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Botulism is a rare gastrointestinal infection, it is a serious condition caused by toxins from bacteria called Clostridium Botulinum. Clostridium Botulinum are a species of anaerobic, gram-positive, rod shaped bacteria in the family Clostridiaceae that produces proteins with characteristics neurotoxicity. The botulinum toxin is a potent neurotoxin that impairs nerve function, including those of the diaphragm, leading to paralysis. It is the etiologic agent of botulism in humans, wild fowl, horses and cattle. There are seven subtypes of these bacteria, each producing a different Botulinum Toxin. The organism and its spores are widely distributed in nature. They can be found in soil, sediments of streams and lakes, and in the intestinal tracts of fish and mammals.
Clostridium botulinum interferes with the presynaptic release of acetylcholine at the neuromuscular junction. Acetylcholine is a neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, and at many other sites in the CNS. Acetylcholine enables muscle contraction therefore without it muscles will not contract. The diaphragm enables breathing hence without acetylcholine the infected animal will die of respiratory failure and asphyxia. Clinical features include abdominal pain, vomiting, acute paralysis, blurred vision, and diplopia. There are eight types of botulism. They are: A, B, CÎ±, CÎ², D, E, F, and G. Out of the eight only three of them are associated with human disease. They are A, B, E and F. A, and B are foodborne related potent strains.
It was first recorded in Europe in 1735 and it was suspected of being associated with a German sausage, hence being named after the Latin word for sausage, "botulus". Several nations produced botulism toxins in the WWII as a potential bacteriological weapon. They were said to have test sprayed over a section of Canadian wilderness killing all animals within 6 hours but they were never used in combat. The bacteria itself is not toxic when ingested and are commonly consumed on fruits, vegetables and seafood. The German physician and poet Justinus Kerner first developed the idea of a possible therapeutic use of botulinum toxin. In 1870, another German physician, Muller, coined the name botulism. In 1895, Professor Emile Van Ermengem, of Belgium, was the first to isolate the bacterium. In 1928, Dr Herman Sommer, at the University of California, was the first to isolate in purified form the toxin type A (BoNT-A) as a stable acid precipitate. Dr Edward J Schantz succeeded in purifying BoNT-A in crystalline form-cultured C blotulinum and isolated the toxin in 1946. In the 1950's, Dr Burgen's ASV group discovered that blotulinum toxins blocks neuromuscular transmission in 1949. Dr Vermon Brooks discovered that when BoNT-A is injected into a hyperactive muscle, it blocks the release of acetycholine from motor nerve endings. Dr Alan B Scott, of Smith-Kettlewell Eye Research Institute used BoNT-A in monkey experiments in 1973, and in 1980 he used if for the first time in humans to treat strabismus.
The incubation period of botulism is 12-80 hours. It can be obtained through inhalation of toxin, consumption of toxin or C botulinum spores, and contamination of a tissue with toxin or C botulinum spores. Signs and symptoms have six presentations. The cardinal signs include afebrile (having no fever); symmetrical neurological manisfestations; normal mental status, though may appear lethargic and have difficulty with communication; normal to slow heart rate without presence of hypotension; and normal sensory nerve function, other than vision. The early presentations include: cranial abnormalities, fatigue and vertigo, double and blurred vision, and difficulty swallowing food. The later presentation include; descending paralysis, difficulty moving eyes and mild pupillary dilation, tongue weakness, decrease gag reflex, indistinct speech, symmetrical descending progressive muscular weakness especially on arms and legs, extreme weakness on postural neck muscles and occasional mouth breathing, and constipation. Ingestional presentation include: dry mouth and dysarthria, and nausea and vomiting. Inhalational presentation include: mucus in throat, and serous nasal discharge, salivation. Lastly the infant presentation include: inability to suck and swallow, constipation, weakened voice and floppy neck.
