Food Poisoning Caused by Gram-Positive Sporeforming Bacteria
581
activated. The high-molecular-weight complexes or the progenitor possess higher resistance to acid
and pepsin.
117 While the derivative toxin was rapidly inactivated, the progenitor was shown to be
resistant to rat intestinal juice in vitro. The progenitor was more stable in the stomachs of rats.
It appears that the nontoxic component of the progenitor provides protection to the toxin activity.
After botulinal toxins are absorbed into the blood stream, they enter the peripheral nervous system.
C. botulinum toxins consist of a series of seven related toxins with the major one having a molecular
weight of ca. 150,000. The toxin binds to presynaptic terminal membranes at nerve-muscle junctions
where the release of acetylcholine is blocked. This leads to flaccid paralysis, which is the basis of the
cosmetic uses of Botox. In contrast to the botulinum toxin, tetanus toxin blocks a nerve factor that
allows muscle relaxation and leads to spastic paralysis. Unlike the staphylococcal enterotoxins and
heat-stable toxins of other foodborne pathogens, the botulinal toxins are heat sensitive and may be
destroyed by heating at 80
◦ C (176
◦ F) for 10 minutes, or boiling temperatures for a few minutes.
The Adult Botulism Syndrome: Incidence and Vehicle Foods
Symptoms of botulism may develop anywhere between 12 and 72 hours after the ingestion of toxincontaining foods. Even longer incubation periods are not unknown. Symptoms consist of nausea,
vomiting, fatigue, dizziness, and headache; dryness of skin, mouth, and throat; constipation, lack of
fever, paralysis of muscles, double vision, and, finally, respiratory failure and death. The duration of
the illness is from 1 to 10 or more days, depending on host resistance and other factors. The mortality
rate varies between 30% and 65%, with the rate being generally lower in European countries than in
the United States. All symptoms are caused by the exotoxin, and treatment consists of administering
specific antisera as early as possible. Although it is assumed that the tasting of toxin-containing foods
allows for absorption from the oral cavity, Lamanna et al.
68 found that mice and monkeys are more
susceptible to the toxins when administered by stomach tube than by exposure to the mouth. The
botulinal toxins are neurotoxins and attach irreversibly to nerves. Early treatment by use of antisera
brightens the prognosis.
Prior to 1963, most cases of botulism in the United States in which the vehicle foods were identified
were traced to home-canned vegetables and were caused by types A and B toxins. In almost 70%
of the 640 cases reported for the period 1899–1967, the vehicle food was not identified. Among the
640 cases, 17.8% were associated with vegetables, 4.1% fruits, 3.6% fish, 2.2% condiments, 1.4%
meats and poultry, and 1.1% for all others. Reported foodborne cases in the United States for the
years 1977–1997 reveal that the largest number of cases occurred in 1977 in a restaurant in Pontiac,
Michigan, following consumption of a hot sauce prepared from home-canned jalape˜ no peppers. No
deaths occurred, and type B toxin was identified. Total cases from all sources in the United States rarely
exceed 50 per year, with the highest 10-year period being 1930–1939, when 384 cases were reported
from noncommercial foods. Between 1899 and 1963, 1561 cases were reported from noncommercial
foods, whereas 219 were reported from commercial foods between 1906 and 1963, with 24 in 1963
alone.
Of 404 verified cases of type E botulism through 1963, 304 or 75% occurred in Japan. No outbreak
of botulism was recorded in Japan prior to 1951. For the period May 1951 through January 1960, 166
cases were recorded, with 58 deaths for a mortality rate of 35%. Most of these outbreaks were traced
to a home-prepared food called izushi, a preserved food consisting of raw fish, vegetables, cooked
rice, malted rice (koji), and a small amount of salt and vinegar. This preparation is packed tightly in
a wooden tub equipped with a lid and held for 3 weeks or longer to permit lactic acid fermentation.
During this time, the Eh potential is lowered, thus allowing for the growth of anaerobes.
