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(2010) demonstrated that both serovars spread through water and infect eels - serovar A
entering mainly by the anus and serovar E by the gills. Also, both serovars were pathogenic
for tilapia (
Oreochromis
spp.), European sea bass and rainbow trout, but not for gilthead
sea bream.
3.2.4 Vibrio ichthyoenteri
Since 1971 a bacterial disease characterized by intestinal necrosis and high rates of mor-
tality has been observed in larval Japanese flounder (
Paralichthys olivaceus
Temminck and
Schlegel). It should be noted that the disease only occurs in the intestine of larval stages with-
out a functional stomach (Muroga
et al.
1990; Ishimaru
et al.
1996; Kim
et al.
2004; Montes
et al.
2006). The disease is one of the most serious diseases in Korean and Japanese hatcheries
and is caused by
Vibrio ichthyoenteri
(Ishimaru
et al.
1996), previously described as
Vibrio
species INFL (intestinal necrosis of flounder larvae) (Masumura
et al.
1989). Little is known
about the pathogenicity of this species.
3.2.5 Vibrio harveyi (Vibrio carchariae)
Although
Vibrio harveyi
(which includes
Vibrio carchariae
as a junior synonym) is often
found in a free-living state in aquatic environments and is often reported to be present in the
GI tract of apparently healthy fish and shellfish, a number of reports have described
V. harveyi
as the aetiological agent of infectious gastroenteritis in a number of fish species (Lee
et al.
2002; Austin and Zhang 2006; Cano-Gomez
etal.
2009). Liu
etal.
(2004) described outbreaks
of disease with serious mortalities in cultured cobia (
Rachycentron canadum
L.) displaying
swollen intestines containing transparent yellow fluid. All moribund/dead fish exhibited
gastroenteritis and
V. harveyi
was shown as the causative agent. A similar syndrome has
also been observed in summer flounder (
Paralichthys dentatus
L.), a commercially important
species in coastal waters of the eastern United States (Soffientino
et al.
1999; Gauger
et al.
2006). The pathogen was identified as
V. harveyi/carchariae
. Histopathological examination
revealed lesions to the peritoneum and posterior intestine. Large numbers of bacteria were
observed in the peritoneum and at the serosal surface of the posterior intestine. The tissue was
associated with necrosis, fibrin deposition, haemorrhaging and inflammatory cell infiltration.
V. harveyi/carchariae
has also been isolated from moribund grouper (
Epinephelus coioides
)
(Yii
et al.
1997) and red drum (
Sciaenops ocellatus
)(Liu
et al.
2003) displaying a swollen
intestine with transparent yellow fluid.
V. harveyi
has also been isolated from diseased
common dentex (
Dentex dentex
L.) and was dominant in samples from diseased animals
(Company
et al.
1999). Necropsy of the diseased fish revealed haemorrhagic liver, empty
digestive tract, enlarged gall bladder and trunk kidney inflammation. Histopathology revealed
the presence of bacteria around the gill lamellae and in the gut lumen and in some samples
the intestinal epithelium appeared highly necrotic.
A recent
ex vivo
study assessed the impact of
V. harveyi
on the intestinal brush border of
European sea bass;
V. harveyi
cells were inoculated into lumen the of posterior intestinal sacs
(
in vitro
) at log 7 CFU g
-1
for 1 h at 20
∘
C (Peggs, Browdy, Davies and Merrifield unpublished
results). After the incubation the brush borders from control samples (exposed to PBS) were
intact and apparently healthy, whereas the intestinal tissue exposed to
V. harveyi
showed
regions with morphological changes, including irregular-shaped enterocytes, disorganized
microvilli and necrotic enterocytes which can ultimately lead to breaching of the epithelial
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