Instruct: Given a question, retrieve documents that can help answer the question.
Query: Does Botulinum toxin cause botulism?
Botulism is a rare and potentially fatal illness caused by a toxin produced by the bacterium Clostridium botulinum.[1] The disease begins with weakness, blurred vision, feeling tired, and trouble speaking.[1] This may then be followed by weakness of the arms, chest muscles, and legs.[1] Vomiting, swelling of the abdomen, and diarrhea may also occur.[1] The disease does not usually affect consciousness or cause a fever.[1]
Botulism is a rare disease caused by "Clostridium botulinum" bacteria. A small number of the bacteria can cause severe poisoning leading to respiratory and muscular problems in adults. In infants, the toxin also affects the intestinal system.
Foodborne botulism
"Signs and symptoms of foodborne botulism typically begin between 18 and 36 hours after the toxin gets into your body, but can range from a few hours to several days, depending on the amount of toxin ingested."Wound botulism
Most people who develop wound botulism inject drugs several times a day, so it's difficult to determine how long it takes for signs and symptoms to develop after the toxin enters the body. Most common in people who inject black tar heroin, wound botulism signs and symptoms include:Infant botulism
If infant botulism is related to food, such as honey, problems generally begin within 18 to 36 hours after the toxin enters the baby's body. Signs and symptoms include:Beneficial effects of botulinum toxin:
Purified botulinum toxin is diluted by a physician for treatment:
The spores require warm temperatures, a protein source, an anaerobic environment, and moisture in order to become active and produce toxin. In the wild, decomposing vegetation and invertebrates combined with warm temperatures can provide ideal conditions for the botulism bacteria to activate and produce toxin that may affect feeding birds and other animals. Spores are not killed by boiling, but botulism is uncommon because special, rarely obtained conditions are necessary for botulinum toxin production from C. botulinum spores, including an anaerobic, low-salt, low-acid, low-sugar environment at ambient temperatures.[24]
Foodborne Botulism: serum analysis for toxins by bioassay in mice should be done, as the demonstration of the toxins is diagnostic.
Only botulinum toxin types A, B, E, F and H cause disease in humans. Types A, B, and E are associated with food-borne illness, with type E specifically associated with fish products. Type C produces limber-neck in birds and type D causes botulism in other mammals. No disease is associated with type G. The "gold standard" for determining toxin type is a mouse bioassay, but the genes for types A, B, E, and F can now be readily differentiated using quantitative PCR. As no antitoxin to type H is yet available, discovered in 2013 and by far the deadliest, details are kept under shroud.
Botulinum toxin produced by Clostridium botulinum is the cause of botulism.[9] Humans most commonly ingest the toxin from eating improperly-canned foods in which C. botulinum has grown. However, the toxin can also be introduced through an infected wound. In infants, the bacteria can sometimes grow in the intestines and produce botulinum toxin within the intestine and can cause a condition known as floppy baby syndrome.[33] In all cases, the toxin can then spread, blocking nerves and muscle function. In severe cases, the toxin can block nerves controlling the respiratory system or heart, resulting in death.[1] Botulism can be difficult to diagnose, as it may appear similar to diseases such as Guillain–Barré syndrome, myasthenia gravis, and stroke. Other tests, such as brain scan and spinal fluid examination, may help to rule out other causes. If the symptoms of botulism are diagnosed early, various treatments can be administered. In an effort to remove contaminated food which remains in the gut, enemas or induced vomiting may be used.[34] For wound infections, infected material may be removed surgically.[34] Botulinum antitoxin is available and may be used to prevent the worsening of symptoms, though it will not reverse existing nerve damage. In severe cases, mechanical respiration may be used to support patients suffering from respiratory failure.[34] The nerve damage heals over time, generally over weeks to months.[4] With proper treatment, the case fatality rate for botulinum poisoning can be greatly reduced.[34]
In all cases, illness is caused by the botulinum toxin produced by the bacterium C. botulinum in anaerobic conditions and not by the bacterium itself. The pattern of damage occurs because the toxin affects nerves that fire (depolarize) at a higher frequency first.[16]
The "Clostridium botulinum" bacteria are the cause of botulism. Vegetative cells of "C. botulinum" may be ingested. Introduction of the bacteria may also occur via endospores in a wound. When the bacteria are in vivo, they induce flaccid paralysis. This happens because "C. botulinum" produces a toxin which blocks the release of acetylcholine. Botulism toxin blocks the exocytosis of presynaptic vesicles containing acetylcholine (ACh). When this occurs, the muscles are unable to contract. Other symptoms associated with infection from this neurotoxin include double vision, blurred vision, drooping eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness. Botulism prevents muscle contraction by blocking the release of acetylcholine, thereby halting postsynaptic activity of the neuromuscular junction. If its effects reach the respiratory muscles, then it can cause respiratory failure, leading to death.