581
activated. The high-molecular-weight complexes or the progenitor possess higher resistance to acid
and pepsin.
117 While the derivative toxin was rapidly inactivated, the progenitor was shown to be
resistant to rat intestinal juice in vitro. The progenitor was more stable in the stomachs of rats.
It appears that the nontoxic component of the progenitor provides protection to the toxin activity.
After botulinal toxins are absorbed into the blood stream, they enter the peripheral nervous system.
C. botulinum toxins consist of a series of seven related toxins with the major one having a molecular
weight of ca. 150,000. The toxin binds to presynaptic terminal membranes at nerve-muscle junctions
where the release of acetylcholine is blocked. This leads to flaccid paralysis, which is the basis of the
cosmetic uses of Botox. In contrast to the botulinum toxin, tetanus toxin blocks a nerve factor that
allows muscle relaxation and leads to spastic paralysis. Unlike the staphylococcal enterotoxins and
heat-stable toxins of other foodborne pathogens, the botulinal toxins are heat sensitive and may be
destroyed by heating at 80
◦ C (176
◦ F) for 10 minutes, or boiling temperatures for a few minutes.
The Adult Botulism Syndrome: Incidence and Vehicle Foods
Symptoms of botulism may develop anywhere between 12 and 72 hours after the ingestion of toxincontaining foods. Even longer incubation periods are not unknown. Symptoms consist of nausea,
vomiting, fatigue, dizziness, and headache; dryness of skin, mouth, and throat; constipation, lack of
fever, paralysis of muscles, double vision, and, finally, respiratory failure and death. The duration of
the illness is from 1 to 10 or more days, depending on host resistance and other factors. The mortality
rate varies between 30% and 65%, with the rate being generally lower in European countries than in
the United States. All symptoms are caused by the exotoxin, and treatment consists of administering
specific antisera as early as possible. Although it is assumed that the tasting of toxin-containing foods
allows for absorption from the oral cavity, Lamanna et al.
68 found that mice and monkeys are more
susceptible to the toxins when administered by stomach tube than by exposure to the mouth. The
botulinal toxins are neurotoxins and attach irreversibly to nerves. Early treatment by use of antisera
brightens the prognosis.
Prior to 1963, most cases of botulism in the United States in which the vehicle foods were identified
were traced to home-canned vegetables and were caused by types A and B toxins. In almost 70%
of the 640 cases reported for the period 1899–1967, the vehicle food was not identified. Among the
640 cases, 17.8% were associated with vegetables, 4.1% fruits, 3.6% fish, 2.2% condiments, 1.4%
meats and poultry, and 1.1% for all others. Reported foodborne cases in the United States for the
years 1977–1997 reveal that the largest number of cases occurred in 1977 in a restaurant in Pontiac,
Michigan, following consumption of a hot sauce prepared from home-canned jalape˜ no peppers. No
deaths occurred, and type B toxin was identified. Total cases from all sources in the United States rarely
exceed 50 per year, with the highest 10-year period being 1930–1939, when 384 cases were reported
from noncommercial foods. Between 1899 and 1963, 1561 cases were reported from noncommercial
foods, whereas 219 were reported from commercial foods between 1906 and 1963, with 24 in 1963
alone.
Of 404 verified cases of type E botulism through 1963, 304 or 75% occurred in Japan. No outbreak
of botulism was recorded in Japan prior to 1951. For the period May 1951 through January 1960, 166
cases were recorded, with 58 deaths for a mortality rate of 35%. Most of these outbreaks were traced
to a home-prepared food called izushi, a preserved food consisting of raw fish, vegetables, cooked
rice, malted rice (koji), and a small amount of salt and vinegar. This preparation is packed tightly in
a wooden tub equipped with a lid and held for 3 weeks or longer to permit lactic acid fermentation.
During this time, the Eh potential is lowered, thus allowing for the growth of anaerobes.