There are five main kinds of botulism. They are foodborne botulism, wound botulism, infant botulism, adult intestinal toxaemia botulism, and iatrogenic botulism. Even though botulism bacteria are common in nature, they can be killed by oxygen. Thereof, the bacteria form spores that protect them from the oxygen. Once on an oxygen-free environment the spores activate. The most common way to get botulism is from improperly canned food. When the can is sealed it creates an oxygen-free environment suitable for the bacteria. If heated properly the spores dies but if not heated properly, the spores activate and the can is filled with toxin, botulin. Since botulin is a protein it can be denatured by heat, however canned food is mostly eaten cold botulism occurs. Affected individuals have difficulty swallowing or speaking, dry mouth, facial weakness on both sides of the face, blurred or double vision, drooping eyelids, trouble breathing, nausea, vomiting and abdominal cramps, and paralysis.
Babies normally obtain botulism from honey in a variety of ways. When collecting nectar from flowers, bees collect botulism spores and mix them into the honey. Most adults can eat these spores without difficulty since the bacteria within the body robust the immune system which eliminates the spores. Since infants still do not have these bacterial defences the spores come to life when they reach the intestine oxygen-free environment. While inside of the baby they produce toxin. This typically occurs between the ages of 2 and 6 months. Complications arise normally within 18 to 36 hours after the toxin enters the baby's body. Signs and symptoms include: constipation, floppy movements due to muscle weakness and trouble controlling head, weak cry, irritability, drooling, drooping eyelids, tiredness, difficulty sucking or feeding, and paralysis.
Wound botulism is the result of wounds contaminated with C botulinum spores. It develops traumatic injury that involves soil contamination among injection drug users (those who use black-tar heroin) and after a caesarean delivery. The wound may appear benign. The involved tissues which are traumatized and devitalized provide a perfect anaerobic medium for the C botulinum spores to germinate into vegetative organisms and produce neurotoxins. The symptoms usually appear 4 to 18 hours after an injury occurs and are similar to food-borne botulism although gastrointestinal symptoms may be absent. They include: difficulty swallowing or speaking, facial weakness on both sides of the face, blurred or double vision, drooping eyelids, trouble breathing, and paralysis.
Adult intestinal toxaemia (adult intestinal colonization) botulism is a very rare kind of botulism that occurs among adults by the same route as infant botulism. The exact prevalence of AITB is unknown. To date, about 20 cases have been reported. The disease affects adults and older children. Characteristics include unknown source of toxin, presence of toxin in stool, and abnormal gastrointestinal pathology (e.g., Billroth surgery, Crohn's disease, and peptic ulcer disease) or antimicrobial drug use.
Lastly, iatrogenic botulism can occur from accidental overdose of botulinum toxin.
It has been noted very rarely after medical use or misuse of the botulinum toxin. Injectable toxins are used to treat a range of spastic and autonomic muscular disorders. These toxins are purified and highly diluted. Toxin type A (Botox) is used in extremely minute doses for the treatment of facial wrinkles and blepharospasm (an abnormal contraction or twitch of the eyelid), cervical dystonia strabismus (an chronic painful neurological disorder characterized by loss of control over one or more parts of the body), glabellar lines( are the vertical lines on the human face and are visible when a person frowns) , and primary axillary hyperhidrosis (excessive sweating). Toxin type B (Myobloc, Neurobloc) is used to treat cervical dystonia.
The diagnosis of this infection can be tricky because symptoms mimic those presented by other diseases. Sepsis (whole body inflammation) is the most common initial diagnosis for infant botulism. Laboratory tests are used for definitive diagnosis. Analysis of blood, stool or vomit for evidence of the toxin may help in the confirmation of the infection.
Treatment includes the use of drugs, respiratory support, surgery, and gastric lavage. Adults with botulism are treated with an antitoxin. The antitoxin is effective against toxins types A, B and E and inactivates only the toxin that is unattached to nerve endings. For infants, BIG (botulism immune globulin) is available neutralizing A, B, C, D, and E before they can even bind to nerves. Infant treatment usually involves respiratory support and tube feeding for weeks even months. Physical therapy is initiated once the baby can breathe unaided. A respirator is often required to help adult patients breathe, and a tracheostomy may also be necessary. Surgery may be necessary to clean an infected wound and remove the source of the bacteria. Antimicrobial therapy may be necessary. In gastric lavage, cathartic agents or enemas are used.
Vaccines against botulism do not exist however scientist have successfully vaccinated mice and ducks against type C and D, which may help in the creation for human vaccination. The toxin cannot be seen, smelled or tasted so the wisest thing to do is to discard any food that seems spoiled without tasting it.