174
nutrient rich cultures (Rahman et al. 1997 ). Nevertheless as a general rule, it is apparent that the pathogen has considerable exo-enzyme potential, including haemolysins,
serine (= caseinase; 68 kDa) – and metalloprotease (= elastase; 31, 44 and 60 kDa)
(Esteve and Birkbeck 2004 ) some of which has relevance in fi sh pathology. The precise function of these ‘toxins’, which number at least six (Bernheimer and Avigad
1974 ; Donta and Haddow 1978 ; Cumberbatch et al. 1979 ) in fi sh pathology, has yet
to be fully elucidated. A 21 kb plasmid has been detected in pathogenic isolates associated with ulcerative disease syndrome, and correlated with antibiotic- resistance.
Curing the plasmid led to loss of virulence in Indian walking catfi sh (Clarias batrachus) whereas pathogenicity was restored when the plasmid was re- introduced into
the bacterial cells (Majumdar et al. 2006 ). There have been more recent developments involving determination of the host response to infection. Thus, it has been
documented that the stress-related genes, i.e. heat-shock protein (HSP) genes with
modulation being greater in liver compared to the kidney or spleen of experimentally
infected rohu particularly with regard to APG2, HSP90, glucose-regulated protein
(GRP) 78, GRP75, and heat shock cognate 70 at 3–24 h after challenge; HSP 70 were
down-regulated during infection. GRP 78, which is a highly conserved HSP gene
essential for its regulatory role in infection and the early developmental phases of the
fi sh, was most highly expressed in liver at 12 h after challenge (Das et al. 2015a , b).
This begs the question about the nature of the host response. In the case of zebra fi sh
skin, two-dimensional gel electrophoresis with mass spectrometry was used to determine the effect on protein expression as a result of infection with Aer. hydrophila .
Thus, the data revealed that 17 proteins were differentially expressed 6 were upregulated, and 11 proteins down-regulated. (Lu et al. 2014 ).
Surface Structures
Studies have emphasised the surface structures of Aer. hydrophila , which appear to
be involved in autoaggregation/hydrophobicity and haemagglutination (e.g. Paula
et al. 1988 ). There is some evidence that a capsule may be produced in vivo (Mateos
and Paniagua 1995 ). The presence or absence of lateral fl agella (as opposed to the
more typical polar pattern) was demonstrated by electron microscopy on three isolates from catfi sh in Nigeria (Nzeako 1991 ). Del Corral et al. ( 1990 ) demonstrated
the presence of pili/fi mbriae, regardless of virulence. These workers considered that
there was not a direct correlation between virulence and haemagglutination.
The surface array matrix, i.e. the S-layer, has been considered to infl uence the
interaction between the bacterial cell and its environment (Esteve et al. 2004 ). A
major function is believed to be the provision of physical protection from lytic components, including serum proteins and bacteriophages (Dooley et al. 1988 ). Work
also links the presence of an S-layer with invasive disease in humans and mice (but
not fi sh!) (Murray et al. 1988 ). As a result of studying one isolate, i.e. TF7 – isolated
from a lesion on trout in Quebec, it was determined that the S-layer did not confer
any increase in surface hydrophobicity or any enhanced association with macrophages, and did not specifi cally bind porphyrin or immunoglobulin (Murray et al.
4 Aeromonadaceae Representatives (Motile Aeromonads)
nutrient rich cultures (Rahman et al. 1997 ). Nevertheless as a general rule, it is apparent that the pathogen has considerable exo-enzyme potential, including haemolysins,
serine (= caseinase; 68 kDa) – and metalloprotease (= elastase; 31, 44 and 60 kDa)
(Esteve and Birkbeck 2004 ) some of which has relevance in fi sh pathology. The precise function of these ‘toxins’, which number at least six (Bernheimer and Avigad
1974 ; Donta and Haddow 1978 ; Cumberbatch et al. 1979 ) in fi sh pathology, has yet
to be fully elucidated. A 21 kb plasmid has been detected in pathogenic isolates associated with ulcerative disease syndrome, and correlated with antibiotic- resistance.
Curing the plasmid led to loss of virulence in Indian walking catfi sh (Clarias batrachus) whereas pathogenicity was restored when the plasmid was re- introduced into
the bacterial cells (Majumdar et al. 2006 ). There have been more recent developments involving determination of the host response to infection. Thus, it has been
documented that the stress-related genes, i.e. heat-shock protein (HSP) genes with
modulation being greater in liver compared to the kidney or spleen of experimentally
infected rohu particularly with regard to APG2, HSP90, glucose-regulated protein
(GRP) 78, GRP75, and heat shock cognate 70 at 3–24 h after challenge; HSP 70 were
down-regulated during infection. GRP 78, which is a highly conserved HSP gene
essential for its regulatory role in infection and the early developmental phases of the
fi sh, was most highly expressed in liver at 12 h after challenge (Das et al. 2015a , b).
This begs the question about the nature of the host response. In the case of zebra fi sh
skin, two-dimensional gel electrophoresis with mass spectrometry was used to determine the effect on protein expression as a result of infection with Aer. hydrophila .
Thus, the data revealed that 17 proteins were differentially expressed 6 were upregulated, and 11 proteins down-regulated. (Lu et al. 2014 ).
Surface Structures
Studies have emphasised the surface structures of Aer. hydrophila , which appear to
be involved in autoaggregation/hydrophobicity and haemagglutination (e.g. Paula
et al. 1988 ). There is some evidence that a capsule may be produced in vivo (Mateos
and Paniagua 1995 ). The presence or absence of lateral fl agella (as opposed to the
more typical polar pattern) was demonstrated by electron microscopy on three isolates from catfi sh in Nigeria (Nzeako 1991 ). Del Corral et al. ( 1990 ) demonstrated
the presence of pili/fi mbriae, regardless of virulence. These workers considered that
there was not a direct correlation between virulence and haemagglutination.
The surface array matrix, i.e. the S-layer, has been considered to infl uence the
interaction between the bacterial cell and its environment (Esteve et al. 2004 ). A
major function is believed to be the provision of physical protection from lytic components, including serum proteins and bacteriophages (Dooley et al. 1988 ). Work
also links the presence of an S-layer with invasive disease in humans and mice (but
not fi sh!) (Murray et al. 1988 ). As a result of studying one isolate, i.e. TF7 – isolated
from a lesion on trout in Quebec, it was determined that the S-layer did not confer
any increase in surface hydrophobicity or any enhanced association with macrophages, and did not specifi cally bind porphyrin or immunoglobulin (Murray et al.
4 Aeromonadaceae Representatives (Motile Aeromonads)