Agriculture Reference
In-Depth Information
3.5.1 Edwardsiella ictaluri
Edwardsiellaictaluri
is the aetiological agent of enteric septicaemia of catfish (ESC) which can
result in high mortalities (Thune
et al.
1993; Birkbeck and Ringø 2005). The pathogenesis of
ESC was previously studied by experimental infections of channel catfish (
Ictaluruspunctatus
Rafinesque) via the gut and water (Shotts
et al.
1986). The gut-exposed fish showed signs of
a systemic infection within 2 weeks, suffering from enteritis, hepatitis, interstitial nephritis
and myositis. Some of the non-injected cohabitants developed systemic infections beginning
in the intestine and nostrils. In another study the pathogenesis of ESC was investigated by
intragastric intubation (Baldwin and Newton 1993). Within 15-30 minutes of exposure
E.
ictaluri
was observed in contact with intestinal brush border and the trunk kidney was positive
for bacteria, indicating a rapid trans-mucosal passage. Additionally, bacteria were observed
in phagocytes of the intestinal mucosa, and later it was documented that
E. ictaluri
is able to
invade, survive and replicate in catfish macrophages (Booth
et al.
2006).
3.5.2 Edwardsiella tarda
Edwardsiellatarda
is a pathogen of several fish species including common carp, mullet (
Mugil
cephalus
L.), tilapia (
Tilapia mossambica
Peters), Japanese eel (
Anguilla japonica
Temminck
and Schlegel), blue gourami (
Trichogaster trichopterus
Pallas), channel catfish and Japanese
flounder (Thune
et al.
1993). The pathogenesis of experimental edwardsiellosis was studied
in Japanese flounder by intraperitoneal injection, immersion and oral intubation (Rashid
et al.
1997). The viable counts of
E. tarda
in the intestine, liver and kidney tissues were always
higher than those in the blood. Histopathological examinations demonstrated massive necrosis
in liver and kidney, and sporadic necrosis in epithelia and lamina propria. Intraphagocytic
multiplication of
E. tarda
was confirmed in these three tissues. In another study the entry of
E. tarda
in the blue gourami was investigated by immersion challenge (Ling
et al.
2001); the
bacteria were detected in all parts of the fish one day after exposure with the highest bacterial
concentration in the anterior section of the intestine. At day seven bacterial numbers were
insignificant in all organs studied except for the intestine.
3.6
PISCIRICKETTSIA SALMONIS
Piscirickettsiosis is caused by a Gram-negative intracellular pathogen,
Piscirickettsia salmo-
nis
, and was first isolated from marine netpen-reared coho salmon in southern Chile (Fryer
et al.
1990; Garcés
et al.
1991; Branson and Diaz-Munoz 1991; Fryer
et al.
1992). The disease
was also observed in other aquacultured salmonids such as Chinook salmon, rainbow trout,
masu salmon (
Oncorhynchus masou
Brevoort) and Atlantic salmon (Fryer and Lannan 1996;
Almendras
et al.
1997; Smith
et al.
1999). The disease has also been reported in Canada,
Norway and Ireland (Marshall
et al.
1998). Piscirickettsia-like bacteria have also been
associated with diseases in non-salmonids. Examples are white sea bass (
Atactoscion noblis
Ayres), black sea bass (
Dicentrarchus
sp.), tilapia (
Oreochromis
,
Tilapia
and
Sarotherodon
spp.) and blue-eyed plecostomus (
Panaque suttoni
Eigenmann and Eigenmann) (Mauel and
Miller 2002).
Coho salmon and Atlantic salmon have previously been tested for their susceptibility to
infection by a rickettsia isolated from cell cultures from diseased coho salmon (Garces
et al.
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