Clostridium botulinum is a gram positive, obligate anaerobe, spore-former that causes the intoxication of any organism that ingests its toxin. The botulinum toxin is a single polypeptide chain that has a molecular weight of about 15 kDa with a low potency. The chain divides to two chains: a light chain (A) and a heavy chain (B). This occurs when the toxin is nicked by a bacterial protease. Chain A has a molecular weight of 50kDa and chain B has a molecular weight of 100kDa. The two chains are still are connected by a disulfide bond. Therefore, chain A becomes the most potent toxin in nature.
There are seven toxigenic types of C. botulinum: A, B, C1, D, E, F, and G. Each produce a different toxin. Type A is the most usually cause of botulism in the U.S. and causes 62% of those cases. Types C and D have lysogenic phages encode toxin and non-lysogenized bacteria. Only type G is plasmid encoded. However, only types A, B, E, and F cause illness in humans, and C and D cause botulism in animals.
There are four types of botulism: food-borne, infant, wound, and an undetermined form. Each form differs in the way it attacks the organism and how it spreads. Also, each infects different kinds of organisms.
Food-borne botulism is caused by ingesting food contain the neurotoxin that is produced by C. botulinum. That toxin is absorbed in the upper part of the GI tract in the jejunum and duodenum and is then passed to the peripheral neuromuscular synapses through the blood stream. Once there, it attacks the presynaptic stimulatory terminals halting stimulation of that muscle. When it attacks the presynaptic stimulatory terminals, it blocks that release of the neurotransmitter acetylcholine, which is a requirement for the nerve to stimulate the muscle. This all occurs because the toxin is specific to the peripheral nerve endings where a motor neuron stimulates the muscle. It is to that neuron that the toxin bonds with and that is how it prevents the release of acetylcholine across the synaptic cleft. The exact procedure of the release of acetylcholine is unknown but studies show that the botulinum toxin is zinc-dependent that needs specific proteins. Therefore, the excretion of the neurotransmitters must be involved with those proteins.
The symptoms of food-borne botulism show between 18 and 36 hours after ingestion. However there have been cases that range from 4 hours to 10 days. The toxin’s infective dose is simply a few nanograms of the toxin, the symptoms for this: lassitude, weakness, and vertigo. If the amount of toxin ingested is larger than the infective dose, the symptoms can include: double vision, difficulty in speaking, difficulty in swallowing, weakness of other muscles, abdominal distention, constipation, and difficulty in breathing. Those respiration problems are the causes of death that occur. This is why if the illness is treated quickly and properly then the chance of death is much less than if respiratory problems occur untreated or unrecognized.
Infant botulism is caused by an infection (instead of the intoxication of food-borne) caused by C. botulinum. It occurs in infants between 5-20 months of age that are exposed to solid food. At this young age the intestinal bacteria are not yet fully developed. Such as normal flora which would compete with the infection. This is why solid food containing C. botulinum spores can colonize and produce toxin in the intestinal tract of the infant. The production of the toxin causes constipation, poor feeding, lethargy, weakness, pooled oral secretions, a wail or altered cry, and, most dramatic, loss of head control. Most of the known cases of infant botulism have recovered, however it is possible that it may have a role in the "sudden infant death syndrome." This possibility is very possible because the toxin has been found in bowel contents of many infants who have died suddenly.
Wound botulism is caused when C. botulinum infects a wound on and organism and then begins to produce its toxin. This toxin then enters the blood stream and goes to other parts of the body. After this, the effects of the toxin are basically the same as the food-borne botulism in which the toxin causes flaccid paralysis by blocking motor nerve terminals at the myoneural junction. The paralysis usually starts at the eyes, moves to the face, then to the throat, the chest, and finally the extremities. Wound botulism can affect animals but mostly infects humans, especially in California because of the use of black-tar heroin.
The undetermined form of botulism occurs in adults only. In these cases, the source of either food or wound cannot be identified. Many theories suggest that it might have been from an intestinal colonization in adults much like infant botulism. Another theory is that some of the victims had had surgical operations of gastrointestinal tract or antibiotic therapy that might have destroyed or altered the normal flora which prevents colonization.
In the United States, there are 110 cases of botulism reported annually. 25% are food-borne, 72% infant botulism, and the rest are wound botulism. However, many may be overlooked because symptoms are weak, death is involved with SIDS or respiratory problems, or it is often misdiagnosed as Guillain - Barre syndrome.
Botulism can be preventing by avoiding foods that have been home-canned or foods that have not undergone sterilization, especially for foods that have a low acid content. To sterilize home-canned food, it can be boiled for at least ten minutes because the toxin is destroyed by high temperatures. In the case of infant botulism, solid food should be avoiding during the developmental stages of the intestinal tract. Also, honey should never be ingested by anyone under 1 year old because it can easily contain the spores of C. botulinum. Cleaning and treating all wounds quickly, and not using injectable street drugs can prevent wound botulism.