Botulism

What is Botulism?

Botulism is an acute toxic-infectious disease associated with eating foods that contain Clostridium botulinum toxin and the pathogens themselves. Characterized by the development of cuts and paralysis of the muscles due to the blockade of acetylcholine release by the toxin in the nerve synapses.

Brief historical information

The term “botulism” (from the Latin. Botulus – sausage) was introduced by the Belgian bacteriologist E. Van-Ermengem (1896), who isolated the pathogen from the intestines of the deceased patient. However, even in the IX-X centuries in Byzantium, and somewhat later in Germany, cases of the disease associated with the use of blood sausage were observed. In 1818, in Russia, a neuroparalytic disease associated with eating smoked fish was described.

Causes of Botulism

The causative agent is a mobile, gram-positive, strictly anaerobic spore-forming bacterium Clostridium botulinum. In brush strokes it looks like rods with rounded ends, arranged in erratic clusters or small chains. Under adverse conditions, it forms sub-terminal and terminal spores, in the form of which it remains in the environment. In the dried state, spores can remain viable for decades. There are 8 known botulism serovars – A, B, Ca2beta, D, E, F, G; however, serovars A, B, E and F dominate human pathology.

Optimum growth of clostridia and toxin formation occurs under anaerobic conditions at a temperature of 35 ° C. Vegetative forms of bacteria die at 80 ° C for 30 minutes, while boiling for 5 minutes. Spores withstand boiling for more than 30 minutes and are destroyed only by autoclaving. Toxin (botulinum toxin) quickly collapses when boiled, is resistant to pepsin and trypsin, withstands high concentrations (up to 18%) of salt, does not collapse in foods containing various spices. The presence of botulinum toxin in food products does not change their organoleptic properties. Botulinum toxin is one of the most powerful biological poisons. Cases of poisoning of people and animals by several toxins produced by bacteria of various serovars are possible.

Epidemiology

The reservoir and sources of infection are soil, wild and synanthropic animals, waterfowl, fish and humans. The causative agent of botulism lives in the intestines of cows, horses, pigs, rabbits, rats, minks, chickens, wild waterfowl and many other representatives of the animal world. In this case, the carriage of pathogens usually does not cause any visible harm to animals. A sick person does not represent an epidemiological hazard to those around them. From the body of infected animals (or humans), bacteria are excreted in faeces and enter the soil, water, livestock feed, etc. Contamination of various elements of the environment can also be caused by the decomposition of corpses of rodents and birds killed by botulism.

The transmission mechanism is fecal-oral. The main cause of the disease is the consumption of home canning products, most often vegetables and mushrooms, as well as sausages, ham, smoked and salted fish contaminated with clostridia. Almost all food products contaminated with soil or the intestinal contents of animals, birds, fish, may contain spores of pathogens of botulism. However, the disease can occur only when using products stored in anaerobic conditions (canned food, cooked at home). Much less common are wound botulism and botulism in newborns, which occurs in the latter when they enter clostridia in the intestine and produce toxin. With injuries in crushed, necrotic tissues, deprived of oxygen access, conditions are created that are close to anaerobic, under which spore germination occurs and botulinum toxin accumulates. The toxin is well absorbed not only from the mucous membrane of the gastrointestinal tract, but also from the mucous membranes of the eyes and upper respiratory tract, which is a great danger if the toxin aerosol is used as a biological weapon.

The natural susceptibility of people is high. Due to the fact that the toxin realizes activity in minimal doses, significant antitoxic immune reactions do not develop and antitoxic immunity is not developed.

