BoNT, an exo-neurotoxin produced by the bacteria Clostridium botulinum, is the cause of the uncommon but potentially fatal disease of widespread, flaccid paralysis known as botulism.
Numerous additional botulism etiologies, such as wound botulism, inhalational botulism, and iatrogenic botulism have been described since the disease was first identified as a foodborne phenomenon in Belgium and Germany there in the 1800s.
Botulism can be treated with weeks of mechanical breathing and some other resource-intensive therapy until the body’s neuromuscular signaling mechanisms heal, even though the administration of polyvalent antitoxin to botulinum neurotoxin slows down the disease’s clinical progression.
The world’s military organizations are very interested in botulinum neurotoxin since it is the most lethal poison currently in use and is very easy to create, store, and distribute.
Epidemiology
The National Botulism Surveillance System was created by the Centers for Disease Control and Prevention (CDC) in 1973 to track botulism cases across the country. An average of 162 cases of botulism per year were reported in the five years between 2011 and 2015.
The proportions of each form of botulism varied from seventy-one to eighty-eight percent in cases of newborn botulism, one to 20 percent in cases of foodborne botulism, five to ten percent in cases of wound botulism, and one to four percent in cases of botulism of other or unknown origin.
The overall number of botulism cases and the proportional shares of each subgroup have largely remained constant for the past ten years, with the exception of sporadic, significant outbreaks (for example, a foodborne botulism outbreak across Ohio in April 2015 that resulted in 27 instances alone).
There has only ever been one incidence of iatrogenic botulism throughout the U.s, which was brought on by the use of an illegal, heavily contaminated type of BoNT; there were no recorded cases of botulism caused by bioterrorism.
Botulism has a low mortality rate. Even before the 1950s, sixty to seventy percent of cases of foodborne botulism resulted in death. Between 1975 and 2009, there were 3,618 cases of botulism, 109 deaths, and an overall fatality rate of 3.0 percent.
A total of 2352 infant botulism incidents resulted in 18 [below 1 percent] fatalities, 854 incidents resulted in 61 [7.1 percent] deaths, 359 incidents resulted in 18 [5.0 percent] deaths, and 53 incidents resulted in 12 [22.6 percent] deaths.
Anatomy
Pathophysiology
One 150 kDa protein known as botox neurotoxin has a 50 kDa light strand and then a 100 kDa heavy string that is joined by something like a singular disulfide bond. Depending on identification via polyclonal serum, BoNT can be divided into eight different serotypes, numbered A (BoNT/A) across H (BoNT/H). Human disease is caused by toxin subtypes A, B, E, and sporadically F, G, and H. BoNT/A and BoNT/B are to blame for the extreme case that is recorded across the Us.
Dual toxin-producing C. botulinum strains have been discovered, albeit the majority of strains only produce one toxin serotype. The most potent toxin is type A, followed by type B by BoNT. Depending on the sort of exposure, the poison enters the bloodstream through a different route. In newborn botulism, a weak immune system enables the spread of toxin-producing C. botulinum cultures in the bronchioles or digestive tract after spore inhalation or ingestion.
When BoNT is released, it crosses the mucosal barrier (either the pulmonary or intestinal epithelium) through transcytosis and enters the bloodstream. Food-borne botulinum, which is absorbed in the digestive tract identical to newborn botulism, is caused by ingesting produced toxins in inadequately stored food.
The most prevalent cause of subcutaneous injection of spore-contaminated illicit substances is wound botulism, which is caused by C. botulinum spores’ maturation in damaged tissue tissues and the discharge of BoNT into surrounding circulation. After entering the bloodstream, BoNT goes to the spontaneous motor as well as autonomic Neuromuscular junctions and attaches to their presynaptic nerve endings.
The toxin’s heavy chain moiety stimulates endocytosis, which is followed by the release of the light chain into the cytosol. The SNARE (SNAP-25, syntaxin, or VAMP) polypeptide combination, which is necessary for the union of acetylcholine-containing vesicles with the presynaptic terminal, has serotype-specific receptors that the light chain seeks out and split.
Fusion enables postsynaptic membrane depolarization and acetylcholine exocytosis at the NMJ. BoNT causes flaccid paralysis by separating all those fusion structures, which limits muscular contraction and prevents presynaptic acetylcholine discharge. All BoNT serogroups exhibit the downstream side effect of flaccid paralysis due to a lack of acetylcholine production at the neuromuscular junctions, irrespective of serotype-specific variations in target locations.
Etiology
The gram-positive, spore-forming, obligatory anaerobic bacterium Clostridium botulinum, rod-shaped, produces an Exo neurotoxin, which has systemic effects and causes the neuroparalytic condition known as botulism. The toxin is also occasionally produced by other Clostridium species, including Clostridium butyricum and Clostridium baratii.