Botulinum toxin is broken into 8 neurotoxins (labeled as types A, B, C [C1, C2], D, E, F, and G), which are antigenically and serologically distinct but structurally similar. Human botulism is caused mainly by types A, B, E, and (rarely) F. Types C and D cause toxicity only in other animals.[20]
The toxin is the protein botulinum toxin produced under anaerobic conditions (where there is no oxygen) by the bacterium Clostridium botulinum.
The effects of botulinum toxin are different from those of nerve agents involved insofar in that botulism symptoms develop relatively slowly (over several days), while nerve agent effects are generally much more rapid and can be instantaneous. Evidence suggests that nerve exposure (simulated by injection of atropine and pralidoxime) will increase mortality by enhancing botulinum toxin's mechanism of toxicity.
Food-borne botulism results, indirectly, from ingestion of food contaminated with Clostridium spores, where exposure to an anaerobic environment allows the spores to germinate, after which the bacteria can multiply and produce toxin. Critically, it is ingestion of toxin rather than spores or vegetative bacteria that causes botulism. Botulism is nevertheless known to be transmitted through canned foods not cooked correctly before canning or after can opening, and so is preventable. Infant botulism cases arise chiefly as a result of environmental exposure and are therefore more difficult to prevent. Infant botulism arising from consumption of honey can be prevented by eliminating honey from diets of children less than 12 months old.[72]
The Botulism Antitoxin Heptavalent (A, B, C, D, E, F, G) - (Equine) (BAT) – BAT, made by Emergent BioSolutions Canada Inc. (formerly Cangene Corporation), – is a licensed, commercially available botulism anti-toxin that effectively neutralizes all seven known botulinum nerve toxin serotypes (types A, B, C, D, E, F and G). It is indicated for sporadic cases of life-threatening botulism and is also stockpiled for the eventuality of botulinum nerve toxins being used in a future bioterrorist attack.
In 1895 (seventy-five years later), Émile van Ermengem, professor of bacteriology and a student of Robert Koch, correctly described Clostridium botulinum as the bacterial source of the toxin. Thirty-four attendees at a funeral were poisoned by eating partially salted ham, an extract of which was found to cause botulism-like paralysis in laboratory animals. Van Ermengem isolated and grew the bacterium, and described its toxin,[41] which was later purified by P Tessmer Snipe and Hermann Sommer.[42]
A few strains from organisms genetically identified as other "Clostridium" species have caused human botulism: "C. butyricum" has produced type E toxin and "C. baratii" had produced type F toxin. The ability of "C. botulinum" to naturally transfer neurotoxin genes to other clostridia is concerning, especially in the food industry, where preservation systems are designed to destroy or inhibit only "C. botulinum" but not other "Clostridium" species.