Major epidemiological signs. Botulism is recorded in the form of sporadic and group diseases; Often, cases of illness are familial as a result of eating contaminated homemade foods. They account for about 38% of all cases of the disease. For botulism is not typical strictly pronounced seasonality. It should be noted that the botulism caused by the use of food produced in industrial conditions has practically disappeared. In Ukraine, diseases associated with the use of homemade mushrooms, smoked or dried fish are more often recorded, in European countries – meat and sausage products, in the USA – canned legumes. The relationship between the typical structure of pathogens and the nature of transmission factors has been determined. Infection after eating canned meat from warm-blooded animals (stews, ham, sausages, etc.) is most often caused by type B bacteria; from fish, bacteria E and F types, canned vegetable products (pickled mushrooms, vegetables, fruits, etc.) – Type A and B bacteria. Local and national peculiarities, traditions and customs in nutrition and methods of food preservation determine the unequal distribution of one or another type of pathogen in different territories. Clinical and epidemiological features of diseases caused by bacteria of different types are also expressed. Type B pathogen causes intoxication with relatively low mortality and foci, which are distinguished by an extended incubation period, late hospitalization and the initiation of specific treatment. At the same time, type E bacteria cause lesions with a very high mortality rate (30% and above), the predominance of severe clinical forms. In recent years, there is a tendency to an increase in morbidity, mortality and the number of outbreaks, which is due to the increasing pace and spontaneity of canning various types of products at home. Most often, the disease is registered among persons of 20-25 years.

Pathogenesis during Botulism

In the overwhelming majority of cases, human infection occurs when the toxin is ingested with food in the gastrointestinal tract, but other ways of infection are also possible (wound botulism, newborn botulism). The good absorbability of the toxin determines its greatest concentration in the blood already on the first day, but the doses of the toxin, which did not manage to contact the nervous tissue, are completely eliminated from the body by urine during the 3-4th day. Pathogenetic mechanisms of intoxication are still not clear enough. It is known that botulinum toxin reversibly disrupts carbohydrate metabolism in nerve cells, providing their energy regime. This disrupts the synthesis of choline acetyltransferase, activating the formation of acetylcholine. As a result, the neuromuscular impulse weakens or disappears, reversible (in case of recovery) paresis or paralysis develop.

Botulinum toxin affects the parasympathetic nervous system, inhibiting its activity, which is manifested by mydriasis, dry mucous membranes and constipation.

Many researchers qualify botulism not as intoxication, but as toxic infection, giving importance to the pathogen. In particular, the rarely occurring long incubation period (up to 10 days) is explained by germination of the pathogen spores in the gastrointestinal tract with subsequent excretion of exotoxin by vegetative forms. In addition, the possibility of the development of vegetative forms from spores in purulent foci or “pockets” for injuries (wound botulism) has been established. These mechanisms maintain the concentration of the toxin in the patient’s body for a long time, which should be considered when performing serum therapy.

Symptoms of Botulism

The incubation period of botulism
In most cases, it is short and is 4-6 hours. However, in rare cases it can be extended to 7-10 days. This makes it necessary for 10 days to monitor the health of all persons who ate the product that caused the first case of the disease.

Initial period
Symptoms of the disease may be unclear, similar to a number of other diseases, which makes it difficult to diagnose early. By the nature of the main clinical manifestations of botulism in the initial period, it is conditionally possible to distinguish the following options.

  • Gastroenteric option. There are pains in the epigastric region of a cramping character, one-time or two-time vomiting of food is eaten, and the stools are relaxed. The disease resembles the manifestations of foodborne illness. At the same time, it should be taken into account that with botulism there is no pronounced increase in body temperature and there is a strong dryness of the mucous membranes of the oral cavity, which cannot be explained by a slight loss of fluid. A frequent symptom during this period is difficulty in passing food through the esophagus (“lump in the throat”).
  • “Eye” option. Manifested by visual impairment – the appearance of fog, a grid, “flies” before the eyes, the clarity of the contours of objects is lost. In some cases, developing “acute hyperopia”, corrected by plus lenses.
  • Variant of acute respiratory failure. The most dangerous variant of botulism with lightning is the development of acute respiratory failure (shortness of breath, cyanosis, tachycardia, pathological types of respiration). The death of the patient can develop in 3-4 hours.

The height of the disease

Clinical manifestations of botulism are quite characteristic and are distinguished by a combination of a number of syndromes. With the development of ophthalmoplegic syndrome, bilateral blepharoptosis, persistent mydriasis, diplopia, impaired movement of the eyeballs (often converging strobism), and vertical nystagmus can be observed. At the same time, the patient has a syndrome of swallowing disorders, manifested in the difficulty of swallowing first solid and then liquid food (when trying to drink water, it pours through the nose through the patient). The latter is due to paresis of swallowing muscles. When examining the oral cavity, a violation or in more severe cases the complete lack of mobility of the soft palate and uvula attracts attention. There is no pharyngeal reflex, language movements are limited.

