329
the aquatic environment, although there is some evidence that the pathogen may be
present in invertebrates that could act as vectors for transmission. A recent study
demonstrated that Edw. ictaluri could be introduced onto theronts and replicate during tomont division of fi sh parasite Ichthyophthirius multifi liis. Theronts arriving on
fi sh (in this case channel catfi sh) could be observed by fl uorescent microscopy with
Edw. ictaluri on the skin and gills (Xu et al. 2012 ). A carrier state in channel catfi sh
has been documented (Klesius 1992 ). Also, data have shown that cells can pass
from dead fi sh to non-infected channel catfi sh (Klesius 1994 ). Of course, the results
of such laboratory-based survival experiments need to be treated cautiously. It is
conceivable that the organism comprises part of the normal microfl ora of fi sh, lurking perhaps in the digestive tract.
Lytic bacteriophage, notably ΦeiAU and ΦeiDWF, have been recovered (Hossain
et al. 2012 ), and it is speculative if such bacteriophage impact on populations of the
pathogen in the environment.
Pathogenicity
Mortalities of up to 50 % have been recorded. In one comparative study, an injection
of 1.5 × 10
3 cells of the pathogen was suffi cient to cause 100 % mortality among a
group of channel catfi sh; tilapia only demonstrated slight susceptibility, whereas
golden shiner, bighead carp and largemouth bass were completely resistant (Plumb
and Sanchez 1983 ), with daily feeding (of channel catfi sh) leading to less mortalities than groups that were fed less often or starved (Lim and Klesius 2003 ). The
LD 50 of ayu was reported at 10
4 CFU/fi sh, with dead animals displaying similar
signs to the natural infection (Sakai et al. 2008 ). Survival of natural outbreaks has
led to high humoral antibody levels and protection from fresh onslaught with Edw.
ictaluri (Vinitnantharat and Plumb 1993 ). The aetiological agent has been also associated with disease outbreaks in non-ictalurid fi sh, e.g. danio ( Danio devario )
(Waltman et al. 1985 ).
Knowledge about the pathogenicity mechanisms of Edw. ictaluri is steadily
increasing, with genome sequencing identifying various virulence mechanisms
including type I fi mbriae, type III and type IV secretion systems, a twin arginine
translocation system, and fl agellins (Williams et al. 2012 ). Extracellular products
have been associated with virulence (Stanley et al. 1994 ; Williams et al. 2003 ). By
comparing virulent with attenuated (these had been subcultured repeatedly in liquid
medium) isolates, the latter lacked a 55 kDa OMP, showed markedly less haemolytic activity, and had differences in the composition of core oligosaccharide sugars
of the LPS compared with the former (Williams et al. 2003 ). Lawrence et al. ( 2001 )
using transposon mutagenesis and O side chain mutants, deduced that the LPS O
side chains were important for virulence. Rabbit antibodies to 3 (22, 31 and 59 kDa)
of 4 major OMPs blocked invasion of cells from fathead minnow ( Pimephales
promelas ) by Edw. ictaluri demonstrating that some if not all of these OMPs are
involved in initial host-pathogen interactions (Skirpstunas and Baldwin 2003 ).
Edwardsiella ictaluri
the aquatic environment, although there is some evidence that the pathogen may be
present in invertebrates that could act as vectors for transmission. A recent study
demonstrated that Edw. ictaluri could be introduced onto theronts and replicate during tomont division of fi sh parasite Ichthyophthirius multifi liis. Theronts arriving on
fi sh (in this case channel catfi sh) could be observed by fl uorescent microscopy with
Edw. ictaluri on the skin and gills (Xu et al. 2012 ). A carrier state in channel catfi sh
has been documented (Klesius 1992 ). Also, data have shown that cells can pass
from dead fi sh to non-infected channel catfi sh (Klesius 1994 ). Of course, the results
of such laboratory-based survival experiments need to be treated cautiously. It is
conceivable that the organism comprises part of the normal microfl ora of fi sh, lurking perhaps in the digestive tract.
Lytic bacteriophage, notably ΦeiAU and ΦeiDWF, have been recovered (Hossain
et al. 2012 ), and it is speculative if such bacteriophage impact on populations of the
pathogen in the environment.
Pathogenicity
Mortalities of up to 50 % have been recorded. In one comparative study, an injection
of 1.5 × 10
3 cells of the pathogen was suffi cient to cause 100 % mortality among a
group of channel catfi sh; tilapia only demonstrated slight susceptibility, whereas
golden shiner, bighead carp and largemouth bass were completely resistant (Plumb
and Sanchez 1983 ), with daily feeding (of channel catfi sh) leading to less mortalities than groups that were fed less often or starved (Lim and Klesius 2003 ). The
LD 50 of ayu was reported at 10
4 CFU/fi sh, with dead animals displaying similar
signs to the natural infection (Sakai et al. 2008 ). Survival of natural outbreaks has
led to high humoral antibody levels and protection from fresh onslaught with Edw.
ictaluri (Vinitnantharat and Plumb 1993 ). The aetiological agent has been also associated with disease outbreaks in non-ictalurid fi sh, e.g. danio ( Danio devario )
(Waltman et al. 1985 ).
Knowledge about the pathogenicity mechanisms of Edw. ictaluri is steadily
increasing, with genome sequencing identifying various virulence mechanisms
including type I fi mbriae, type III and type IV secretion systems, a twin arginine
translocation system, and fl agellins (Williams et al. 2012 ). Extracellular products
have been associated with virulence (Stanley et al. 1994 ; Williams et al. 2003 ). By
comparing virulent with attenuated (these had been subcultured repeatedly in liquid
medium) isolates, the latter lacked a 55 kDa OMP, showed markedly less haemolytic activity, and had differences in the composition of core oligosaccharide sugars
of the LPS compared with the former (Williams et al. 2003 ). Lawrence et al. ( 2001 )
using transposon mutagenesis and O side chain mutants, deduced that the LPS O
side chains were important for virulence. Rabbit antibodies to 3 (22, 31 and 59 kDa)
of 4 major OMPs blocked invasion of cells from fathead minnow ( Pimephales
promelas ) by Edw. ictaluri demonstrating that some if not all of these OMPs are
involved in initial host-pathogen interactions (Skirpstunas and Baldwin 2003 ).
Edwardsiella ictaluri