330
Saeed ( 1983 ) showed that cells are highly piliated, and inferred that the pili might
be associated with virulence. By means of intragastric intubation and a comparatively high dose of 1 × 10
9 cells, Edw. ictaluri crossed the intestinal mucosa of channel catfi sh in 15 min (Baldwin and Newton 1993 ). Using 1 × 10
6 cells/ml and an
application directly into the olfactory organs of channel catfi sh, light and electron
microscopy revealed damage after 1 h (Morrison and Plumb 1994 ). The importance
of entry across the intestinal epithelium is becoming widely accepted, with actin
polymerization and receptor-mediated endocytosis as likely mechanisms of uptake
(Li et al. 2012 ). It has been fi rmly established that channel catfi sh are highly susceptible to the organism, with an injected dose of 1.5 × 10
3 cells capable of killing the
host within 10 days at a water temperature of 26 °C (Plumb and Sanchez 1983 ). It
does not appear that the organism produces abundant exo-enzymes, which would
function as exotoxins in fi sh. It has been argued that both gut and nares are primary
sites for the invasion of Edw. ictaluri in natural outbreaks of disease (Shotts et al.
1986 ). Fluorescence microscopy evidence pointed to the localisation of the organism on the gill within 5 min and within gill epithelia after 45 min and to the kidney
within 4 h of a waterborne route (Nusbaum and Morrison 2002 ); the outcome was a
bacteraemia within 24 h (Wise et al. 1997 ). By 72 h, the pathogen was recoverable
from the blood. Then by 216 h, there was evidence of the pathogen clearing from
the blood, with all survivors developing agglutinating antibodies to Edw. ictaluri.
Entry, survival (many organisms were present in vacuoles) and replication in head
kidney macrophages of channel catfi sh has been observed microscopically.
Opsonisation with normal serum led to even greater internalization of Edw. ictaluri
at 0 h, but did not affect replication once internalized (Booth et al. 2006 ). Uptake of
the pathogen into host (epithelial) cells may well involve actin polymerization and
receptor-mediated endocytosis (Skirpstunas and Baldwin 2002 ). The infection process was accompanied by shedding of the pathogen into the water; a process contributing to transmission of the disease (Wise et al. 1997 ). It does not appear that the
level of dietary iron affected antibody production and thereby infl uenced the course
of an infection (Sealey et al. 1997 ).
Another approach to understanding pathogenicity is to determine the nature of
the host’s response to infection. Thus using qPCR, the transcriptional levels of 7 key
channel catfi sh antimicrobial peptides genes was followed with data revealing a
total lack of signifi cant upregulation at 2 h post infection (Pridgeon et al. 2012 ).
At 4 h onwards, hepcidin was upregulated. Additionally at 24 h after infection,
upregulation of NK-lysin type 1 and type 3, and cathepsin D occurred. Administration
of lethal but not sub-lethal doses of Edw. ictaluri led to upregulation of hepcidin in
the posterior kidney, the signifi cance of which may be related to the inhibition of
replication of the pathogen. The suggestion was that hepcidin may well be important
as a defence mechanism against Edw. ictaluri infection in channel catfi sh (Pridgeon
et al. 2012 ).
6 Enterobacteriaceae Representatives
Saeed ( 1983 ) showed that cells are highly piliated, and inferred that the pili might
be associated with virulence. By means of intragastric intubation and a comparatively high dose of 1 × 10
9 cells, Edw. ictaluri crossed the intestinal mucosa of channel catfi sh in 15 min (Baldwin and Newton 1993 ). Using 1 × 10
6 cells/ml and an
application directly into the olfactory organs of channel catfi sh, light and electron
microscopy revealed damage after 1 h (Morrison and Plumb 1994 ). The importance
of entry across the intestinal epithelium is becoming widely accepted, with actin
polymerization and receptor-mediated endocytosis as likely mechanisms of uptake
(Li et al. 2012 ). It has been fi rmly established that channel catfi sh are highly susceptible to the organism, with an injected dose of 1.5 × 10
3 cells capable of killing the
host within 10 days at a water temperature of 26 °C (Plumb and Sanchez 1983 ). It
does not appear that the organism produces abundant exo-enzymes, which would
function as exotoxins in fi sh. It has been argued that both gut and nares are primary
sites for the invasion of Edw. ictaluri in natural outbreaks of disease (Shotts et al.
1986 ). Fluorescence microscopy evidence pointed to the localisation of the organism on the gill within 5 min and within gill epithelia after 45 min and to the kidney
within 4 h of a waterborne route (Nusbaum and Morrison 2002 ); the outcome was a
bacteraemia within 24 h (Wise et al. 1997 ). By 72 h, the pathogen was recoverable
from the blood. Then by 216 h, there was evidence of the pathogen clearing from
the blood, with all survivors developing agglutinating antibodies to Edw. ictaluri.
Entry, survival (many organisms were present in vacuoles) and replication in head
kidney macrophages of channel catfi sh has been observed microscopically.
Opsonisation with normal serum led to even greater internalization of Edw. ictaluri
at 0 h, but did not affect replication once internalized (Booth et al. 2006 ). Uptake of
the pathogen into host (epithelial) cells may well involve actin polymerization and
receptor-mediated endocytosis (Skirpstunas and Baldwin 2002 ). The infection process was accompanied by shedding of the pathogen into the water; a process contributing to transmission of the disease (Wise et al. 1997 ). It does not appear that the
level of dietary iron affected antibody production and thereby infl uenced the course
of an infection (Sealey et al. 1997 ).
Another approach to understanding pathogenicity is to determine the nature of
the host’s response to infection. Thus using qPCR, the transcriptional levels of 7 key
channel catfi sh antimicrobial peptides genes was followed with data revealing a
total lack of signifi cant upregulation at 2 h post infection (Pridgeon et al. 2012 ).
At 4 h onwards, hepcidin was upregulated. Additionally at 24 h after infection,
upregulation of NK-lysin type 1 and type 3, and cathepsin D occurred. Administration
of lethal but not sub-lethal doses of Edw. ictaluri led to upregulation of hepcidin in
the posterior kidney, the signifi cance of which may be related to the inhibition of
replication of the pathogen. The suggestion was that hepcidin may well be important
as a defence mechanism against Edw. ictaluri infection in channel catfi sh (Pridgeon
et al. 2012 ).
6 Enterobacteriaceae Representatives