Botulism - Causes, symptoms and treatment. MF.

Botulism is one of the most severe, acute, saprozonotic bacterial toxic infections, with a fecal-oral transmission mechanism, characterized by central and autonomic nervous system damage, paresis and paralysis of striated and smooth muscles.

The name comes from the Latin word botulus - sausage, because the pathogen was found there, and it is in the bodies of dead people who used it. The occurrence of this disease and to this day is associated with eating salted or smoked fish, as well as hams.

causative agent of botulism

The causative agent is Clostridium botulinum, it is a stick with flagella on the periphery, therefore called peritrich - they provide mobility. In the structure of the pathogen there is a small number of features that predetermine the symptoms:

• Botulinum toxin - is the strongest exotoxin( even in comparison with tetanus), ie a biologically active substance, excreted from the pathogen always. There are several types of this toxin - proteolytic and non-proteolytic, that is, they are divided according to their abilities to ferment substances for self-activation and H₂S products. People are most susceptible to 7 types of toxins( A, B, C, D, E, F, G) - but these are all variations of the same botulinum toxin, but specificity and lethality are determined by various functional components, such as the presence of a neurotoxin and the ability tohemagglutination.

• A special feature of botulinum toxin activation is the action of proteolytic enzymes( either its own or in the digestive tract), as a result of which the neurotoxin( botulinum toxin) is divided into 2 chains: the H chain provides attachment of the toxin to the cell membrane receptor, by binding to the synoptic membrane of the neuro-muscular cholinergic synapses( joints) innervating transversely striated and smooth musculature. The L-chain has a blocking effect on the cholinergic transfer by cleavage of specific synaptic proteins( SNAP-25 and synaptobrevin-similarly as in tetanus), the synaptic vesicle is not connected to the presynoptic membrane, the nerve impulse is blocked during normal production of acetylcholine and cholinesterase.

• The toxin types B, C, D, F are also dangerous, because they can activate their own neurotoxin with their own enzymes, without getting into the digestive tract. In this case, not only is the incubation period shortened, moreover, the symptoms appear even when the infected product was in the mouth, but was not swallowed.

• Specific activity:
- Leukotoxic( phagocytosis suppression without leukocyte damage, ie phagocytic cells),
- Hemolytic( destroys red blood cells);
- Leukocyte( cleaves the phospholipids of the cell membrane).

• The causative agent can be in two forms - vegetative( indicated by the arrow in the figure below) and spore( blue arrow) - this is important in preventive measures, because vegetative forms are most pathogenic and resistant to harmful factors. Spore form - the ability to spore, that is, the emergence of almost nothing unshakable stability. The spore is formed in a terminal way, ie practically at the end, the causative agent takes the form of a "tennis racket".

botulinum causative agent Clostridium botulinum

Stability:

1. Spore form - at a temperature of 6 ° C - persists for several months, at 100 ° - 1-2 hours, at 120 ° - perishes within 30 minutes, but some strains may persistand a few hours at this temperature. Spores are resistant to freezing and drying, even to direct UV.In the dried state, decades remain. The action of disinfectant solutions is activated for several hours: a 20% formalin solution kills the pathogen within 24 hours;ethyl alcohol for 2 months;10% solution of hydrochloric acid - in an hour.

2. The vegetative form is unstable in the external environment and, at 80 ° C, dies within 30 minutes.

3. The toxin is destroyed at the same temperature as the vegetative form: 100 ° -10 minutes, well neutralized in alkali, but resistant to acidic. In the gastrointestinal tract reduces its activity, in addition to type E, which, on the contrary, increases its activity by 10,000 times.

Botulism occurs in all regions, but is more often recorded in countries where the population consumes a large number of different canned foods( both vegetable and animal), it can be said that there are no territorial restrictions. All people are highly sensitive to toxin, with no restrictions in the field and age. Seasonality is also not marked.

Features of the application of botulinum toxin in everyday life:

1. As a biological weapon, by obtaining a pure toxin, where 1r = 1 million lethal doses, ie it can be used as a means of mass destruction.
2. As a medicine for the treatment of muscle contractures in cosmetology( "Botex")

Causes of infection with boltulism

The natural habitat and, as a consequence, the source, is the soil, so the causative agent is called saprozonosis. Also, the source is water, dust, food contaminated with soil, intestinal contents of fish and birds, honey - but in these habitats, the causative agent is more often in spore form and becomes vegetative when creating favorable conditions: t ° = 28-35 ° C,anaerobic = anoxic conditions( canned food), activation by proteolytic enzymes in the digestive tract. Infection often occurs in vegetative forms, infection with spores is possible only in two cases - with wound infection, and with newborn botulism. Ways - food and contact-household.

