Infectious diseases. Botulism. Etiology. Epidemiology. Pathogenesis (most important)

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Infectious diseases. Botulism. Etiology. Epidemiology. Pathogenesis (most important)

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22. Botulism. Etiology. Epidemiology. Pathogenesis

Botulism is an acute infectious disease with a leading enteral route of infection, caused by C. botulinum exotoxins and characterized by a severe course with a predominant lesion of the central and autonomic nervous system. There are three forms of botulism:

1. food, caused by food intake, in which botulinum toxin accumulates during storage;

2. wound, caused by infection of wounds by the causative agent of this disease, which produces a toxin;

3. a disease of infants caused by the pathogen entering the intestines, its reproduction and the release of a toxin.

Etiology. C. botulinum is an anaerobic, motile Gram-positive bacillus that produces heat-resistant spores.

If the spores survive the cooking process, they germinate, multiply, and produce toxins. Seven antigenically distinct toxins (A, B, C, D, E, F, and G) have been identified, of which only types A, B, E, F, and G are responsible for human disease.

Epidemiology. Botulism in young children. Most often, children under 1 year old get sick, the peak of the disease occurs at the age of 2-6 months. The etiological factor can be pathogens of types A and B. The main reservoir and source of infection are warm-blooded herbivores, less often - fish, crustaceans, mollusks.

From a sick person to a healthy person, the disease is not transmitted. The main route of infection is food, more often with the use of home-made canned food. In infants, foodborne botulism may be derived from infant formula.

Pathogenesis. The entrance gate of infection is the gastrointestinal tract. Botulism in young children occurs when C. botulinum spores enter the child's intestines, germinate, multiply, and release the toxin. Spores are constantly present in the soil and in the environment, but in adults such a genesis of the disease does not occur. Food botulism occurs when botulinum toxin is absorbed from the intestines, which has entered the body along with improperly cooked food. Wound botulism is characterized by the formation of a toxin in the wound itself.

It is assumed that the transport of the toxin to the nerve endings occurs not only with the blood flow, but also with the participation of lymphocytes. Different toxins have different affinity for nervous tissue. It is most pronounced in type A toxin, less in type E and weakly in type B. The last toxin circulates in the blood longer than others and is determined in it even 3 weeks after ingestion of contaminated food.

The toxin selectively acts on the endings of motor nerve fibers, inhibiting the formation of acetylcholine. Its inhibitory effect on the motor neurons of the spinal cord has been proven. The effect of the toxin on the brain is slightly pronounced, the endings of the cranial nerves are affected early, and therefore the patients develop shortness of breath or asphyxia and arrhythmia.

Author: Pavlova N.V.

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