259
In a study of uptake of Aer. salmonicida by rainbow trout, it was observed that
the pathogen could be detected in the blood and kidney within 5 min of immersion
in a suspension containing 10
5 cells/ml (Hodgkinson et al. 1987 ). Interestingly, it
was also found that uptake of the pathogen was enhanced by the addition of particulates, e.g. latex, to the bacterial suspension. If latex was indeed added, Aer. salmonicida was isolated from blood at 12 min, and from kidney, spleen and faeces at 4 h
post-challenge. The organism was also cultured from the skin, gills, blood and faeces for up to 48 h. In the absence of latex, the pathogen could be again recovered at
12 min, but from a wider range of sites including kidney, spleen and the lower
intestine. However by 24 h, the pathogen was no longer recovered from the fi sh.
From culturing methods alone, it may not, however, be assumed that Aer. salmonicida had been totally removed from the animals. In fact, cultures of the pathogen
were isolated from kidney, spleen and faeces within 1 to 4 h of immunosuppression
of the fi sh at 7 days post-challenge. In addition, the method of challenge yielded
different results. Thus, when the entire fi sh was immersed in the bacterial suspension, superior uptake occurred compared to exposing only the head or tail regions.
The explanation of this phenomenon is unclear, but such results suggest that uptake
may occur through several locations rather than a single site, e.g. mouth, nares, gill
or anus. It is possible that the pathogen gains entry via all these sites or additionally
through the lateral line and/or skin (Hodgkinson et al. 1987 ). Perhaps, the most
signifi cant observation resulting from these experiments was the rapidity by which
Aer. salmonicida entered the rainbow trout. Other investigators have not sampled so
close to the initial time of challenge. McCarthy ( 1980 ) reported uptake to occur
from the oral route within 5 h, with the organism found in the kidney. Tatner et al.
( 1984 ) fi rst sampled the fi sh at 24 h post-challenge. However, all these studies indicate the localisation of Aer. salmonicida principally within the reticulo-endothelial
systems of fi sh (Tatner et al. 1984 ). Notwithstanding, evidence continues to be
fi rmly pointed at the role of gills and skin/mucus in the uptake of Aer. salmonicida
into fi sh (Ferguson et al. 1998 ).
Another route of infection that has been proposed is via the gastro-intestinal
tract, due to intake of contaminated food. However, there is disagreement as to
whether or not this in fact occurs. Plehn ( 1911 ) and Blake and Clark ( 1931 ) reported
success in experimentally infecting fi sh by feeding contaminated food. However,
Krantz et al. ( 1964a , b ) and McCarthy ( 1980 ) failed to infect brown trout by feeding
with food containing the pathogen. Klontz and Wood ( 1972 ) reported clinical furunculosis in the sable fi sh apparently caused by ingestion of carrier coho salmon.
Evidence has been published that shows Aer. salmonicida may translocate across
the intestinal epithelia (Jutfelt et al. 2006 ). Here, the authors exposed intestinal segments of rainbow trout for 90 min to isothiocyanate-labelled cells of virulent Aer.
salmonicida and demonstrated translocation. In addition, in laboratory-based experiments that compared various methods designed to induce the carrier state of Aer.
salmonicida in juvenile spring chinook salmon, Markwardt and Klontz (1989)
observed that gastric intubation (of ca. 1 × 10
8 bacteria) resulted in a 65 % carrier
state. This result was a signifi cantly higher percentage than those recorded for exposure to a broth culture as a bath, ingestion of broth culture coated food, and exposure
Aeromonas salmonicida
In a study of uptake of Aer. salmonicida by rainbow trout, it was observed that
the pathogen could be detected in the blood and kidney within 5 min of immersion
in a suspension containing 10
5 cells/ml (Hodgkinson et al. 1987 ). Interestingly, it
was also found that uptake of the pathogen was enhanced by the addition of particulates, e.g. latex, to the bacterial suspension. If latex was indeed added, Aer. salmonicida was isolated from blood at 12 min, and from kidney, spleen and faeces at 4 h
post-challenge. The organism was also cultured from the skin, gills, blood and faeces for up to 48 h. In the absence of latex, the pathogen could be again recovered at
12 min, but from a wider range of sites including kidney, spleen and the lower
intestine. However by 24 h, the pathogen was no longer recovered from the fi sh.
From culturing methods alone, it may not, however, be assumed that Aer. salmonicida had been totally removed from the animals. In fact, cultures of the pathogen
were isolated from kidney, spleen and faeces within 1 to 4 h of immunosuppression
of the fi sh at 7 days post-challenge. In addition, the method of challenge yielded
different results. Thus, when the entire fi sh was immersed in the bacterial suspension, superior uptake occurred compared to exposing only the head or tail regions.
The explanation of this phenomenon is unclear, but such results suggest that uptake
may occur through several locations rather than a single site, e.g. mouth, nares, gill
or anus. It is possible that the pathogen gains entry via all these sites or additionally
through the lateral line and/or skin (Hodgkinson et al. 1987 ). Perhaps, the most
signifi cant observation resulting from these experiments was the rapidity by which
Aer. salmonicida entered the rainbow trout. Other investigators have not sampled so
close to the initial time of challenge. McCarthy ( 1980 ) reported uptake to occur
from the oral route within 5 h, with the organism found in the kidney. Tatner et al.
( 1984 ) fi rst sampled the fi sh at 24 h post-challenge. However, all these studies indicate the localisation of Aer. salmonicida principally within the reticulo-endothelial
systems of fi sh (Tatner et al. 1984 ). Notwithstanding, evidence continues to be
fi rmly pointed at the role of gills and skin/mucus in the uptake of Aer. salmonicida
into fi sh (Ferguson et al. 1998 ).
Another route of infection that has been proposed is via the gastro-intestinal
tract, due to intake of contaminated food. However, there is disagreement as to
whether or not this in fact occurs. Plehn ( 1911 ) and Blake and Clark ( 1931 ) reported
success in experimentally infecting fi sh by feeding contaminated food. However,
Krantz et al. ( 1964a , b ) and McCarthy ( 1980 ) failed to infect brown trout by feeding
with food containing the pathogen. Klontz and Wood ( 1972 ) reported clinical furunculosis in the sable fi sh apparently caused by ingestion of carrier coho salmon.
Evidence has been published that shows Aer. salmonicida may translocate across
the intestinal epithelia (Jutfelt et al. 2006 ). Here, the authors exposed intestinal segments of rainbow trout for 90 min to isothiocyanate-labelled cells of virulent Aer.
salmonicida and demonstrated translocation. In addition, in laboratory-based experiments that compared various methods designed to induce the carrier state of Aer.
salmonicida in juvenile spring chinook salmon, Markwardt and Klontz (1989)
observed that gastric intubation (of ca. 1 × 10
8 bacteria) resulted in a 65 % carrier
state. This result was a signifi cantly higher percentage than those recorded for exposure to a broth culture as a bath, ingestion of broth culture coated food, and exposure
Aeromonas salmonicida