respective neurotoxins produced. Human botulism is caused by types A, B,
E, and rarely type F (Franciosa et al., 1994). Types C and D cause botulism in
animals. Type G is not associated with neurotoxicity in humans or animals.
All isolates of C. botulinum can be placed into one of four groups based on
physiological differences: group I, all type A strains and proteolytic B and F
types; group II, all type E strains and nonproteolytic B and F strains; group
III, C and D type strains; and group IV, G type strains. 16s and 23S rRNA
gene sequence studies (Hutson et al. 1993a, b and Hutson et al. 1994) have
confi rmed this grouping and have documented a high level of relatedness
among strains within each group and little relatedness between members
of the different groups (Hatheway, 1993).
Relationship Between Botulism and Seafood
In recent years an average of 450 botulism outbreaks have been annually
reported in the international literature; 12% of the outbreaks being caused
by Type E (Hatheway, 1995). Coastal marine environments usually exhibit
serotype E as predominant although certain marine sediments have been
found to contain predominantly serotype B. Although isolates of types B,
E, and F are known to be psychrotolerant only isolates of type E are truly
psychrotrophic and exhibit the ability to grow in seafood tissue under
refrigerated conditions (~ 4°C). Type E has been the most frequent cause
of botulism derived from seafood.
There is a well established history of salted fi sh causing type E
botulism. Uneviscerated, salt-cured fi sh have been implicated in a
number of additional botulism outbreaks (Badhey et al., 1986; Kotev et
al. 1987; Telzak et al. 1990). The intestines of uneviscerated, salted fi sh are
thought to result in a low-salt environment allowing spores of C. botulism
to germinate, grow and produce toxin. Weber et al. (1993) reported on a
massive outbreak of type E botulism associated with the consumption of
traditional salted fi sh in Cairo, Egypt. Low levels of type E toxin are known
to result in primarily gastrointestinal (GI) symptoms. Sobel et al. (2007)
reported on an outbreak of clinically mild botulism type E illness among
fi ve individuals resulting in predominantly GI symptoms consisting of
nausea, vomiting, abdominal pain, dry mouth, shortness of breath and in
one individual diplopia (double vision). Fresh, uneviscerated whitefi sh
with salt had been placed in a sealed ziplock bag and stored for ~ 1 mon at
ambient temperature prior to consumption. Remnant fi sh tested positive
for botulinum type E toxin.
Commercially produced vacuum-packaged hot-smoked fi sh is
presently considered one of the most important botulism food vehicles.
Hot-smoked Canadian whitefi sh was reported by Korkeala et al. (1998)
to be the cause of a single family outbreak of type E botulism in 1997.
The fi sh was smoked only 5 d before consumption indicating that toxin