A heterogeneous and widespread class of bacteria known as C. botulinum is typically split into four categories (categories I, II, III, or IV) depending on physiologic traits. Soil, shellfish, marine sediment, vegetables, and fruits can all be quickly and readily isolated from C. botulinum.
In anaerobic, substrate-rich circumstances, it produces heat-resistant pollen that germinates to become bacilli that produce toxins. Due to its great potency and toxicity, botox neurotoxin is regarded as the most lethal toxin now in use. Its fatal dose (LD50) ranges from 1 to 3 ng (nanograms) of toxin per kilogram (kg) of body mass, making it the deadliest toxin currently in use.
The permanent suppression of acetylcholine release at the presynaptic nerve ending of the body’s NMJs causes flaccid paralysis associated with botulism. In addition to systemic release of the toxin in vivo, as in the cases of baby and wound botulism, botulism can be contracted from exposure to the pre-formed toxin through incorrectly food stored, bioterrorism, or iatrogenic injection.
(in infants is caused by either toxin type A or type B):
Below 1 yr: 100 mg/kg Intravenous infusion; give at 25 mg/kg/hr over first 15 mins; when well tolerated, gradually increase to 50 mg/kg/hr.
Above 1 yr: not indicated
The reconstituted product has at least 15 IU/mL of antibodies against the type A botulinum toxins and at least 2.7 IU/mL of antibodies against type B toxins.
Dose Adjustments
Renal Impairment
Reduce the rate and concentration of infusion.
Local epidemiology divisions can be consulted
BabyBIG (protects against both forms of botulism toxin) can be obtained by calling the California Infant Botulism Programme.
Type F child botulism has been treated using heptavalent botulinum antitoxin. Future instances of newborn botulism may also be treated with it on a case-by-case basis.
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Media Gallary
References
https://www.ncbi.nlm.nih.gov/books/NBK459273/
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BoNT, an exo-neurotoxin produced by the bacteria Clostridium botulinum, is the cause of the uncommon but potentially fatal disease of widespread, flaccid paralysis known as botulism.
Numerous additional botulism etiologies, such as wound botulism, inhalational botulism, and iatrogenic botulism have been described since the disease was first identified as a foodborne phenomenon in Belgium and Germany there in the 1800s.
Botulism can be treated with weeks of mechanical breathing and some other resource-intensive therapy until the body’s neuromuscular signaling mechanisms heal, even though the administration of polyvalent antitoxin to botulinum neurotoxin slows down the disease’s clinical progression.
The world’s military organizations are very interested in botulinum neurotoxin since it is the most lethal poison currently in use and is very easy to create, store, and distribute.
The National Botulism Surveillance System was created by the Centers for Disease Control and Prevention (CDC) in 1973 to track botulism cases across the country. An average of 162 cases of botulism per year were reported in the five years between 2011 and 2015.
The proportions of each form of botulism varied from seventy-one to eighty-eight percent in cases of newborn botulism, one to 20 percent in cases of foodborne botulism, five to ten percent in cases of wound botulism, and one to four percent in cases of botulism of other or unknown origin.
The overall number of botulism cases and the proportional shares of each subgroup have largely remained constant for the past ten years, with the exception of sporadic, significant outbreaks (for example, a foodborne botulism outbreak across Ohio in April 2015 that resulted in 27 instances alone).
There has only ever been one incidence of iatrogenic botulism throughout the U.s, which was brought on by the use of an illegal, heavily contaminated type of BoNT; there were no recorded cases of botulism caused by bioterrorism.
Botulism has a low mortality rate. Even before the 1950s, sixty to seventy percent of cases of foodborne botulism resulted in death. Between 1975 and 2009, there were 3,618 cases of botulism, 109 deaths, and an overall fatality rate of 3.0 percent.
A total of 2352 infant botulism incidents resulted in 18 [below 1 percent] fatalities, 854 incidents resulted in 61 [7.1 percent] deaths, 359 incidents resulted in 18 [5.0 percent] deaths, and 53 incidents resulted in 12 [22.6 percent] deaths.
One 150 kDa protein known as botox neurotoxin has a 50 kDa light strand and then a 100 kDa heavy string that is joined by something like a singular disulfide bond. Depending on identification via polyclonal serum, BoNT can be divided into eight different serotypes, numbered A (BoNT/A) across H (BoNT/H). Human disease is caused by toxin subtypes A, B, E, and sporadically F, G, and H. BoNT/A and BoNT/B are to blame for the extreme case that is recorded across the Us.
Dual toxin-producing C. botulinum strains have been discovered, albeit the majority of strains only produce one toxin serotype. The most potent toxin is type A, followed by type B by BoNT. Depending on the sort of exposure, the poison enters the bloodstream through a different route. In newborn botulism, a weak immune system enables the spread of toxin-producing C. botulinum cultures in the bronchioles or digestive tract after spore inhalation or ingestion.
