509
slightly longer, i.e. 4–5 days. These results support the earlier fi ndings of Janssen
and Surgalla ( 1968 ) that the organism does not appear to survive well away from
fi sh. However, there is some evidence that has demonstrated the discharge of viable
cells from experimentally infected yellowtail for 1–2 days before death (Matsuoka
and Kamada 1995 ). The survival of starved cells in seawater needs to be clarifi ed
(Magariños et al. 1997a ). Furthermore, it was speculated that transmission of the
disease is likely to be fi sh to fi sh. Data suggest that the gill is key to the development
of the disease cycle insofar as the pathogen has been located in the gills of apparently healthy amberjack (Nagano et al. 2011b ). Although the arguments are reminiscent of the debate about the spread of furunculosis, it should not be overlooked that
Ph. damselae subsp . piscicida may survive in water, albeit in a non-culturable, dormant or altered form. Indeed, a view was expressed that the pathogen may well
exhibit a dormant phase (Magariños et al. 1994a ). Plate count data revealed that Ph.
damselae subsp. piscicida could survive in seawater and sediment for 6–12 days,
with metabolism being reduced by 80 %. Indeed, in terms of numbers, culturable
cells persisted in sediment better than in seawater. However, when culture techniques inferred a reduction in bacterial numbers, microscopy using acridine orange
suggested that the populations remain at 10
5 (Magariños et al. 1994a ).
A possibly useful tool for epizootiology is ribotyping, which has already successfully discriminated between European and Japanese isolates (Magariños et al.
1997b ).
Pathogenicity
Experimental infection may be achieved by i.m. injection, oral uptake or immersion, with maximum mortalities at 18 and 20 but less at 15 °C (Magariños et al.
2001 ). Medium composition, and in particular the presence of yeast extract and/or
(fi sh) peptone, enhanced the toxicity of ECPs and the virulence of cells administered via immersion or i.p. injection (Bakopoulos et al. 2002 ). The fate of the pathogen has been examined by FAT (Kawahara et al. 1989 ). Thus following i.m.
injection, the pathogen became located initially in the kidney and spleen, before
spreading to the gills, heart, intestine and pyloric caeca. The pathogenic has the ability to adhere to, invade and survive within cells, and has been observed to adhere to
and invade the epithelial cell line SAF-1 (Acosta et al. 2009 ). Following oral uptake,
the pathogen appeared in the stomach, before spreading to the internal organs. After
immersion, Ph. damselae subsp . piscicida located in the gills, and then spread
widely to the heart, kidney, liver, pyloric caeca and spleen (Kawahara et al. 1989 ).
Within the tissues of infected fi sh, Ph. damselae subsp . piscicida was seen to accumulate and multiply in the macrophages (Nelson et al. 1989 ; Elkamel et al. 2003 )
perhaps after an initial cell adherence stage (Magariños et al. 1996a , b ), which
appears to involve capsular polysaccharide [this is dependent on the presence of
iron and younger, i.e. logarithmic rather than lag phase cultures] (Magariños et al.
1996b ; do Vale et al. 2001 ), which has a minor role in the binding of haemin (do
Photobacterium damselae subsp. piscicida (= Pasteurella piscicida)
slightly longer, i.e. 4–5 days. These results support the earlier fi ndings of Janssen
and Surgalla ( 1968 ) that the organism does not appear to survive well away from
fi sh. However, there is some evidence that has demonstrated the discharge of viable
cells from experimentally infected yellowtail for 1–2 days before death (Matsuoka
and Kamada 1995 ). The survival of starved cells in seawater needs to be clarifi ed
(Magariños et al. 1997a ). Furthermore, it was speculated that transmission of the
disease is likely to be fi sh to fi sh. Data suggest that the gill is key to the development
of the disease cycle insofar as the pathogen has been located in the gills of apparently healthy amberjack (Nagano et al. 2011b ). Although the arguments are reminiscent of the debate about the spread of furunculosis, it should not be overlooked that
Ph. damselae subsp . piscicida may survive in water, albeit in a non-culturable, dormant or altered form. Indeed, a view was expressed that the pathogen may well
exhibit a dormant phase (Magariños et al. 1994a ). Plate count data revealed that Ph.
damselae subsp. piscicida could survive in seawater and sediment for 6–12 days,
with metabolism being reduced by 80 %. Indeed, in terms of numbers, culturable
cells persisted in sediment better than in seawater. However, when culture techniques inferred a reduction in bacterial numbers, microscopy using acridine orange
suggested that the populations remain at 10
5 (Magariños et al. 1994a ).
A possibly useful tool for epizootiology is ribotyping, which has already successfully discriminated between European and Japanese isolates (Magariños et al.
1997b ).
Pathogenicity
Experimental infection may be achieved by i.m. injection, oral uptake or immersion, with maximum mortalities at 18 and 20 but less at 15 °C (Magariños et al.
2001 ). Medium composition, and in particular the presence of yeast extract and/or
(fi sh) peptone, enhanced the toxicity of ECPs and the virulence of cells administered via immersion or i.p. injection (Bakopoulos et al. 2002 ). The fate of the pathogen has been examined by FAT (Kawahara et al. 1989 ). Thus following i.m.
injection, the pathogen became located initially in the kidney and spleen, before
spreading to the gills, heart, intestine and pyloric caeca. The pathogenic has the ability to adhere to, invade and survive within cells, and has been observed to adhere to
and invade the epithelial cell line SAF-1 (Acosta et al. 2009 ). Following oral uptake,
the pathogen appeared in the stomach, before spreading to the internal organs. After
immersion, Ph. damselae subsp . piscicida located in the gills, and then spread
widely to the heart, kidney, liver, pyloric caeca and spleen (Kawahara et al. 1989 ).
Within the tissues of infected fi sh, Ph. damselae subsp . piscicida was seen to accumulate and multiply in the macrophages (Nelson et al. 1989 ; Elkamel et al. 2003 )
perhaps after an initial cell adherence stage (Magariños et al. 1996a , b ), which
appears to involve capsular polysaccharide [this is dependent on the presence of
iron and younger, i.e. logarithmic rather than lag phase cultures] (Magariños et al.
1996b ; do Vale et al. 2001 ), which has a minor role in the binding of haemin (do
Photobacterium damselae subsp. piscicida (= Pasteurella piscicida)