Characterized by violations of phonation, consistently passing through 4 stages. First, there is hoarseness or a decrease in its tone, due to the dryness of the mucous membrane of the vocal cords. Subsequently, dysarthria develops, which is explained by a violation of the mobility of the tongue (“porridge in the mouth”), followed by nasal voices (paresis or paralysis of the palatine curtain), and, finally, complete aphonia occurs, caused by paresis of the vocal cords. The patient does not have a cough push, which leads to an attack of suffocation when mucus or fluid enters the larynx.

In some cases, but not always, violations of innervation from the facial nerve of the muscles of the mimic muscles: bias of the face, impossibility of grinning teeth, etc., are revealed.

In the midst of illness, patients complain of great muscular weakness; their gait becomes unstable (“drunk” gait). From the first hours of the disease, severe dryness of the mucous membranes of the oral cavity is typical. Constipation associated with intestinal paresis develops. Body temperature remains normal and only occasionally rises to subfebrile numbers. Typical tachycardia, in some cases, there is a slight arterial hypertension. Consciousness and hearing fully preserved. There are no disturbances on the part of the sensitive sphere.

Botulism complication

In botulism, the fatal development of pneumonia is observed, primarily due to a decrease in the volume of external respiration in patients. At the same time, the preventive administration of antibiotics for botulism does not prevent the onset of this complication.

The most terrible complications, often leading to death, are respiratory disorders, which can occur in any period of botulism. In the initial stage, they are distinguished by an increase in respiration up to 40 per minute, the patient’s motive anxiety, intercostal spacing, paralysis of the diaphragm, involvement of the brachial muscles in the breathing process. Already in this stage it is necessary to transfer the patient to mechanical ventilation.

With the introduction of heterogeneous antibotulinic serum, anaphylactic shock can develop, and in later periods (on the 10-12th day after its use) serum sickness.

Recently, a number of reports of fairly frequent myocarditis have emerged as a complication of botulism. Its clinical course and prognosis are similar to myocarditis in diphtheria.

Diagnosis of Botulism

Differential diagnostics

Botulism should be distinguished from food toxicoinfection, poisoning from bleached and poisonous fungi, the bulbar form of polio, diphtheria, stem encephalitis.

Of particular importance is the differential diagnosis of the disease in its initial period. When botulism may be dyspeptic phenomena (gastroenteric version of the disease), but there is no pronounced increase in body temperature; characterized by severe dry mouth, often noted difficulty in swallowing (“lump in the throat”). In other variants of the initial period of botulism, visual disturbances (an “eye variant”) or acute respiratory failure develop at a normal body temperature. In the midst of the disease characterized by significant muscle weakness, severe dryness of the mucous membranes of the mouth, constipation. Patients simultaneously develop manifestations of ophthalmoplegic syndrome, swallowing disorders, sequential disorders of phonation (hoarseness – dysarthria – nasalism – aphonia); in some cases, pathology is detected by the facial nerve. There are no disturbances on the part of the sensitive sphere.

Laboratory diagnosis

Currently, there are no laboratory tests to identify botulinum toxin in human biological media in the early stages of the disease. The objectives of bacteriological research are the detection and identification of the toxin; pathogen isolation is carried out in the second stage. To do this, put a biological sample on laboratory animals (white mice, guinea pigs). A batch of 5 animals is selected for the experiment. The first is infected only with the test material, the rest with the test material with the introduction of 2 ml of 200 AE antitoxic serum types A, B, C and E. If there is toxin in the material, the animal survives, which received antiserum neutralizing the toxin of the corresponding type. For the express indication of toxins, an RPHA with an antibody diagnosticum (erythrocytes sensitized with corresponding types of antitoxins) is installed.

Current promising methods are based on the indication of antigens in ELISA, RIA or PCR.

Isolation of the pathogen does not provide a basis for confirming the diagnosis, since germination of C. botulinum spores is possible, which may be found in the intestines of a large number of healthy people.

Treatment of Botulism

Due to the danger to life, hospitalization of patients is necessary in all cases, even if botulism is suspected. Patients are sent to any hospital where there is equipment for mechanical ventilation.

