 and 26 °C, but no deaths occurred
if the water temperature was at 16 °C. In comparison, an eel population suffered
10 % mortalities within 5 days at a water temperature of 21 °C, and 30 % deaths in
3–7 days at 26 °C. Clearly, this information suggests that V. cholerae is likely to be
troublesome only in higher water temperatures.
Vibrio furnissii
There has been an indication that V. furnissii may be associated with eel disease in
Spain (Esteve 1995 ). However, isolates were recovered from water rather than diseased eels. Therefore, the association with fi sh pathology is dubious.
10 Vibrios