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Pseudomonas mosselii
The organism was recovered from Nile tilapia in Mexico. The disease signs included
lethargy, erratic swimming, melanosis, scale loss, blindness, exophthalmia and/or
red or opaque eyes. Diseased tissues were inoculated onto TSA supplemented with
0.5 % (/v) glucose, BHIA supplemented with 5 % (v/v) sheep blood, MacConkey
agar, glutamate- starch-phenol red agar, and TCBS with incubation at 30 +/− 1 °C
for 24–48 h. Identifi cation was achieved by sequencing of the 16S rRNA gene.
Pathogenicity was confi rmed in laboratory-based infectivity experiments using tilapia ( Oreochromis mossambicus ). ECPs displayed cytotoxic effects to HeLa cells
(Soto-Rodriguez et al. 2013 ).
Pseudomonas plecoglossicida
Characteristics of the Disease
A new bacterial disease emerged during the 1990s, and caused mass mortalities in
pond-cultured ayu in Japan (Wakabayashi et al. 1996 ) and subsequently with diseased large yellow croaker ( Larimichthys crocea ) in China (Zhang et al. 2014 ). The
term bacterial haemorrhagic ascites is descriptive, with affected ayu displaying
lesions in the gills, heart, intestine, kidney, liver and spleen. In particular, lesions in
the spleen and haematopoietic tissues were profound. Those in the kidney, liver and
spleen were necrotic. Abscesses were apparent in the liver. In contrast, the brain did
not reveal the presence of any lesions (Kobayashi et al. 2004 ). In olive fl ounder, the
pathogen caused visceral granulomas (Zhang et al. 2014 ).
Characteristics of the Pathogen
The pathogen was regarded as having phenetic similarities with Ps. putida biovar A,
but on the basis 16S rRNA sequencing was regarded as distinct, and elevated into a
new species, as Ps. plecoglossicida (Nishimori et al. 2000 ).
Pseudomonas plecoglossicida
Pseudomonas mosselii
The organism was recovered from Nile tilapia in Mexico. The disease signs included
lethargy, erratic swimming, melanosis, scale loss, blindness, exophthalmia and/or
red or opaque eyes. Diseased tissues were inoculated onto TSA supplemented with
0.5 % (/v) glucose, BHIA supplemented with 5 % (v/v) sheep blood, MacConkey
agar, glutamate- starch-phenol red agar, and TCBS with incubation at 30 +/− 1 °C
for 24–48 h. Identifi cation was achieved by sequencing of the 16S rRNA gene.
Pathogenicity was confi rmed in laboratory-based infectivity experiments using tilapia ( Oreochromis mossambicus ). ECPs displayed cytotoxic effects to HeLa cells
(Soto-Rodriguez et al. 2013 ).
Pseudomonas plecoglossicida
Characteristics of the Disease
A new bacterial disease emerged during the 1990s, and caused mass mortalities in
pond-cultured ayu in Japan (Wakabayashi et al. 1996 ) and subsequently with diseased large yellow croaker ( Larimichthys crocea ) in China (Zhang et al. 2014 ). The
term bacterial haemorrhagic ascites is descriptive, with affected ayu displaying
lesions in the gills, heart, intestine, kidney, liver and spleen. In particular, lesions in
the spleen and haematopoietic tissues were profound. Those in the kidney, liver and
spleen were necrotic. Abscesses were apparent in the liver. In contrast, the brain did
not reveal the presence of any lesions (Kobayashi et al. 2004 ). In olive fl ounder, the
pathogen caused visceral granulomas (Zhang et al. 2014 ).
Characteristics of the Pathogen
The pathogen was regarded as having phenetic similarities with Ps. putida biovar A,
but on the basis 16S rRNA sequencing was regarded as distinct, and elevated into a
new species, as Ps. plecoglossicida (Nishimori et al. 2000 ).
Pseudomonas plecoglossicida