What causes botulism?

The cause of botulism is Clostridium botulinum, a gram-positive anaerobic (in young cultures) motile rod. Depending on the antigenic properties of the produced toxin, eight serovars are distinguished - A, B, C _1, C ₂, D, E, F and G.

In Ukraine, the disease is caused by serovars A, B and E. During its life cycle, the botulism pathogen produces a specific neurotoxin. Optimal conditions for toxin formation by vegetative forms are extremely low residual oxygen pressure (0.4-1.33 kPa) and a temperature range of 28-35°C, with the exception of the pathogen type E, which does not require strict anaerobic conditions and whose reproduction is possible at the temperature of a household refrigerator (3°C). This toxin is the strongest of all known toxins of any origin. Strains of the pathogen obtained in laboratory conditions produce a toxin that in purified crystalline form contains up to 1 million lethal doses for humans per 1 g. Unique toxicity and relative ease of production allow us to consider the possibility of its use as a biological weapon and a means of mass destruction. Botulinum toxin is used as a drug for the treatment of muscle contractures and in cosmetology. Botulinum toxin, produced by different serovars of the pathogen, has a single mechanism of action and differs in antigenic and physical properties and molecular weight.

Heating at 80 °C for 30 minutes causes the death of vegetative forms of the pathogen. Spores, unlike the vegetative form, are extremely resistant to various physical and chemical factors: in particular, they can withstand boiling for 4-5 hours, exposure to high concentrations of various disinfectants. They are resistant to freezing and drying, and to ultraviolet radiation. Botulinum toxin is preserved in normal environmental conditions for up to 1 year, and in canned products - for years. It is stable in an acidic environment, withstands high concentrations (up to 18%) of table salt, and is not destroyed in products containing various spices. The toxin is relatively quickly inactivated under the influence of alkalis; when boiled, it completely loses its toxic properties within 10 minutes. In the gastrointestinal tract, the toxin reduces its toxicity, with the exception of toxin E, which, when activated by trypsin, increases it 10,000 times. Ethanol and liquids containing it reduce the toxicity of botulinum toxin; its presence in food products does not cause changes in their appearance and organoleptic properties. "Bombing" of canned food, the smell and taste of rancid oil are usually associated with the presence of accompanying anaerobic flora, in particular Cl. perfringens.

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Pathogenesis of botulism

The toxin plays a leading role in the pathogenesis of botulism. In case of alimentary infection, it enters the body together with food, which also contains vegetative forms of the pathogen. The effect of the toxin on the human body is highly specific and is not related to its antigen structure and molecular weight. The H-chain of the toxin binds to the synaptic membrane of neuromuscular cholinergic synapses that innervate striated muscles, i.e., the a-motor neurons of the anterior horns of the spinal cord and the motor nuclei of the cranial nerves, as well as the smooth muscles that are innervated by the vagus nerve. The toxin, having protease activity, breaks down specific synaptic proteins: SNAP-25 (broken down by toxins of serovars A and E) and synaptobrevin (broken down by toxin of serovar B), which disrupts the fusion of synaptic vesicles and the synaptic membrane, i.e. blocks the passage of a nerve impulse with normal production of acetylcholine and cholinesterase. Blockade of impulse transmission leads to myasthenia and paralytic syndrome in the absence of anatomical damage, therefore it is more correct to interpret this syndrome as pseudoparalytic, since inactivation of the toxin can completely restore the functions of neuromuscular synapses. Primarily affected are muscles with high functional activity: oculomotor, pharynx and larynx, respiratory. The effect of the toxin is potentiated by aminoglycosides, antipolarizing muscle relaxants. ionizing radiation and repeated entry of new doses of toxin into the body. Blockade of the muscles innervated by the vagus nerve causes intestinal paresis, reduces the production of saliva and gastric juice. Additional factors of pathogenesis include ventilation hypoxia, aspiration of oropharyngeal secretions, and secondary bacterial infection. The clinical picture of botulism is completely formed by the toxin, but a certain role is played by the pathogen, the vegetative forms of which can produce the toxin under the conditions of the body (wound botulism, botulism in newborns, cases of the disease with prolonged incubation, sudden deterioration in the late stages of the disease). This is evidenced by the presence of antimicrobial antibodies in some patients. [ 6 ], [ 7 ]

Epidemiology of botulism

Spore forms of the pathogen can be found in dust, water and silt. Almost all food products contaminated with soil or the intestinal contents of animals, birds, fish may contain spore forms of botulism pathogens. Under natural conditions, the formation of vegetative forms and botulinum toxin most intensively occurs after the death of the animal, when the body temperature drops to the optimum for the pathogen. When creating anaerobic conditions as a result of oxygen consumption by aerobic bacteria, algae in the soil, bottom silt of small bodies of water, reproduction of vegetative forms of the pathogen and toxin formation are also possible.

The overwhelming majority of cases of botulism are associated with the consumption of canned food (mushrooms, beans, vegetables), fish and home-cooked meat. If a solid-phase product (sausage, smoked meat, fish) is contaminated, then "nested" formation of the toxin is possible in it, so not all people who have consumed this product become ill. Cases of the disease as a result of infection with only spores of the pathogen Cl. botulinum are much less common. These include so-called wound botulism and neonatal botulism.

Wound botulism can occur due to contamination of wounds, which create anaerobic conditions. In this case, vegetative forms germinate from the spores that get into the wound, which produce botulinum toxins. Infant botulism is observed mainly in children in the first 6 months of life. Most of the patients were partially or completely bottle-fed. Sometimes spores were isolated from honey used to prepare nutritional mixtures, or found in the child's environment: soil, household dust in rooms, and even on the skin of nursing mothers. Susceptibility to botulism is universal. Immunity to botulism is type-specific antibacterial, weakly expressed, so a second infection is possible.

Botulism is common in all countries where home canning is practiced.

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