When BoNT is released, it crosses the mucosal barrier (either the pulmonary or intestinal epithelium) through transcytosis and enters the bloodstream. Food-borne botulinum, which is absorbed in the digestive tract identical to newborn botulism, is caused by ingesting produced toxins in inadequately stored food.
The most prevalent cause of subcutaneous injection of spore-contaminated illicit substances is wound botulism, which is caused by C. botulinum spores’ maturation in damaged tissue tissues and the discharge of BoNT into surrounding circulation. After entering the bloodstream, BoNT goes to the spontaneous motor as well as autonomic Neuromuscular junctions and attaches to their presynaptic nerve endings.
The toxin’s heavy chain moiety stimulates endocytosis, which is followed by the release of the light chain into the cytosol. The SNARE (SNAP-25, syntaxin, or VAMP) polypeptide combination, which is necessary for the union of acetylcholine-containing vesicles with the presynaptic terminal, has serotype-specific receptors that the light chain seeks out and split.
Fusion enables postsynaptic membrane depolarization and acetylcholine exocytosis at the NMJ. BoNT causes flaccid paralysis by separating all those fusion structures, which limits muscular contraction and prevents presynaptic acetylcholine discharge. All BoNT serogroups exhibit the downstream side effect of flaccid paralysis due to a lack of acetylcholine production at the neuromuscular junctions, irrespective of serotype-specific variations in target locations.
The gram-positive, spore-forming, obligatory anaerobic bacterium Clostridium botulinum, rod-shaped, produces an Exo neurotoxin, which has systemic effects and causes the neuroparalytic condition known as botulism. The toxin is also occasionally produced by other Clostridium species, including Clostridium butyricum and Clostridium baratii.
A heterogeneous and widespread class of bacteria known as C. botulinum is typically split into four categories (categories I, II, III, or IV) depending on physiologic traits. Soil, shellfish, marine sediment, vegetables, and fruits can all be quickly and readily isolated from C. botulinum.
In anaerobic, substrate-rich circumstances, it produces heat-resistant pollen that germinates to become bacilli that produce toxins. Due to its great potency and toxicity, botox neurotoxin is regarded as the most lethal toxin now in use. Its fatal dose (LD50) ranges from 1 to 3 ng (nanograms) of toxin per kilogram (kg) of body mass, making it the deadliest toxin currently in use.
The permanent suppression of acetylcholine release at the presynaptic nerve ending of the body’s NMJs causes flaccid paralysis associated with botulism. In addition to systemic release of the toxin in vivo, as in the cases of baby and wound botulism, botulism can be contracted from exposure to the pre-formed toxin through incorrectly food stored, bioterrorism, or iatrogenic injection.
(in infants is caused by either toxin type A or type B):
Below 1 yr: 100 mg/kg Intravenous infusion; give at 25 mg/kg/hr over first 15 mins; when well tolerated, gradually increase to 50 mg/kg/hr.
Above 1 yr: not indicated
The reconstituted product has at least 15 IU/mL of antibodies against the type A botulinum toxins and at least 2.7 IU/mL of antibodies against type B toxins.
Dose Adjustments
Renal Impairment
Reduce the rate and concentration of infusion.
Local epidemiology divisions can be consulted
BabyBIG (protects against both forms of botulism toxin) can be obtained by calling the California Infant Botulism Programme.
Type F child botulism has been treated using heptavalent botulinum antitoxin. Future instances of newborn botulism may also be treated with it on a case-by-case basis.
https://www.ncbi.nlm.nih.gov/books/NBK459273/
medtigo
Botulism
Updated :
August 22, 2023
BoNT, an exo-neurotoxin produced by the bacteria Clostridium botulinum, is the cause of the uncommon but potentially fatal disease of widespread, flaccid paralysis known as botulism.
Numerous additional botulism etiologies, such as wound botulism, inhalational botulism, and iatrogenic botulism have been described since the disease was first identified as a foodborne phenomenon in Belgium and Germany there in the 1800s.
Botulism can be treated with weeks of mechanical breathing and some other resource-intensive therapy until the body’s neuromuscular signaling mechanisms heal, even though the administration of polyvalent antitoxin to botulinum neurotoxin slows down the disease’s clinical progression.
The world’s military organizations are very interested in botulinum neurotoxin since it is the most lethal poison currently in use and is very easy to create, store, and distribute.
The National Botulism Surveillance System was created by the Centers for Disease Control and Prevention (CDC) in 1973 to track botulism cases across the country. An average of 162 cases of botulism per year were reported in the five years between 2011 and 2015.
