522
Epizootiology
Vibrios abound in the marine and estuarine environments (see Kaneko and Colwell
1974 ), and therefore present a constant threat for any susceptible host. In particular,
V. alginolyticus has been recovered from the water in marine fi sh tanks (Gilmour
1977 ).
Pathogenicity
V. alginolyticus adheres to intestinal mucus of the large yellow croaker
( Pseudosciaena crocea ), possibly involving glycoproteins, with adhesion infl uenced by environmental parameters, namely pH, salinity and temperature. Maximal
adhesion occurred in acid conditions, at 30 °C and at marine salinities [35%o]
(Yan et al. 2007 ). The portal of entry into large yellow croaker has been identifi ed
as the intestinal tract rather than gill or skin (Chen et al. 2008 ). A type III secretion
system has been determined to rapidly cause cell death by inducing rapid apoptosis,
characterized by membrane blebbing, nuclear condensation and DNA fragmentation, rounding of the cells, and lysis (Zhao et al. 2010 ).
ECPs, growth in iron-limited conditions, and survival in fi sh serum have been
associated with virulence (Kahla-Nakbi et al. 2009 ). Lee ( 1995 ) revealed that the
organism produced ECP, which was lethal at 0.52 μg/g of fi sh. The ECP contained
a 44 kDa toxic protease, for which the minimum lethal dose was 0.17 μg/g of fi sh.
In comparison, the LD 50 for ECP to silver sea bream was reported as 0.92 μg/g of
fi sh, with haemolysins and proteases featuring in pathogenicity (Li et al. 2003 ).
Also, administration of ECP led to a reduction in one of the hepatic heat shock protein (HSP), specifi cally HSP90 during the latter stages of acute infection in silver
sea bream (Deane et al. 2004 ). The LD 50 of the pathogen to silver sea bream was
reported as 4.85 × 10
4 , 5.01 × 10
5 , 3.16 × 10
6 and >2.5 × 10
8 CFU/ml for i.m., i.p.,
injury coupled with immersion and immersion, respectively (Li et al. 2003 ). From,
these data, the impact of injury leading to infection is apparent. Following infection
of sea bream, there was a rapid and substantial decline in Na
+ , K
+ and ATPase activity in the kidney, and a decreased expression of HSP70 in the kidney and liver
(Deane and Woo 2005 ). Subsequently, virulence of V. alginolyticus was linked to
genotype, viz. the collagenase gene (Yishan et al. 2011 ). A virulence-associated
toxR gene has been described in a pathogenic isolate, coined ZJ51-O, and linked to
resistance to bile salts and the ability to form a biofi lm and thus colonise the surface
of fi sh intestine. A deletion mutant, lacking toxR , lacked a 37 kDa OMP [a homolog
of OmpT] whereas a second OMP of 43 kDa [a homolog of OmpN] was reduced
(Chen et al. 2012 ).
A thermostable haemolysin, TLH, has been described, and shown to induce caspase- 3, 8, −9/6 activities followed by apoptotic DNA fragmentation, membrane
10 Vibrios
Epizootiology
Vibrios abound in the marine and estuarine environments (see Kaneko and Colwell
1974 ), and therefore present a constant threat for any susceptible host. In particular,
V. alginolyticus has been recovered from the water in marine fi sh tanks (Gilmour
1977 ).
Pathogenicity
V. alginolyticus adheres to intestinal mucus of the large yellow croaker
( Pseudosciaena crocea ), possibly involving glycoproteins, with adhesion infl uenced by environmental parameters, namely pH, salinity and temperature. Maximal
adhesion occurred in acid conditions, at 30 °C and at marine salinities [35%o]
(Yan et al. 2007 ). The portal of entry into large yellow croaker has been identifi ed
as the intestinal tract rather than gill or skin (Chen et al. 2008 ). A type III secretion
system has been determined to rapidly cause cell death by inducing rapid apoptosis,
characterized by membrane blebbing, nuclear condensation and DNA fragmentation, rounding of the cells, and lysis (Zhao et al. 2010 ).
ECPs, growth in iron-limited conditions, and survival in fi sh serum have been
associated with virulence (Kahla-Nakbi et al. 2009 ). Lee ( 1995 ) revealed that the
organism produced ECP, which was lethal at 0.52 μg/g of fi sh. The ECP contained
a 44 kDa toxic protease, for which the minimum lethal dose was 0.17 μg/g of fi sh.
In comparison, the LD 50 for ECP to silver sea bream was reported as 0.92 μg/g of
fi sh, with haemolysins and proteases featuring in pathogenicity (Li et al. 2003 ).
Also, administration of ECP led to a reduction in one of the hepatic heat shock protein (HSP), specifi cally HSP90 during the latter stages of acute infection in silver
sea bream (Deane et al. 2004 ). The LD 50 of the pathogen to silver sea bream was
reported as 4.85 × 10
4 , 5.01 × 10
5 , 3.16 × 10
6 and >2.5 × 10
8 CFU/ml for i.m., i.p.,
injury coupled with immersion and immersion, respectively (Li et al. 2003 ). From,
these data, the impact of injury leading to infection is apparent. Following infection
of sea bream, there was a rapid and substantial decline in Na
+ , K
+ and ATPase activity in the kidney, and a decreased expression of HSP70 in the kidney and liver
(Deane and Woo 2005 ). Subsequently, virulence of V. alginolyticus was linked to
genotype, viz. the collagenase gene (Yishan et al. 2011 ). A virulence-associated
toxR gene has been described in a pathogenic isolate, coined ZJ51-O, and linked to
resistance to bile salts and the ability to form a biofi lm and thus colonise the surface
of fi sh intestine. A deletion mutant, lacking toxR , lacked a 37 kDa OMP [a homolog
of OmpT] whereas a second OMP of 43 kDa [a homolog of OmpN] was reduced
(Chen et al. 2012 ).
A thermostable haemolysin, TLH, has been described, and shown to induce caspase- 3, 8, −9/6 activities followed by apoptotic DNA fragmentation, membrane
10 Vibrios