The seven toxin types (A-G) have different tertiary structures and sequence differences.[36][37] While the different toxin types all target members of the SNARE family, different toxin types target different SNARE family members.[35] The A, B, and E serotypes cause human botulism, with the activities of types A and B enduring longest in vivo (from several weeks to months).[36]
The growth of the spores releases botulinum toxin, which is then absorbed into the bloodstream and taken throughout the body, causing paralysis by blocking the release of acetylcholine at the neuromuscular junction. Typical symptoms of infant botulism include constipation, lethargy, weakness, difficulty feeding and an altered cry, often progressing to a complete descending flaccid paralysis. Although constipation is usually the first symptom of infant botulism, it is commonly overlooked.[10]
Most strains produce one type of neurotoxin, but strains producing multiple toxins have been described. "C. botulinum" producing B and F toxin types have been isolated from human botulism cases in New Mexico and California. The toxin type has been designated Bf as the type B toxin was found in excess to the type F. Similarly, strains producing Ab and Af toxins have been reported. Evidence indicates the neurotoxin genes have been the subject of horizontal gene transfer, possibly from a viral source. This theory is supported by the presence of integration sites flanking the toxin in some strains of "C. botulinum". However, these integrations sites are degraded, indicating that the "C. botulinum" acquired the toxin genes quite far in the evolutionary past.
Toxoids are used as vaccines because they induce an immune response to the original toxin or increase the response to another antigen since the toxoid markers and toxin markers are preserved. For example, the tetanus toxoid is derived from the tetanospasmin produced by "Clostridium tetani". The latter causes tetanus and is vaccinated against by the DTaP vaccine. Botulin is produced by "Clostridium botulinum" and causes the deadly disease botulism. While patients may sometimes complain of side effects after a vaccine, these are associated with the process of mounting an immune response and clearing the toxoid, not the direct effects of the toxoid. The toxoid does not have virulence as the toxin did before inactivation.
"Clostridium botulinum" is a soil-borne bacterium, which may be better known for producing clinical signs of botulism. It may cause grass sickness when the spores of "C. botulinum" type C are ingested and produce their toxin locally within the intestine.
Foodborne botulism results from contaminated foodstuffs in which "C. botulinum" spores have been allowed to germinate and produce botulism toxin, and this typically occurs in canned non-acidic food substances that have not received a strong enough thermal heat treatment. "C. botulinum" prefers low oxygen environments and is a poor competitor to other bacteria, but its spores are resistant to thermal treatments. When a canned food is sterilized insufficiently, most other bacteria besides the "C. botulinum" spores are killed, and the spores can germinate and produce botulism toxin. Botulism is a rare but serious paralytic illness, leading to paralysis that typically starts with the muscles of the face and then spreads towards the limbs. The botulinum toxin is extremely dangerous because it cannot be detected by sight or smell, and ingestion of even a small amount of the toxin can be deadly. In severe forms, it leads to paralysis of the breathing muscles and causes respiratory failure. In view of this life-threatening complication, all suspected cases of botulism are treated as medical emergencies, and public health officials are usually involved to prevent further cases from the same source.
"HBAT" is the only product available for treating botulism in adults, and for botulism in infants caused by botulinum toxins other than types A and B. "HBAT" has been used to treat a case of type F infant botulism and, on a case-by-case basis, may be used for future cases of non-type A and non-type B infant botulism.
Two preparations of botulinum antitoxins are available for treatment of botulism. Trivalent (A,B,E) botulinum antitoxin is derived from equine sources using whole antibodies. The second antitoxin is Heptavalent (A,B,C,D,E,F,G) botulinum antitoxin, which is derived from equine antibodies which have been altered to make them less immunogenic. This antitoxin is effective against all known strains of botulism.
Botulinum toxin (BTX) is a neurotoxic protein produced by the bacterium Clostridium botulinum and related species.[1] It prevents the release of the neurotransmitter acetylcholine from axon endings at the neuromuscular junction and thus causes flaccid paralysis. Infection with the bacterium causes the disease botulism. The toxin is also used commercially in medicine, cosmetics and research.