Symptoms of botulism

The incubation period is considered from the moment of introduction of the pathogen to the first clinical manifestations. It lasts up to a day, but it can vary from 2-12 days, which is extremely rare and happens only with wound botulism and botulism of newborns. Penetrating through the gastrointestinal tract, the activator activates lecithinase and leukopenic activity( more details in the description of the pathogen) - they facilitate the penetration of the pathogen into the glibrous tissue with parallel protection from phagocytosis. At the introduction stages, the toxin begins to act due to activation by the proteolytic enzymes of the gastrointestinal tract and, as soon as the toxin is activated, symptoms appear.

Cholinergic synapses - target for botulinum toxin

The period of clinical manifestations begins acutely and lasts for 3 weeks, with a gradual decrease in clinical symptoms. This period is characterized by the following:

• Acute sudden onset in the form of general clinical symptoms( headache, dizziness, possible rise in body temperature up to 38 ° C)

• Symptoms of gastroenteritis in 90% of cases come first in the first 24 hours from the time of ingestion, manifests cramping pain in the epigastric region( roughly in the region of the stomach), vomiting, diarrhea.

• Within a few hours, neurologic symptoms are combined in the form of a different combination of myoneurovascular syndromes:

• ophthalmoplegic syndrome;
• bulbar syndrome in the form of paresis of the pharyngeal muscles in lesion IX( glossopharyngeal), X( wandering), XII( sublingual) pairs of cranial nerves;
• parasympathetic involvement and change from CAS;

Neurological symptoms explain

• tropicity( selective lesion) to neurons of the medulla oblongata and motor neurons of the spinal cord;
• toxin action - increases permeability of affected tissues;
• First of all, muscles with high functional activity are affected, those that are in constant tension / movement( oculomotor, throat muscles, etc.)

It happens that there may not be any symptoms of gastroenteritis, and the first manifestations are neurological symptoms.

• Ophthalmoplegic syndrome:

• mesh or fog in front of the eyes;
• the inability to read and see nearby objects, but with good foresight - this is due to the paresis of ciliary muscles, those that change the configuration of the lens, as a result of their defeat, the lens is in a constant relaxed state that happens when focusing on distant objects;
• strabismus;
• double vision( diplopia);
• ovulation of the eyelids( ptosis);
• dilated pupils that do not respond to light( mydriasis);
• pupillary irregularity( anisocoria);
• nystagmus( involuntary movements of the eyeballs);
• in severe cases, there may be immobility of eyeballs.

• Bulbar syndrome is manifested by aphonia and dysphagia. Afoniya: speech is indistinct, with a nasal hue, the paresis of the musculature of the tongue, the hoarseness of the voice. Dysphagia is caused by the paresis of the muscles of the pharynx, epiglottis and soft palate, as a result manifests itself: a violation of the swallowing of both solid and liquid foods, the latter flows through the nose, and they also note a bump when trying to swallow even saliva.

• Two-sided paresis of the facial nerve is manifested by a "mask-like face" due to impaired mimic muscles.

• Paresis of the diaphragm and ancillary respiratory muscles:

• , the limitation of the mobility of the pulmonary margin is due to the paralysis of the intercostal muscles, patients complain of a feeling of chest compression "as if hoop";
• is the severance of speech due to a feeling of lack of air;
• tachypnoe( ↑ respiratory rate) and shallow breathing;
• respiratory failure may increase either gradually or suddenly - there is a sharp cessation of breathing( apnea) and "death occurs on the floor of the word";
• in the formation of respiratory failure, contributes to the contribution of bulbar syndrome.

• Parasympathetic nervous system damage:

• dry skin and mucous membranes;
• decreased salivation;
• violation of innervation of the gastrointestinal tract until the development of paralytic intestinal obstruction;
• violation of urodynamics in the form of acute urinary retention or involuntary urination.

• Cardiovascular change:

• bradycardia( decrease in heart rate) alternates with tachycardia( increased heart rate);
• tendency to increase blood pressure;
• impaired excitation, with the onset of atrioventricular blockade( AV blockade);
• increase of dyspnea.

