582 Modern Food Microbiology
Sixty-two outbreaks of botulism resulting from commercially canned foods were recorded for the
period 1899–1973,
74 with 41 prior to 1930. Between 1941 and 1982, 7 outbreaks occurred in the United
States involving commercially canned foods in metal containers, with 17 cases and 8 deaths.
89 Three
of these outbreaks were caused by type A and the remainder by type E. In five of the outbreaks, can
leakage or underprocessing occurred.
89 Canned mushrooms have been incriminated in several botulism
outbreaks. A study in 1973 and 1974 turned up 30 cans of mushrooms containing botulinal toxin (29
were type B). An additional 11 cans contained viable spores of C. botulinum without preformed
toxin.
74 The capacity of the commercial mushroom (Agaricus bisporus) to support the growth of
inoculated spores of C. botulinum was studied by Sugiyama and Yang.
119 Following inoculation of
various parts of mushrooms, they were sealed with plastic film and incubated. Toxin was detected
as early as 3–4 days later, when products were incubated at 20
◦ C. Although the plastic film used to
wrap the inoculated mushrooms allowed for gas exchange, the respiration of the fresh mushrooms
apparently consumed oxygen at a faster rate than it entered the film. No toxin was detected in products
stored at refrigerator temperatures.
An unusual outbreak of 36 cases occurred in 1985 with victims in three countries: Canada, the
Netherlands, and the United States. The vehicle food was chopped garlic in soybean oil that was
packaged in glass bottles. Although labeled with instructions to refrigerate, unopened bottles were
stored unrefrigerated for 8 months. The product was used to make garlic-buttered bread, which in
turn was used to prepare beef dip sandwiches. Proteolytic type B spores were found, and toxin was
produced within 2 weeks when proteolytic and nonproteolytic B strains were inoculated into bottles
of chopped garlic and held at 25
◦ C.
111 Type A toxin was produced in bottled chopped garlic in 20 days
at 35
◦ C when inoculated with 1 spore/g and by type B toxin in 20 days.
106 In the latter study, highly
toxic bottles looked and smelled acceptable. An outbreak of type E involving 91 cases with 20 deaths
occurred in Egypt in 1991, and the vehicle was an ungutted, salted raw fish product called faseikh.
84 In
1994, there were 30 victims in El Paso, Texas, after consuming potato-based dip and eggplant-based
dip, both of which contained baked potato. The baked potatoes were wrapped in aluminum foil and
held at room temperature for several days and, thus, they became toxigenic.
8 Although not common,
this is not the first time that botulinal toxin was detected in baked potatoes.
One of the recorded outbreaks of botulism (five cases with one death) due to type F involved
homemade liver paste. The U.S. outbreak occurred in 1966 from home-prepared venison jerky, with
three clinical cases.
82
The greatest hazards of botulism come from home-prepared and home-canned foods that are improperly handled or given insufficient heat treatments to destroy botulinal spores. Such foods are often
consumed without heating. The best preventive measure is the heating of suspect foods to boiling
temperatures for a few minutes, which is sufficient to destroy the neurotoxins.
Infant Botulism
First recognized as such in California in 1976, infant botulism has since been confirmed in most
states in the United States and in many other countries. In the adult form of botulism, preformed
toxins are ingested; in infant botulism, viable botulinal spores are ingested, and upon germination
in the intestinal tract, toxin is synthesized. Although it is possible that in some adults under special
conditions botulinal endospores may germinate and produce small quantities of toxin, the colonized
intestinal tract does not favor spore germination. Infants over one year of age tend not to be affected
by this syndrome because of the establishment of a more normal intestinal biota. The disease is mild
in some infants; in others, it can be severe. High numbers of spores are found in the feces of infants
during the acute phase of the disease, and as recovery progresses, the number of organisms abate.
Sixty-two outbreaks of botulism resulting from commercially canned foods were recorded for the
period 1899–1973,
74 with 41 prior to 1930. Between 1941 and 1982, 7 outbreaks occurred in the United
States involving commercially canned foods in metal containers, with 17 cases and 8 deaths.
89 Three
of these outbreaks were caused by type A and the remainder by type E. In five of the outbreaks, can
leakage or underprocessing occurred.
89 Canned mushrooms have been incriminated in several botulism
outbreaks. A study in 1973 and 1974 turned up 30 cans of mushrooms containing botulinal toxin (29
were type B). An additional 11 cans contained viable spores of C. botulinum without preformed
toxin.
74 The capacity of the commercial mushroom (Agaricus bisporus) to support the growth of
inoculated spores of C. botulinum was studied by Sugiyama and Yang.
119 Following inoculation of
various parts of mushrooms, they were sealed with plastic film and incubated. Toxin was detected
as early as 3–4 days later, when products were incubated at 20
◦ C. Although the plastic film used to
wrap the inoculated mushrooms allowed for gas exchange, the respiration of the fresh mushrooms
apparently consumed oxygen at a faster rate than it entered the film. No toxin was detected in products
stored at refrigerator temperatures.
An unusual outbreak of 36 cases occurred in 1985 with victims in three countries: Canada, the
Netherlands, and the United States. The vehicle food was chopped garlic in soybean oil that was
packaged in glass bottles. Although labeled with instructions to refrigerate, unopened bottles were
stored unrefrigerated for 8 months. The product was used to make garlic-buttered bread, which in
turn was used to prepare beef dip sandwiches. Proteolytic type B spores were found, and toxin was
produced within 2 weeks when proteolytic and nonproteolytic B strains were inoculated into bottles
of chopped garlic and held at 25
◦ C.
111 Type A toxin was produced in bottled chopped garlic in 20 days
at 35
◦ C when inoculated with 1 spore/g and by type B toxin in 20 days.
106 In the latter study, highly
toxic bottles looked and smelled acceptable. An outbreak of type E involving 91 cases with 20 deaths
occurred in Egypt in 1991, and the vehicle was an ungutted, salted raw fish product called faseikh.
84 In
1994, there were 30 victims in El Paso, Texas, after consuming potato-based dip and eggplant-based
dip, both of which contained baked potato. The baked potatoes were wrapped in aluminum foil and
held at room temperature for several days and, thus, they became toxigenic.
8 Although not common,
this is not the first time that botulinal toxin was detected in baked potatoes.
One of the recorded outbreaks of botulism (five cases with one death) due to type F involved
homemade liver paste. The U.S. outbreak occurred in 1966 from home-prepared venison jerky, with
three clinical cases.
82
The greatest hazards of botulism come from home-prepared and home-canned foods that are improperly handled or given insufficient heat treatments to destroy botulinal spores. Such foods are often
consumed without heating. The best preventive measure is the heating of suspect foods to boiling
temperatures for a few minutes, which is sufficient to destroy the neurotoxins.
Infant Botulism
First recognized as such in California in 1976, infant botulism has since been confirmed in most
states in the United States and in many other countries. In the adult form of botulism, preformed
toxins are ingested; in infant botulism, viable botulinal spores are ingested, and upon germination
in the intestinal tract, toxin is synthesized. Although it is possible that in some adults under special
conditions botulinal endospores may germinate and produce small quantities of toxin, the colonized
intestinal tract does not favor spore germination. Infants over one year of age tend not to be affected
by this syndrome because of the establishment of a more normal intestinal biota. The disease is mild
in some infants; in others, it can be severe. High numbers of spores are found in the feces of infants
during the acute phase of the disease, and as recovery progresses, the number of organisms abate.