Botulism - Symptoms

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

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The main symptoms of botulism and the dynamics of their development

Botulism begins acutely. There are two variants of onset: the first is with a picture of gastroenteritis followed, within a few hours, by the addition of neurological symptoms, and the second is a variant in which there is no dyspeptic syndrome and CNS damage comes to the forefront from the very beginning.

In the first case, the symptoms of botulism begin with cramping pains in the epigastrium, vomiting, diarrhea, and an increase in body temperature. These phenomena last from several 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 variant is characterized by the fact that the symptoms of botulism begin with a sharply expressed myasthenia, dizziness, headache, fever. Pain is not typical. Almost simultaneously, vision is impaired (blurred, "net" before the eyes, inability to read, although distant objects are clearly visible) due to paresis of the ciliary muscle. Other disorders appear simultaneously: strabismus, diplopia, convergence disorder, mydriasis, anisocoria, ptosis. In severe cases, ophthalmoplegia is possible: the eyeballs are motionless, the pupils are wide, do not react to light. Ophthalmoplegic syndrome appears earlier than other neurological symptoms and persists longer, especially pathological hyperopia.

A few hours later, paresis of the pharyngeal-glossus muscles (IX, X, XII pairs of cranial nerves) appears with the development of aphonia and dysphagia. Speech becomes slurred, with a nasal tint, swallowing is impaired, choking on food and liquid appears. Tongue movements are limited, the soft palate hangs down, the palatal reflex is absent, and the glottis gapes during laryngoscopy. Bilateralparesis of the facial nerve is observed less often. Somewhat later (and in the most severe cases simultaneously), paresis of the diaphragm and accessory respiratory muscles appears. Paresis of the diaphragm is expressed in limited mobility of the pulmonary edge. Respiratory failure may initially be compensated and is detected only on the basis of a reduced minute respiratory volume, pO2, and arterial blood. Then, incoherence of speech, a feeling of shortness of breath, cyanosis of the lips, tachypnea, and shallow breathing appear. Respiratory failure may develop gradually over two to three days. But rapid, over several hours, and even sudden development of apnea ("death in mid-sentence") is possible. Development of acute respiratory failure is facilitated by bulbar paralysis, accompanied by obstruction of the upper respiratory tract. Aspiration of fluid and secretion of the oropharynx, high standing of the diaphragm, atelectasis of the lower segments of the lungs.

The syndrome of parasympathetic nervous system damage is detected in all patients, it is characterized by dry skin, mucous membranes, decreased salivation, which is expressed in the corresponding complaints of patients. In addition, damage to the autonomic nervous system is associated with a violation of the innervation of the gastrointestinal tract, up to the development of paralytic intestinal obstruction and, less often, urodynamic disorders in the form of acute urinary retention or involuntary constant urination. Innervation of the intestine and urinary tract is impaired only in severe cases of botulism.

Changes in the cardiovascular system: bradycardia alternating with tachycardia, a tendency to increase in blood pressure, changes in the terminal part of the ventricular complex on the ECG, increased activity of "cardiospecific" enzymes (MB-creatine phosphokinase, aspartic transaminase and hydroxybutyrate dehydrogenase), troponin levels - are detected in moderate and severe cases. In severe cases of the disease and severe myocardial damage, conduction disorders may develop, up to complete AV block, electrical instability of the myocardium, up to ventricular fibrillation, impaired myocardial contractility with the development of heart failure in the systemic circulation. Such changes can be the direct cause of death in these patients. In convalescents, shortness of breath, tachycardia, changes in the ECG, and decreased myocardial contractility may persist for a long time.

Symptoms of uncomplicated botulism are characterized by clarity of consciousness, absence of meningeal symptoms, and fever-intoxication syndrome.

Recovery occurs slowly - in severe forms usually not earlier than the second week of the disease. One of the early signs of improvement is the restoration of salivation. Neurological symptoms gradually regress. Visual acuity and muscle strength are completely restored last of all. Intermittent visual disturbances can occur over several months. Despite the most severe, sometimes incompatible with life, neurological disorders, those who have recovered from botulism do not have any consequences or persistent dysfunction of the nervous system or internal organs.

Wound botulism and infant botulism have some peculiarities. In both cases, there is no gastrointestinal syndrome and general infectious intoxication. Wound botulism has a longer incubation period (4-14 days), and the same neurological symptoms as food botulism.

Botulism in infants (infant botulism) is more often observed with artificial feeding. In addition to Cl. botulinum, the causative agents are Cl. butyricum and Cl. baratii. The first manifestations of the disease may be lethargy in children, weak sucking or refusal to suck, and constipation. When ophthalmoplegic symptoms of botulism appear, hoarse crying, weakening of the pharyngeal and sucking reflexes, choking, this should suggest the possibility of botulism and the need to urgently carry out appropriate diagnostic and therapeutic measures. Paralytic syndrome increases over 1-2 weeks. With early damage to the respiratory muscles, sudden death is possible. Severe pneumonia develops early and often.

Classification of botulism

The clinical picture distinguishes between mild, moderate and severe forms of the disease. In mild cases, the paralytic syndrome in patients is limited to damage to the oculomotor muscles: in moderate cases, it extends to the glossopharyngeal muscles. Severe cases are characterized by respiratory failure and severe bulbar disorders.

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Complications of botulism

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 patient's condition. Most often, the femoral, occipital and gastrocnemius muscles are affected. The following symptoms of botulism appear: swelling, sharp pain upon palpation, muscle infiltration, pain and difficulty in movement. Much more serious consequences can be caused by the development of secondary bacterial complications, which occur in almost all patients with severe botulism. The most typical are aspiration pneumonia, atelectasis, purulent tracheobronchitis, pyelitis, pyelonephritis, sepsis or their combinations.

Iatrogenic complications of botulism are associated with a large volume of drug therapy and invasive diagnostic and treatment methods. Since botulinum toxin significantly reduces the body's immune resistance, complications associated with invasive treatment methods (intubation, tracheostomy, artificial ventilation, urinary bladder catheterization, etc.) and caused by the addition of a secondary infection pose a certain danger. One of the most common complications of drug therapy for botulism is serum sickness, which develops in approximately every third patient who received heterologous antibotulinum serum. It usually occurs during the period of regression of neurological symptoms of botulism. A large group of complications, such as hyperglycemia, hypophosphatemia (causes weakness of the respiratory muscles, hemolysis and decreased dissociation of oxyhemoglobin in tissues), fatty liver disease,_CO2 retention in the body, electrolyte imbalance (hyponatremia, hypokalemia, hypocalcemia ), intestinal atrophy, and acalculous cholecystitis, are associated with the administration of parenteral nutrition to patients with paralytic intestinal obstruction.

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Mortality and causes of death

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