• As the course of the disease grows, muscle weakness, at first it is most pronounced in the occipital muscles and therefore the head can hang, the patients try to hold it. Muscle asthenia can persist for up to 6 months.

• In exacerbation of symptoms, hypoxia( ↓ O₂ in the peripheral blood) of various genesis is of great importance:

• respiratory( due to paresis of the diaphragm and ancillary respiratory musculature);
• toxic( direct and indirect toxin action through inhibition of enzymes of the pentose phosphate shunt and K-Na pump);
• circulatory( due to hemodynamic disorders)

The duration of the disease is on average 3 weeks, provided that the treatment is performed. Neurological symptoms are restored in the reverse order: first breath, and then swallowing. Other manifestations - headache, nasal, ophthalmoplegic, parasympathetic and other neurological symptoms - go without a certain sequence and can persist for a long time( up to 1.5 months or more).In patients who have recovered, all the symptoms pass without leaving a trace and leave no disabling effects. Without treatment, the most lethal outcome is possible.

Features of wound and infant botulism:

• Long incubation period;
• Infection is not vegetative, but spore-forming forms;
• There is no gastrointestinal period;
• Newborn botulism manifests itself as lethargy, weakness of sucking or rejection of it, stool retention, ophthalmoplegic symptoms, hoarse cry, weakening of the swallowing or sucking reflex;
• Children more often experience complications in the form of pneumonia and more often lethal outcomes occur.

Diagnosis of botulism

1. According to epidemiological data - the use of canned food at home.

2. According to clinical data - localization and symmetry of the nervous system, absence of febrile / intoxication / cerebral and meningeal syndromes.

3. Laboratory diagnostics: it is aimed at detection of the pathogen in the food and biomaterials of the patient( blood, rinsing water, feces and urine), with the use of pH neutralization and ELISA - these results can be ready within 8 hours.

Pathogen of botulism under a microscope( spores)

4. Determination of the level of cardiospecific enzymes for establishing the degree of compensation from the heart and blood vessels: MB-creatine phosphokinase, aspartic transaminase, hydroxybutyrate dehydrogenase, tropanin. For this, an additional ECG is performed.

Botulism treatment

1. Antitoxic anti-turbulent horse serum mono / or polyvalent( in the case of an unknown type of botulotoxin) or human anti-botulinum immunoglobulin.

2. Prednisolone is administered in parallel with a therapeutic dose of serum to avoid anaphylactic shock. By the same reason, before the introduction of serum, the sample is administered in small doses and, if an allergic reaction is observed, the dose of prednezolone is increased.

3. Because of the paresis of the tongue-lingual muscles, the risk of aspiration( blockage of the respiratory tract) is high, and due to the paresis of the diaphragm and the respiratory muscles, respiratory failure is formed - as a result of these two life-threatening factors, the patients are transferred to probing and parenteral nutrition, andconnect to the ventilator.

4. In case of myocardial damage, cytoprotectors are prescribed.

5. For bacterial complications, antibiotics with a wide spectrum of action are prescribed.

6. In the early stages of the pathogen act through the gastrointestinal tract, by washing the stomach and setting cleansing enemas, and also assign sorbents.

Nutrition during and after illness

Therapeutic diet provides for the exclusion of foods rich in extractives, spices and fatty foods. And also prescribe a diet number 10.Preferably transfer to a mixture with high energy activity. Bed or half-bed mode.

Botulism complications

1. Specific: myositis( often affects the femoral, occipital and calf muscle, it manifests itself in the form of swelling, tenderness and difficulty in movement) and defeat of the nerve nodes of the heart with the subsequent formation of arrhythmias.

2. Secondary bacterial complications: pneumonia, atelectasis, purulent tracheobranchitis, pyelonephritis, sepsis.

3. Iatrogenic( post-treatment): serum sickness, hyperglycemia, hyperphosphataemia, intestinal atrophy.

Botulism prevention

1. Specific antitoxic anti-botulinum serum polyvalent( from A, B, E type of botulinum toxin).
2. Nonspecific:

strict adherence to the rules for the preparation and storage of fish / meat / vegetable semi-finished products;

heat treatment before using canned food by boiling in a water bath for 15 minutes, while recalling that only vegetative forms die and spores remain intact, therefore before consuming the remaining contents of canned food, it is necessary to boil again to destroy those spores that have sprouted into the vegetativeshape.

