416
of the lectin for >24 h. Exposure to lectin ligands, i.e. D-galactose and L-rhamnose,
protected the catfi sh against columnaris (Beck et al. 2012 ).
Extracellular proteases have been implicated with Fla. columnare (Newton et al.
1997 ), including collagenase, chondroitinase and proteases (Stringer-Roth et al.
2002 ; Olivares-Fuster and Arias 2008 ). Using cell-free extracts (culture supernatants) of Fla. columnare , Pacha ( 1961 ) obtained muscle damage following injection
with the material. However, the result could not be substantiated by detailed in vitro
chemical analyses of the supernatant. Later, two proteases of 53 and 58 kDa were
isolated from Fla. columnare (Newton et al. 1997 ), and we assume that these are
responsible for tissue damage. Iron may infl uence the pathogenicity of Fla. columnare, insofar as the presence of 0.35–1.4 mg of iron/100 g of fi sh reduced the survival time following experimental challenge with the pathogen from 20 days to 1
day (Kuo et al. 1981 ). In contrast, transferrin exerted a negligible effect. Fla. johnsoniae has infected barramundi and goldfi sh via waterborne challenge (Soltani et al.
1994 ).
Fla. columnare cells have been detected in the gill, mucus and skin within 5 min
of immersion challenge of previously abraded fi sh (15 min without abrading) (Bader
et al. 2003a ). There is evidence that mucus promotes the growth of Fla. columnare,
increasing extracellular protease production and the ability to form biofi lms
(Staroscik and Nelson 2008 ).
A siderophore-mediated iron uptake system has been found. With iron- limitation,
synthesis of an OMP, a TonB-dependent ferrichrome-iron receptor precursor, of
86 kDa was upregulated. A putative ferric uptake regulator protein was also identifi ed in the genome (Guan et al. 2013 ).
Disease Control
Management Techniques Columnaris is most severe at high water temperatures;
it has been suggested that control may be exercised by keeping the water as cool as
possible, although this approach may be diffi cult for many fi sh farms. Using a high
virulent culture, there was a high level of colonization and destruction; invasion of
gill tissue was observed to spread from the fi lament tips towards the base, with outer
membrane vesicles surrounding most of the fl avobacterial cells. Higher virulent
cultures led to signifi cantly higher apoptotic cell counts in carp and rainbow trout
(Declercq et al. 2015 ).
Vaccine Development Fujihara and Nakatani ( 1971 ) experimented with heatkilled cells, which were administered via food to juvenile coho salmon. The fi sh
responded with the production of antibody (titre = 1:5120). Schachte and Mora
( 1973 ) concurred with the general view by demonstrating agglutinating antibody in
channel catfi sh. Survivors of infection experiments resisted re-infection, suggesting
the presence of a protective immune response (Fujihara et al. 1971 ). Formalised
cells of Fla. columnare were administered to eel by immersion and injection, result7 Flavobacteria and Cytophagas
of the lectin for >24 h. Exposure to lectin ligands, i.e. D-galactose and L-rhamnose,
protected the catfi sh against columnaris (Beck et al. 2012 ).
Extracellular proteases have been implicated with Fla. columnare (Newton et al.
1997 ), including collagenase, chondroitinase and proteases (Stringer-Roth et al.
2002 ; Olivares-Fuster and Arias 2008 ). Using cell-free extracts (culture supernatants) of Fla. columnare , Pacha ( 1961 ) obtained muscle damage following injection
with the material. However, the result could not be substantiated by detailed in vitro
chemical analyses of the supernatant. Later, two proteases of 53 and 58 kDa were
isolated from Fla. columnare (Newton et al. 1997 ), and we assume that these are
responsible for tissue damage. Iron may infl uence the pathogenicity of Fla. columnare, insofar as the presence of 0.35–1.4 mg of iron/100 g of fi sh reduced the survival time following experimental challenge with the pathogen from 20 days to 1
day (Kuo et al. 1981 ). In contrast, transferrin exerted a negligible effect. Fla. johnsoniae has infected barramundi and goldfi sh via waterborne challenge (Soltani et al.
1994 ).
Fla. columnare cells have been detected in the gill, mucus and skin within 5 min
of immersion challenge of previously abraded fi sh (15 min without abrading) (Bader
et al. 2003a ). There is evidence that mucus promotes the growth of Fla. columnare,
increasing extracellular protease production and the ability to form biofi lms
(Staroscik and Nelson 2008 ).
A siderophore-mediated iron uptake system has been found. With iron- limitation,
synthesis of an OMP, a TonB-dependent ferrichrome-iron receptor precursor, of
86 kDa was upregulated. A putative ferric uptake regulator protein was also identifi ed in the genome (Guan et al. 2013 ).
Disease Control
Management Techniques Columnaris is most severe at high water temperatures;
it has been suggested that control may be exercised by keeping the water as cool as
possible, although this approach may be diffi cult for many fi sh farms. Using a high
virulent culture, there was a high level of colonization and destruction; invasion of
gill tissue was observed to spread from the fi lament tips towards the base, with outer
membrane vesicles surrounding most of the fl avobacterial cells. Higher virulent
cultures led to signifi cantly higher apoptotic cell counts in carp and rainbow trout
(Declercq et al. 2015 ).
Vaccine Development Fujihara and Nakatani ( 1971 ) experimented with heatkilled cells, which were administered via food to juvenile coho salmon. The fi sh
responded with the production of antibody (titre = 1:5120). Schachte and Mora
( 1973 ) concurred with the general view by demonstrating agglutinating antibody in
channel catfi sh. Survivors of infection experiments resisted re-infection, suggesting
the presence of a protective immune response (Fujihara et al. 1971 ). Formalised
cells of Fla. columnare were administered to eel by immersion and injection, result7 Flavobacteria and Cytophagas