Therapeutic measures begin with washing the stomach with a thick probe; during the procedure, it is necessary to ensure that the probe inserted is in the stomach, taking into account the fact that, in the absence of the pharyngeal reflex, the probe can be introduced into the respiratory tract. It is advisable to carry out gastric lavage in the first 1-2 days of the disease, when there may still be contaminated food in the stomach.

To neutralize the toxin on the territory of Ukraine, polyvalent antibotulinic sera are used in a single initial dose of type A – 10 000 ME, type B – 5000 ME, type E – 10 000 ME, sometimes type C-10 000 ME. Serum is injected intravenously or intramuscularly after prior desensitization (the method is uncommon). With the introduction of serum intravenously, it is necessary to pre-mix it with 250 ml of saline, heated to 37 ° C. In most cases, a single injection of the above doses of serum is sufficient. If after 12-24 h after the end of its introduction, the patient progresses neuroparalytic disorders, the introduction of serum should be repeated in the initial dose.

A sufficiently good clinical effect is provided by the use of human antibotulinic plasma, but its use is difficult due to the short shelf life (4-6 months). There is evidence of the effectiveness of human anti-immunotin immunoglobulin.

Simultaneously with the introduction of antibotulinic serum, massive detoxification therapy is carried out, including intravenous drip infusion. It is advisable to use compounds based on polyvinylpyrrolidone (hemodez, reopolyglukine, etc.), which adsorb well the freely circulating botulinum toxin and remove it through the kidneys with urine.

Due to the fact that the patient cannot swallow, his feeding is carried out through a thin probe. Food should be not only complete, but also necessarily liquid, passed through the probe. It is undesirable to leave the probe until the next feeding, since with the dry mucous membranes the rapid development of bedsores is possible.

Given the toxic and infectious nature of the disease and the possibility of the development of vegetative forms of the pathogen from the spores located in the gastrointestinal tract, antibiotics are prescribed to the patient. The drug of choice – chloramphenicol in a daily dose of 2.5 g course of 5 days.

The complex of treatment of patients includes the appointment of a 3% solution of adenosine triphosphate (ATP) and cocarboxylase. There are reports of a fairly good therapeutic effect of hyperbaric oxygenation. With the development of pneumonia, antibiotic therapy is carried out according to standard schemes. At the first signs of the onset of respiratory disorders, the patient should be transferred to a ventilator. After the disappearance of signs of intoxication for a more rapid recovery of the neuromuscular apparatus, it is possible to use physiotherapeutic procedures.

Prevention of Botulism

Epidemiological surveillance is basically similar to that of intestinal infections, includes bacteriological control of food raw materials used in the preparation of canned meat, fish and vegetables, monitoring compliance with the mode of sterilization. The sale in the trading network of canned food, their appearance (bomb) and the timing of implementation are subject to systematic control. Analysis of the incidence is carried out taking into account the type of pathogen and the type of food product. There remains a need to improve the methods of laboratory control of food products and diagnosis of the disease.

Prevention of botulism is based on strict observance of sanitary and technological rules of food preservation. Meat and fish are allowed to preserve only fresh. Vegetables and fruits before canning should be thoroughly washed to remove soil particles. It is also unacceptable to preserve overripe fruit. It is necessary to strictly observe the regime of guarantee sterilization Sterilization should be carried out in autoclaves, since elevated pressure and high temperature (120 ° C) destroy not only bacterial cells and toxin, but also spores. At home, plant-derived products can be stored for the future only by marinating or salting with the addition of enough acid and salt and always in an open container for access to air. Of great importance is the prevention of botulism in the trading network. The most important point – compliance with the storage conditions of perishable goods. The spoiled ones (with bombardment) and expired cans should not be allowed into the trading network. An important role is played by explanatory work among the population about the danger of botulism and the rules for preserving food at home.

Activities in the epidemic outbreak. Hospitalization of the patient is carried out according to clinical indications. It was recommended to discharge those who had recovered from the hospital no earlier than 7-10 days after clinical recovery. In case of detection of cases, suspicious products are subject to seizure and laboratory research, and the persons who used them are subject to medical observation for 10–12 days. It is advisable to intramuscularly administer antibacterial serum containing 2000 ME each to toxins A, B and E, as well as the administration of enterosorbents. Active immunization is not widely used.

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