24
Epizootiology
Cl. botulinum is widespread in soil, marine and freshwater sediments and in the
gastro-intestinal tract of man and other animals, including fi sh (Bott et al. 1968 ;
Cato et al. 1986 ). In one study of 530 trout from Danish earthern ponds, Cl. botulinum type E was discovered to occur in 5–100 % of the fi sh in winter, increasing to
85–100 % of the population in late summer (Huss et al. 1974a ). It was supposed that
the principal source of contamination with this organism was from minced trash fi sh
used as feed, although soil and water could also be involved (Huss et al. 1974a ).
Moreover, it was considered likely that clostridia become established in the mud
and bottom-living invertebrates in trout ponds (Huss et al. 1974b ). In Britain, it has
been determined from an examination of 1400 trout collected from 17 fi sh farms,
that the incidence of Cl. botulinum in whole fi sh and viscera was 9.4 % and 11.0 %
respectively. Nevertheless, Cl. botulinum lingers in the fi sh farm environment for
considerable periods following outbreaks of disease. Thus, at the English trout
farm, which experienced botulism, the organism (possibly as endospores) was
recovered for a year after the outbreak of disease. The numbers ranged from 1 to
800 organisms/g of sediment, compared to <1/g at an unaffected control site (Cann
and Taylor 1982 ). There are no data available to assess the level of contamination in
wild fi sh stocks (Cann et al. 1975 ). Similarly, there is no evidence to suggest that
trout contaminated with Cl. botulinum could comprise a human health hazard (Bach
et al. 1971 ).
Pathogenicity
Botulinum toxin has been introduced into fi sh to determine the level of toxicity.
Thus using channel catfi sh fi ngerlings, Chatla et al. ( 2012 ) established that the MLD
of serotype E toxin as 13.7 pg of toxin/fi sh of 5.3 g weight. This was determined
after 96 h of intracoelomical injection of the toxin. Initially, the fi sh displayed
hyperactivity, which led to erratic swimming leading to death. The mortalities
revealed exophthalmia, ascites, congestion of the spleen, and the cutting off (intussusception) of the blood supply and thus blanching of the intestine, i.e. visceral toxicosis (Chatla et al. 2012 ).
Disease Control
Disinfection As there is no effective chemotherapy for botulism in fi sh, disinfection of the ponds has been advocated. Success has resulted from moving the stock
to clean areas, draining the contaminated ponds, and removing surface mud and
detritus before disinfecting with slaked lime at 1.6 kg/m
2
. The disinfectant should
be worked well into the layers at the bottom of the ponds, left for a period of not less
2 Gram-Positive Bacteria (Anaerobes and ‘Lactic Acid’ Bacteria)
Epizootiology
Cl. botulinum is widespread in soil, marine and freshwater sediments and in the
gastro-intestinal tract of man and other animals, including fi sh (Bott et al. 1968 ;
Cato et al. 1986 ). In one study of 530 trout from Danish earthern ponds, Cl. botulinum type E was discovered to occur in 5–100 % of the fi sh in winter, increasing to
85–100 % of the population in late summer (Huss et al. 1974a ). It was supposed that
the principal source of contamination with this organism was from minced trash fi sh
used as feed, although soil and water could also be involved (Huss et al. 1974a ).
Moreover, it was considered likely that clostridia become established in the mud
and bottom-living invertebrates in trout ponds (Huss et al. 1974b ). In Britain, it has
been determined from an examination of 1400 trout collected from 17 fi sh farms,
that the incidence of Cl. botulinum in whole fi sh and viscera was 9.4 % and 11.0 %
respectively. Nevertheless, Cl. botulinum lingers in the fi sh farm environment for
considerable periods following outbreaks of disease. Thus, at the English trout
farm, which experienced botulism, the organism (possibly as endospores) was
recovered for a year after the outbreak of disease. The numbers ranged from 1 to
800 organisms/g of sediment, compared to <1/g at an unaffected control site (Cann
and Taylor 1982 ). There are no data available to assess the level of contamination in
wild fi sh stocks (Cann et al. 1975 ). Similarly, there is no evidence to suggest that
trout contaminated with Cl. botulinum could comprise a human health hazard (Bach
et al. 1971 ).
Pathogenicity
Botulinum toxin has been introduced into fi sh to determine the level of toxicity.
Thus using channel catfi sh fi ngerlings, Chatla et al. ( 2012 ) established that the MLD
of serotype E toxin as 13.7 pg of toxin/fi sh of 5.3 g weight. This was determined
after 96 h of intracoelomical injection of the toxin. Initially, the fi sh displayed
hyperactivity, which led to erratic swimming leading to death. The mortalities
revealed exophthalmia, ascites, congestion of the spleen, and the cutting off (intussusception) of the blood supply and thus blanching of the intestine, i.e. visceral toxicosis (Chatla et al. 2012 ).
Disease Control
Disinfection As there is no effective chemotherapy for botulism in fi sh, disinfection of the ponds has been advocated. Success has resulted from moving the stock
to clean areas, draining the contaminated ponds, and removing surface mud and
detritus before disinfecting with slaked lime at 1.6 kg/m
2
. The disinfectant should
be worked well into the layers at the bottom of the ponds, left for a period of not less
2 Gram-Positive Bacteria (Anaerobes and ‘Lactic Acid’ Bacteria)