490
DNA:DNA hybridisation levels were <50 % with reference Pseudomonas spp.
(Nishimori et al. 2000 ).
Epizootiology
Immersion leads to infection of ayu, with gills and gill epithelia being the likely
portals of entry as determined by real-time quantitative PCR. At 6 h after infection,
the pathogen was located in the kidney, liver and spleen; septicaemia was apparent
after 48 h when the organism was found in the blood (Sukenda and Wakabayashi
2000 ).
Pathogenicity
During surveys of dead ayu (with bloody ascites) in Japan during 1999 and 2001
with the exception of one isolate, all the others were non-motile. Moreover, nonmotile cells were injected intramuscularly into ayu leading to the recovery of both
motile and non-motile cells from the kidney. However, motile cells were recovered
after the injection of motile cultures (Park et al. 2002 ). By use of GFP-labelled cells,
the pathogen has been observed to adhere predominantly to the site of microscopic
injuries in the fi ns and skin (Sukenda and Wakabayashi 2001 ).
Box 9.7: Pseudomonas plecoglossicida
The 6 cultures (a brown-pigmented culture has been subsequently recovered;
Park et al. 2000 ) examined in the initial study comprises a homogeneous
group of strictly aerobic Gram-negative motile (several polar fl agella) rods
that produce catalase and oxidase, and reduce nitrate to nitrite, and grow at
10–30 °C but not at 4 or 41 °C, in 0–5 % (w/v) NaCl. Arginine dihydrolase is
produced, but not lysine or ornithine decarboxylase. Blood is degraded, but
not gelatin, lecithin, starch or Tween 80. Caprate, citrate, D-fructose,
2- ketogluconate, L-alanine, glucose, D-malate, propylene glycol, L-lysine,
succinate and L-citrulline are utilised, but not L-arabinose, m -inositol, mannitol, D-mannose, sucrose, D-tartrate, testosterone, trehalose, L-tryptophan or
D-xylose. A weak fl uorescent pigment is produced on King medium B. The
G + C ratio of the DNA is 62.8 mol% (Nishimori et al. 2000 ).
9 Pseudomonads
DNA:DNA hybridisation levels were <50 % with reference Pseudomonas spp.
(Nishimori et al. 2000 ).
Epizootiology
Immersion leads to infection of ayu, with gills and gill epithelia being the likely
portals of entry as determined by real-time quantitative PCR. At 6 h after infection,
the pathogen was located in the kidney, liver and spleen; septicaemia was apparent
after 48 h when the organism was found in the blood (Sukenda and Wakabayashi
2000 ).
Pathogenicity
During surveys of dead ayu (with bloody ascites) in Japan during 1999 and 2001
with the exception of one isolate, all the others were non-motile. Moreover, nonmotile cells were injected intramuscularly into ayu leading to the recovery of both
motile and non-motile cells from the kidney. However, motile cells were recovered
after the injection of motile cultures (Park et al. 2002 ). By use of GFP-labelled cells,
the pathogen has been observed to adhere predominantly to the site of microscopic
injuries in the fi ns and skin (Sukenda and Wakabayashi 2001 ).
Box 9.7: Pseudomonas plecoglossicida
The 6 cultures (a brown-pigmented culture has been subsequently recovered;
Park et al. 2000 ) examined in the initial study comprises a homogeneous
group of strictly aerobic Gram-negative motile (several polar fl agella) rods
that produce catalase and oxidase, and reduce nitrate to nitrite, and grow at
10–30 °C but not at 4 or 41 °C, in 0–5 % (w/v) NaCl. Arginine dihydrolase is
produced, but not lysine or ornithine decarboxylase. Blood is degraded, but
not gelatin, lecithin, starch or Tween 80. Caprate, citrate, D-fructose,
2- ketogluconate, L-alanine, glucose, D-malate, propylene glycol, L-lysine,
succinate and L-citrulline are utilised, but not L-arabinose, m -inositol, mannitol, D-mannose, sucrose, D-tartrate, testosterone, trehalose, L-tryptophan or
D-xylose. A weak fl uorescent pigment is produced on King medium B. The
G + C ratio of the DNA is 62.8 mol% (Nishimori et al. 2000 ).
9 Pseudomonads