569
decarboxylase, acid from mannitol or sorbitol, or grow at 42 °C. These differences
add weight to assigning the fi sh pathogens to a new biogroup. However, the results
of DNA:DNA hybridisation, which show 90 % homology between V. vulnifi cus and
the group of fi sh pathogens (Tison et al. 1982 ), confi rm taxonomic (species)
relatedness.
Results of serology have clearly demonstrated that isolates of V. vulnifi cus contain heterologous surface antigens. It must be emphasised, however, that the fi sh
isolates are distinctly homogeneous (Nishibuchi and Muroga 1980 ). There are common soluble intracellular antigens, which are homologous in all isolates. In particular, there is a V. vulnifi cus specifi c antigen, which may have value in the development
of rapid diagnostic tests.
Diagnosis
Serology An ELISA was developed for V. vulnifi cus and fi eld tested, the results of
which indicated a sensitivity of 10
4 –10
5 cells/well, and an ability to detect non culturable cells (Biosca et al. 1997b ).
Molecular Methods González et al. ( 2004 ) used a multiplex PCR and DNA
microarray, and achieved the simultaneous and differential diagnosis of Aer. salmonicida, Ph. damselae subsp. damselae, V. anguillarum, V. parahaemolyticus and
V. vulnifi cus, with a minimum detection limit of <20 fg per reaction, which equates
to 4–5 bacterial cells. A multiplex PCR was developed that detected biotype 2 with
differentiation from the zoonotic serovar E (Sanjuán and Amaro 2007 ).
Epizootiology
V. vulnifi cus is ubiquitous in the coastal marine and estuarine environment, where it
occurs routinely in low numbers (Oliver et al. 1983 ), although serovar E (biotype 2)
is regarded as being rare in natural waters but extended survival occurs in sterile
microcosms (Marco-Noales et al. 2004 ). Populations of the pathogen are almost
certainly controlled by grazing and microbial antagonism (Marco-Noales et al.
2004 ). However, the reservoir is almost certainly the aquatic, especially seawater,
environment (Høi et al. 1998 ), with spread occurring through water (Fouz et al.
2010 ). It has been documented to survive in brackish water and on the surfaces of
eels for 14 days (Amaro et al. 1995 ). It is feasible that fi sh are constantly exposed to
the potential vagaries of this organism. Serotype A and E enter mostly via the anus
and gills, respectively, with pathogenicity recorded for a range of species, including
rainbow trout, sea bass and tilapia (Fouz et al. 2010 ).
Vibrio vulnifi cus
decarboxylase, acid from mannitol or sorbitol, or grow at 42 °C. These differences
add weight to assigning the fi sh pathogens to a new biogroup. However, the results
of DNA:DNA hybridisation, which show 90 % homology between V. vulnifi cus and
the group of fi sh pathogens (Tison et al. 1982 ), confi rm taxonomic (species)
relatedness.
Results of serology have clearly demonstrated that isolates of V. vulnifi cus contain heterologous surface antigens. It must be emphasised, however, that the fi sh
isolates are distinctly homogeneous (Nishibuchi and Muroga 1980 ). There are common soluble intracellular antigens, which are homologous in all isolates. In particular, there is a V. vulnifi cus specifi c antigen, which may have value in the development
of rapid diagnostic tests.
Diagnosis
Serology An ELISA was developed for V. vulnifi cus and fi eld tested, the results of
which indicated a sensitivity of 10
4 –10
5 cells/well, and an ability to detect non culturable cells (Biosca et al. 1997b ).
Molecular Methods González et al. ( 2004 ) used a multiplex PCR and DNA
microarray, and achieved the simultaneous and differential diagnosis of Aer. salmonicida, Ph. damselae subsp. damselae, V. anguillarum, V. parahaemolyticus and
V. vulnifi cus, with a minimum detection limit of <20 fg per reaction, which equates
to 4–5 bacterial cells. A multiplex PCR was developed that detected biotype 2 with
differentiation from the zoonotic serovar E (Sanjuán and Amaro 2007 ).
Epizootiology
V. vulnifi cus is ubiquitous in the coastal marine and estuarine environment, where it
occurs routinely in low numbers (Oliver et al. 1983 ), although serovar E (biotype 2)
is regarded as being rare in natural waters but extended survival occurs in sterile
microcosms (Marco-Noales et al. 2004 ). Populations of the pathogen are almost
certainly controlled by grazing and microbial antagonism (Marco-Noales et al.
2004 ). However, the reservoir is almost certainly the aquatic, especially seawater,
environment (Høi et al. 1998 ), with spread occurring through water (Fouz et al.
2010 ). It has been documented to survive in brackish water and on the surfaces of
eels for 14 days (Amaro et al. 1995 ). It is feasible that fi sh are constantly exposed to
the potential vagaries of this organism. Serotype A and E enter mostly via the anus
and gills, respectively, with pathogenicity recorded for a range of species, including
rainbow trout, sea bass and tilapia (Fouz et al. 2010 ).
Vibrio vulnifi cus