The proportions of each form of botulism varied from seventy-one to eighty-eight percent in cases of newborn botulism, one to 20 percent in cases of foodborne botulism, five to ten percent in cases of wound botulism, and one to four percent in cases of botulism of other or unknown origin.
The overall number of botulism cases and the proportional shares of each subgroup have largely remained constant for the past ten years, with the exception of sporadic, significant outbreaks (for example, a foodborne botulism outbreak across Ohio in April 2015 that resulted in 27 instances alone).
There has only ever been one incidence of iatrogenic botulism throughout the U.s, which was brought on by the use of an illegal, heavily contaminated type of BoNT; there were no recorded cases of botulism caused by bioterrorism.
Botulism has a low mortality rate. Even before the 1950s, sixty to seventy percent of cases of foodborne botulism resulted in death. Between 1975 and 2009, there were 3,618 cases of botulism, 109 deaths, and an overall fatality rate of 3.0 percent.
A total of 2352 infant botulism incidents resulted in 18 [below 1 percent] fatalities, 854 incidents resulted in 61 [7.1 percent] deaths, 359 incidents resulted in 18 [5.0 percent] deaths, and 53 incidents resulted in 12 [22.6 percent] deaths.
One 150 kDa protein known as botox neurotoxin has a 50 kDa light strand and then a 100 kDa heavy string that is joined by something like a singular disulfide bond. Depending on identification via polyclonal serum, BoNT can be divided into eight different serotypes, numbered A (BoNT/A) across H (BoNT/H). Human disease is caused by toxin subtypes A, B, E, and sporadically F, G, and H. BoNT/A and BoNT/B are to blame for the extreme case that is recorded across the Us.
Dual toxin-producing C. botulinum strains have been discovered, albeit the majority of strains only produce one toxin serotype. The most potent toxin is type A, followed by type B by BoNT. Depending on the sort of exposure, the poison enters the bloodstream through a different route. In newborn botulism, a weak immune system enables the spread of toxin-producing C. botulinum cultures in the bronchioles or digestive tract after spore inhalation or ingestion.
When BoNT is released, it crosses the mucosal barrier (either the pulmonary or intestinal epithelium) through transcytosis and enters the bloodstream. Food-borne botulinum, which is absorbed in the digestive tract identical to newborn botulism, is caused by ingesting produced toxins in inadequately stored food.
The most prevalent cause of subcutaneous injection of spore-contaminated illicit substances is wound botulism, which is caused by C. botulinum spores’ maturation in damaged tissue tissues and the discharge of BoNT into surrounding circulation. After entering the bloodstream, BoNT goes to the spontaneous motor as well as autonomic Neuromuscular junctions and attaches to their presynaptic nerve endings.
The toxin’s heavy chain moiety stimulates endocytosis, which is followed by the release of the light chain into the cytosol. The SNARE (SNAP-25, syntaxin, or VAMP) polypeptide combination, which is necessary for the union of acetylcholine-containing vesicles with the presynaptic terminal, has serotype-specific receptors that the light chain seeks out and split.
Fusion enables postsynaptic membrane depolarization and acetylcholine exocytosis at the NMJ. BoNT causes flaccid paralysis by separating all those fusion structures, which limits muscular contraction and prevents presynaptic acetylcholine discharge. All BoNT serogroups exhibit the downstream side effect of flaccid paralysis due to a lack of acetylcholine production at the neuromuscular junctions, irrespective of serotype-specific variations in target locations.
The gram-positive, spore-forming, obligatory anaerobic bacterium Clostridium botulinum, rod-shaped, produces an Exo neurotoxin, which has systemic effects and causes the neuroparalytic condition known as botulism. The toxin is also occasionally produced by other Clostridium species, including Clostridium butyricum and Clostridium baratii.
A heterogeneous and widespread class of bacteria known as C. botulinum is typically split into four categories (categories I, II, III, or IV) depending on physiologic traits. Soil, shellfish, marine sediment, vegetables, and fruits can all be quickly and readily isolated from C. botulinum.
In anaerobic, substrate-rich circumstances, it produces heat-resistant pollen that germinates to become bacilli that produce toxins. Due to its great potency and toxicity, botox neurotoxin is regarded as the most lethal toxin now in use. Its fatal dose (LD50) ranges from 1 to 3 ng (nanograms) of toxin per kilogram (kg) of body mass, making it the deadliest toxin currently in use.
The permanent suppression of acetylcholine release at the presynaptic nerve ending of the body’s NMJs causes flaccid paralysis associated with botulism. In addition to systemic release of the toxin in vivo, as in the cases of baby and wound botulism, botulism can be contracted from exposure to the pre-formed toxin through incorrectly food stored, bioterrorism, or iatrogenic injection.
https://www.ncbi.nlm.nih.gov/books/NBK459273/
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