341
with lipid A as a biologically active determinant (Wang et al. 2010 ). Mutation of the
tryptophanase gene, tnaA, has been correlated with reduced virulence in zebra fi sh,
with a tnaA deletion mutant leading to a ~55 increase in LD 50 dose (Han et al. 2012 ).
A type III secretion system has been documented (Xie et al. 2010 ) and its presence
linked to virulence notably in connection with the intracellular replication of the
pathogen in phagocytes (Rao et al. 2004 ; Okuda et al. 2009 ; Li et al. 2011c ); defective mutants having reduced virulence (Tan et al. 2005 ). Secreted proteins of the
type III secretion system were of 22, 25 and 55 kDa, being identifi ed as EseD, EseC
and EseB, and may function as a translocon (Okuda et al. 2009 ). Pathogenic and
non-pathogenic cultures have been differentiated on the basis of detection of a type
III secretion system using a PCR targeting the type III component gene esaV with
the result that 18 pathogenic cultures were positive but not so the same number of
non-pathogenic isolates (Li et al. 2011 ). It has been proposed that the type III secretion system (T3SS), which is involved in translocating proteins involved with virulence into the host cell, facilitates survival and replication of Edw. tarda in
macrophages with the pathogen causing caspase-1-mediated macrophage death (=
pyroptosis) and enhanced secretion of interleukin 1ß (Xie et al. 2014 ). Deletion of
the fl agellin gene, fl iC, decreased macrophage cytotoxicity, but did not decrease
virulence. The proposal was made that Edw. tarda evades the innate immune
response of the host by downregulating the expression of FliC (Xie et al. 2014 ).
Also, a type VI secretion system (T6SS) has been reported (Nakamura et al. 2014 ).
ECPs have been attributed with stimulating a chemotactic and chemokinetic
response by macrophages that may be involved in the infl ammatory response by
infected fi sh (Widenemayer et al. 2008 ). Variable OMP patterns, including some
major (25–40 kDa) and many minor proteins (~10-120 kDa), have been identifi ed
in isolates when cultured at 25 °C. Interestingly, salinity affected OMP composition
in some cultures, suggesting heterogeneity in the taxon (Darwish et al. 2001 ). Four
immuno-reactive OMPs have been detected, and using matrix-assisted laser desorption/ionization mass spectrometry analyses, two of these were identifi ed as OmpA
and murein lipoprotein (Yu et al. 2013 ).
Haemolysins and dermatotoxins, but not lipases or proteolytic enzymes, were
produced in vitro , and it was postulated that these exo-enzymes may confer pathogenicity on Edw. tarda (Ullah and Arai 1983a , b ). Furthermore, the pathogenic role
of dermatotoxins was highlighted in additional experiments (Ullah and Arai 1983b ).
This work concluded that two high molecular weight, heat sensitive dermatotoxins
were produced, which in rabbits (not fi sh!) were found to have separate functions.
Thus, one toxin caused erythema within 3–8 h of intracutaneous injection, whereas
the second caused oedema followed by necrotic erythema in 5–7 days. Hopefully at
some point, this work will be repeated in fi sh. Proteolytic toxins (molecular
weight = 37 kDa), from ECP, have been purifi ed from avirulent cultures (the toxin is
not present in avirulent isolates) and the LD 50 equated to 1.6 g of toxin/g of fi sh
(Suprapto et al. 1996 ). The organism has been associated with the development of
liver hypertrophy following experimental infection of Japanese fl ounder (Miwa and
Mano 2000 ).
Edwardsiella tarda
with lipid A as a biologically active determinant (Wang et al. 2010 ). Mutation of the
tryptophanase gene, tnaA, has been correlated with reduced virulence in zebra fi sh,
with a tnaA deletion mutant leading to a ~55 increase in LD 50 dose (Han et al. 2012 ).
A type III secretion system has been documented (Xie et al. 2010 ) and its presence
linked to virulence notably in connection with the intracellular replication of the
pathogen in phagocytes (Rao et al. 2004 ; Okuda et al. 2009 ; Li et al. 2011c ); defective mutants having reduced virulence (Tan et al. 2005 ). Secreted proteins of the
type III secretion system were of 22, 25 and 55 kDa, being identifi ed as EseD, EseC
and EseB, and may function as a translocon (Okuda et al. 2009 ). Pathogenic and
non-pathogenic cultures have been differentiated on the basis of detection of a type
III secretion system using a PCR targeting the type III component gene esaV with
the result that 18 pathogenic cultures were positive but not so the same number of
non-pathogenic isolates (Li et al. 2011 ). It has been proposed that the type III secretion system (T3SS), which is involved in translocating proteins involved with virulence into the host cell, facilitates survival and replication of Edw. tarda in
macrophages with the pathogen causing caspase-1-mediated macrophage death (=
pyroptosis) and enhanced secretion of interleukin 1ß (Xie et al. 2014 ). Deletion of
the fl agellin gene, fl iC, decreased macrophage cytotoxicity, but did not decrease
virulence. The proposal was made that Edw. tarda evades the innate immune
response of the host by downregulating the expression of FliC (Xie et al. 2014 ).
Also, a type VI secretion system (T6SS) has been reported (Nakamura et al. 2014 ).
ECPs have been attributed with stimulating a chemotactic and chemokinetic
response by macrophages that may be involved in the infl ammatory response by
infected fi sh (Widenemayer et al. 2008 ). Variable OMP patterns, including some
major (25–40 kDa) and many minor proteins (~10-120 kDa), have been identifi ed
in isolates when cultured at 25 °C. Interestingly, salinity affected OMP composition
in some cultures, suggesting heterogeneity in the taxon (Darwish et al. 2001 ). Four
immuno-reactive OMPs have been detected, and using matrix-assisted laser desorption/ionization mass spectrometry analyses, two of these were identifi ed as OmpA
and murein lipoprotein (Yu et al. 2013 ).
Haemolysins and dermatotoxins, but not lipases or proteolytic enzymes, were
produced in vitro , and it was postulated that these exo-enzymes may confer pathogenicity on Edw. tarda (Ullah and Arai 1983a , b ). Furthermore, the pathogenic role
of dermatotoxins was highlighted in additional experiments (Ullah and Arai 1983b ).
This work concluded that two high molecular weight, heat sensitive dermatotoxins
were produced, which in rabbits (not fi sh!) were found to have separate functions.
Thus, one toxin caused erythema within 3–8 h of intracutaneous injection, whereas
the second caused oedema followed by necrotic erythema in 5–7 days. Hopefully at
some point, this work will be repeated in fi sh. Proteolytic toxins (molecular
weight = 37 kDa), from ECP, have been purifi ed from avirulent cultures (the toxin is
not present in avirulent isolates) and the LD 50 equated to 1.6 g of toxin/g of fi sh
(Suprapto et al. 1996 ). The organism has been associated with the development of
liver hypertrophy following experimental infection of Japanese fl ounder (Miwa and
Mano 2000 ).
Edwardsiella tarda