Epidemiology: Open Access
Open Access

Clostridium botulinum is a Gram-positive, anaerobic spore-forming rod. When breathed, botulinum toxin is one of the most potent known toxins: one microgram is deadly to humans. It works by inhibiting the release of the excitatory neurotransmitter acetylcholine from the presynaptic membrane of neuromuscular junctions in the somatic nervous system, hence limiting nerve activity (neuromuscular blockade). This results in paralysis.

By paralyzing the muscles of the chest, advanced botulism can induce respiratory failure, which can lead to respiratory arrest. Furthermore, acetylcholine release from muscarinic nerve synapses' presynaptic membranes is inhibited. This might result in the aforementioned autonomic signs and symptoms.

The botulinum toxin generated by the bacterium C. botulinum in anaerobic circumstances causes sickness in all cases, not the organism itself. Because the poison targets neurons that fire (depolarize) at a greater frequency first, the pattern of damage develops.

The mechanisms of botulinum toxin entrance into the human body are detailed here.

Colonization of the gut

Infant botulism is the most prevalent type in Western nations. This happens in infants who have the bacteria colonized in their small intestine throughout their early lives. The toxin is then produced by the bacteria and taken into the circulation. Honey eating during the first year of life has been found as a risk factor for newborn botulism, with a fifth of all cases including the substance. Adult intestinal toxemia is the adult equivalent of baby botulism, and it is extremely uncommon.

Food

The most prevalent cause of food-borne botulism is a toxin generated by the bacteria in containers of food that have been inadequately maintained. Pickled fish without the salinity or acidity of brine containing acetic acid and excessive salt levels, as well as smoked fish stored at too high a temperature, and inadequately canned food, all pose a concern.

Food-borne botulism is caused by C. botulinum spores that have been allowed to grow in low-oxygen conditions in contaminated food. This is most common in poorly prepared home-canned foods and fermented recipes with insufficient salt or acidity. Because numerous people frequently consume food from the same source, it is normal for multiple people to be impacted at the same time. Symptoms often develop 12-36 hours after eating, however they might appear anywhere between 6 and 10 days.

Wound

Botulism of the wound is caused by bacteria infecting the wound and secreting the toxin into the circulation. Since the 1990s, this has grown more frequent among intravenous drug users, particularly those who use black tar heroin and inject heroin into the skin rather than the veins. Wound botulism is responsible for 29% of cases.

Injection

Botulism symptoms can appear far from the injection site of botulinum toxin. This can include weakness, clouded vision, and a change in speech, or difficulty breathing, all of which can lead to death. After an injection, symptoms might appear anywhere from hours to weeks later. This usually happens when botulinum toxin is employed in incorrect strengths for aesthetic purposes or when greater dosages are utilised to treat movement issues.

Diagnosis

Signs and symptoms should be used to make a diagnosis. A brain scan, cerebrospinal fluid examination, nerve conduction test (electromyography, or EMG), and an edrophonium chloride (Tensilon) test for myasthenia gravis may be used to confirm the diagnosis. If botulinum toxin is found in food, stomach or intestinal contents, vomit, or faeces, a definitive diagnosis can be made. In peracute instances, the toxin is occasionally seen in the blood. A range of procedures, including enzyme-linked immunosorbent assays (ELISAs), electrochemiluminescent (ECL) tests, and mice inoculation or feeding experiments, can be used to identify botulinum toxin.