Doctor's consultation on botulism:

Question: Is the patient contagious?
Answer: No

Question: Bomb banks are talking about the availability of botulism?
Answer: it's impossible to reject product contamination, because it does not manifest itself in any way, and is an inveterate myth about "bloating, softening and unpleasant odor, rancid taste", because it speaks only of the microflora more enzymatically active than the causative agent of botulismin particular Clostridium Perfringens - the causative agent of gas gangrene).The causative agent of botulism can only produce H₂S( hydrogen sulphide), which is a weak gas in density and it certainly can not create the pressure inside the can. But still a frequent source are homemade, unchanged and unremarkable canned food, because when twisting, favorable anaerobic conditions( without O₂) are created for the pathogen, where they multiply.

Question: Is immunity formed?
Answer: it is formed, but extremely rarely, because the immune dose corresponds lethal. But even if the immunity is formed, then it is strictly type-specific, weakly expressed and not long.

Question: Are disabling post-infectious complications?
Answer: no, because the blockade of nerve impulses occurs on the synoptic, or rather at the subcellular level( the features of the action of L and H toxin chains), leaving the anatomical and tissue structures intact, the toxin action is not paralytic, but pseudo-paralytic and, itscan be eliminated without a trace by inactivation of the toxin, as a result, there will be a complete recovery of neuromuscular excitation. All types of neuromuscular stimulation are restored, in all organs and tissues, with the exception of the heart - if the ectopic focus is formed once there, as a result of uncoordinated movement, it can only be removed surgically.

Therapist doctor Shabanova I.Е.

Rehabilitation after the transferred botulism

Botulism is a serious infectious disease caused by the action of botulinum toxin( neurotoxin) with the defeat of the predominantly nervous system and the development of the neuromuscular syndrome( breathing, speech, swallowing, and damage to the organs of vision).The severity of the changes largely depends on the dose of botulinum toxin, and the symptoms( breathing disorders, speech, swallowing) with timely assistance are still reversible. However, often visual disturbances( paresis and paralysis of accommodation, damage to the optic nerves with the limitation or decrease of vision, narrowing of the visual fields) have certain consequences in the form of atrophy of the optic nerves.
Features of the development of the disease determine the promptness of the provision of medical care to such patients, and also require a serious attitude towards adherence to the entire range of rehabilitation activities during the recovery( or reconvalescence).

Rehabilitation program after the transferred botulism

1) Regimens( inpatient treatment up to 10 days after the disappearance of all neurological disorders with subsequent issuance at discharge of the sick leave, extended for another 7-14 days depending on the severity of the transferred form of the disease).

2) Medical supervision( clinical examination) of patients implies monitoring of the patient's resident site within 14 days after discharge, and consultation and observation by a neurologist and cardiologist( if there is a myocarditis in the hospital), an eye specialist with consequences on the organs of vision. In the future, the observation is established until complete recovery with a frequency of once every 6 months. Medication in the recovery period is prescribed according to indications depending on the residual phenomena and is determined by the attending physician( cardiovascular drugs, nootropics, vitamin therapy, drugs for the treatment of optic atrophy, and others).

3) Recommendations for physical activity include: restriction of physical activity for a period of 3 or more( if necessary) a month, release from heavy physical labor, exclusion from specialized sports, any work related to stress on the visual analyzer. In other words, rational employment for a period of at least 2-3 months. The conclusion on rational employment is determined by the KEK( clinico-expert commission) of the medical-prophylactic institution( polyclinic), including a therapist, neurologist or cardiologist, deputy. Ch.doctor and others.

4) Health food during the recovery period should include a full-fledged diet for composition and calories. However, several basic principles should be observed: adherence to the food intake( 4x intake at approximately the same time);preservation of the principle of chemical shivering of the gastrointestinal tract during the period of convalescence after botulism( restriction of acute and fatty foods, restriction of salt intake, predominance of vegetable fats over animals, sufficient intake of protein);sufficient intake of vitamins with food intake or with the help of specialized multivitamin complexes( vitrum, centers, compliment, alphabet and many others).

5) Physiotherapy procedures can be widely applied after the transferred botulism. Water procedures( baths, showers), hardening procedures, electrosleep, hyperbaric oxygenation( inhalation of oxygen at excess or normal pressure), which will eliminate the residual effects of hypoxia in acute course of botulism, are carried out to them. Shows general health procedures( general massage, exercise therapy, swimming pool).

6) Sanatorium treatment during rehabilitation with visits to institutions for patients with diseases of the nervous system.

The doctor infektsionist Bykova N.I.