Botulism: symptoms

Botulism has an incubation period that lasts up to a day, less often up to 2-3 days, in single cases up to 9-12 days. With a shorter incubation period, the more severe course of the disease is observed, though not always.

[1], [2], [3], [4], [5], [6], [7], [8], [9]

The main symptoms of botulism and the dynamics of their development

Botulism begins acutely. There are two variants of the beginning: the first - with a picture of gastroenteritis followed by, for several hours, the addition of neurological symptoms and the second - an option in which dyspeptic syndrome is absent and the defeat from the very beginning is the CNS.

In the first case, the symptoms of botulism begin with cramping pain in epigastrium, with vomiting, with diarrhea, an increase in body temperature. These phenomena last from a few hours to a day, then symptoms of damage to the nervous system are revealed. Dyspeptic syndrome is associated with concomitant anaerobic flora (Cl. Perfringens) and other pathogens of food toxic infections.

The second option is characterized by the fact that the symptoms of botulism begin with a pronounced myasthenia gravis, dizziness, headache, fever. Pain is not characteristic. Almost simultaneously, impaired vision (blurred vision, "mesh" in front of the eyes, the inability to read, while clearly visible distant objects) due to the paresis of the ciliary muscle. At the same time there are other violations: strabismus, diplopia, violation of convergence, mydriasis, anisocoria, ptosis. In severe cases, ophthalmoplegia is possible: the eyeballs are immovable, the pupils are wide, do not respond to light. Ophthalmoplegic syndrome appears earlier than other neurological symptoms and lasts longer, especially pathological hyperopia.

A few hours later there are paresis of the pharyngeal muscles (IX, X, XII pairs of cranial nerves) with the development of aphonia and dysphagia. Speech becomes vague, with a nasal hue, swallowing is broken, there is a shuffling of food and liquid. The movements of the tongue are limited, the soft palate hangs, the palatine reflex is absent, with the laryngoscopy, the vocal cleft gap. Less often observed bilateral paresis of the facial nerve. Somewhat later (and in the most severe cases at the same time) a paresis of the diaphragm and auxiliary respiratory muscles appears. The paresis of the diaphragm is expressed in the limitation of the pulmonary margin. Respiratory failure can initially be compensated and can be detected only on the basis of a reduced minute volume of respiration, pO2, arterial blood. Then there is a ruptured speech, a feeling of lack of air, cyanosis of the lips, tachypnea, shallow breathing. Respiratory failure may increase gradually, for two to three days. But perhaps fast, within a few hours, and even a sudden development of apnea ("death in the middle"). The development of acute respiratory failure contributes to bulbar paralysis, which is accompanied by a violation of patency of the upper respiratory tract. Aspiration of fluid and secretion of the oropharynx, high diaphragm standing, atelectasis of the lower segments of the lungs.

Syndrome of parasympathetic nervous system lesion is revealed in all patients, it is characterized by dry skin, mucous membranes, reduced salivation, which is expressed in the corresponding complaints of patients. In addition, with the defeat of the autonomic nervous system, there is a violation of the innervation of the gastrointestinal tract, up to the development of paralytic intestinal obstruction and less frequent urodynamic disturbances in the form of acute urinary retention or involuntary permanent urination. Innervation of the intestine and urinary tract is disrupted only in the case of severe botulism.

Changes in the cardiovascular system: a bradycardia alternating with tachycardia, a tendency to increase blood pressure, changes in the final part of the ventricular complex on the ECG, increased activity of "cardiospecific" enzymes (MB-creatine phosphokinase, asparagine transaminase and hydroxybutyrate dehydrogenase), troponin levels - are detected with an average and heavy current. With a severe course of the disease and severe myocardial damage, it is possible to develop conduction disorders, up to a complete AV blockade. Electrical instability of the myocardium, up to ventricular fibrillation. Violations of the contractility of the myocardium with the development of heart failure in a large range of blood circulation. Such changes are the direct cause of death in these patients. Convalescents may persist for a long time, shortness of breath, tachycardia, changes in the ECG, a decrease in the contractile function of the myocardium.

Symptoms of botulism without complications are characterized by clarity of consciousness, lack of meningeal symptoms, febrile-intoxication syndrome.

Recovery comes slowly - with severe forms usually not earlier than from the second week of illness. One of the early signs of improvement is the restoration of salivation. Gradually regresses the neurological symptoms. Later, the visual acuity and muscular strength are completely restored. Intermittent vision disorders can occur within a few months. Despite the hardest, sometimes incompatible with life neurological disorders, those who have recovered from botulism do not have consequences and any persistent impairment of the functions of the nervous system or internal organs.

Some features are wound botulism and botulism of infants. In both cases, there is no gastrointestinal syndrome and a common infectious intoxication. With wound botulism, longer periods of the incubation period (4-14 days), the same as in food botulism, neurological symptoms. Botulism in infants (botulism of infants) is more often observed with artificial feeding. Besides Cl. Botulinum, causative agents are Cl. Butyricum and Cl. Baratii. The first manifestations of the disease may become child fatigue, weak sucking or refusal, stool retention. When ophthalmoplegic symptoms of botulism appear, hoarse cries, weakening of pharyngeal and sucking reflexes, tumbling, this should lead to the thought of the possibility of botulism and the need to urgently carry out appropriate diagnostic and therapeutic measures. Paralytic syndrome builds up within 1-2 weeks. With an early defeat of the respiratory muscles, sudden death is possible. Early and often develop severe pneumonia.

Classification of botulism

In the clinical picture, light, moderate and severe forms of the disease are isolated. With a mild course in patients, the paralytic syndrome is limited to the defeat of the oculomotor muscles: with an average patient, it spreads to the glossopharyngeal musculature. Severe course is characterized by respiratory failure and severe bulbar disorders.

[10], [11], [12], [13], [14]

Botulism Complications

Botulism has specific, secondary bacterial and iatrogenic complications.

A characteristic specific complication of botulism is myositis, which usually occurs in the second week of the disease. As a rule, its development does not affect the severity of the condition of patients. Femoral, occipital and calf muscles are more often affected. The following symptoms of botulism appear: swelling, sharp tenderness in palpation, muscle infiltration, pain and difficulty in moving. Much more serious consequences may have the development of secondary bacterial complications that occur in almost all patients with severe botulism. The most typical aspiration pneumonia, atelectasis, purulent tracheobronchitis, pyelitis, pyelonephritis, sepsis, or a combination thereof.

Iatrogenic complications of botulism are associated with a large volume of drug therapy and invasive methods of diagnosis and treatment. Since botulinum toxin significantly reduces the immune resistance of the body, complications associated with invasive methods of treatment (intubation, tracheostomy, ventilation, bladder catheterization, etc.) and a secondary infection are of particular danger. One of the most frequent complications of medicinal therapy of botulism is serum sickness, which develops in about one in every third patient who received heterologous anti-butulinic serum. It, as a rule, occurs in the period of regression of neurological symptoms of botulism. A large group of complications, such as hyperglycemia, hypophosphataemia (causes weakness of the respiratory muscles, hemolysis and a decrease in the dissociation of oxyhemoglobin in tissues), fatty liver disease, delay in the body of CO ₂, electrolyte imbalance hyponatremia, hypokalemia, hypocalcemia), intestinal atrophy, acalculous cholecystitis, is associated with the appointment of parenteral nutrition to patients with paralytic intestinal obstruction.

[15], [16], [17], [18], [19], [20], [21], [22]

Mortality and causes of death

Botulism has a fairly high lethality of 5-50%. The main causes of death are respiratory failure, secondary bacterial complications, myocardial damage, and multiple organ failure.