Botulism - Causes, Symptoms and Treatment .MF .

August 12, 2017 17:52 | Infectious Diseases

Botulism - one of the most severe, ostroprotekayuschih, saprozoonoznyh bacterial poisoning, with the fecal-oral transmission mechanism, characterized by lesions of the central and autonomic nervous system, with the occurrence of paresis and paralysis of striated and smooth muscle.

name comes from the Latin word botulus - sausage, because the pathogen was found there, and he's in the bodies of dead people who've also mentioned it.The emergence of this disease and to this day is associated with the consumption of salty or smoked fish and ham.

causative agent of botulism

causative agent is Clostridium botulinum, it is a wand with flagella on the periphery, so called peritrih - they provide mobility.The causative agent of the structure has a small number of features that predetermine symptoms:

• Botulinum toxin - is the most powerful exotoxin (even in comparison with tetanus), ie biologically active substances secreted from the pathogen always.There are several types of the toxin - and proteolytic non

proteolytic, ie divided by ability fermentatirovat substances for self-activation and H₂S products.People most susceptible to the 7 types of toxins (A, B, C, D, E, F, G) - but it's all variations of the same botulinum toxin, but specificity and mortality are determined by various functional components, such as the presence of the neurotoxin and the ability tohemagglutination.

• Feature activation of botulinum toxin - the action of proteolytic enzymes (or his, or gastrointestinal tract), resulting in the neurotoxin (botulinum toxin) is divided into two circuits: the H chain secures toxin receptor cell membrane, due to binding with synoptic membrane neuromuscular-Muscular cholinergic synapses (connections), innervating striated and smooth muscles.L-chain has a blocking effect on the cholinergic transmission by cleavage of specific synaptic protein (SNAP-25 and synaptobrevin - the same as in tetanus), the connection is broken synoptic bubbles presinopticheskoy membrane occurs blockage of nerve impulse transmission at normal production of acetylcholine and cholinesterase.

• toxin types B, C, D, F are also dangerous, because they can activate their own neurotoxin same enzymes, without falling into the gastrointestinal tract.In this case, moreover, that the incubation period is reduced to the same symptoms vidpoyavlyayutsya even when the product was contaminated in the mouth, but it was not swallowed.

• Specific Activity:
- Leykotoksicheskaya (inhibition of leukocyte phagocytosis without damage, ie phagocytes),
- Hemolytic (destroys red blood cells);
- Leukocyte (cleaves phospholipids of the cell membrane).

• The pathogen can be in two forms - the autonomic (zhetoy indicated by the arrow in the figure below) and spore (blue arrow) - this is important when preventive measures, because most vegetative forms of pathogenic and low stability to harmful factors.Spore forms - the ability to sporulation, ie the emergence of virtually nothing unwavering stability.Spore produced terminally, ie almost at the end, the agent takes the form of "tennis racket".

causative agent of botulism Clostridium botulinum

Stability:

1. spore form - at a temperature of 6 ° C - is stored for several months at 100 ° - 1-2 hours at 120 ° - are killed within 30minutes, but some strains can persist for several hours at this temperature.The spores are resistant to freezing and drying, even to direct UV radiation.In the dried state saved decade.The action of disinfectants is activated within a few hours of 20% formalin solution kills the pathogen within 24 hours;ethyl alcohol for 2 months;10% hydrochloric acid solution - one hour.

2. The vegetative form are unstable in the environment and, at 80 ° C die within 30 minutes.

3. toxin is destroyed at the same temperature as the vegetative form: 100 ° -10 minutes, the well is neutralized in alkali but resistant to acidic.In reducing its gastrointestinal activity than type E, which on the contrary, increases its activity 10000 times.

Botulism occurs in all regions, but more often registered in countries where the population uses a wide variety of canned food (both plant and animal content), we can say that there are no territorial restrictions.All humans are highly sensitive to the toxin, but not limited to sex and age.Seasonality also noted.

Features of the application of botulinum toxin in everyday life:

1. As biological weapons, through the production of pure toxin, where 1 g = 1 million lethal doses, ie it might be used as weapons of mass destruction.
2. As a drug for the treatment of muscle contractures in cosmetology ( "Boteks»)

Causes infection boltulizmom

natural habitat and as a result, the source is the soil, so called pathogen saprozoonozom.Water is also a source of dust, foods infected soil and intestinal contents of fish birds, honey - but in these habitats, the agent is often in the form of spore-formers and autonomic converted when creating favorable conditions: t ° = 28-35 ° C= anaerobic anoxic conditions (canned), activation of proteolytic enzymes in the digestive tract.Infection often occurs in the vegetative forms, infection with spores is possible only in two cases - when wound infection, and neonatal botulism.Way - food and contact-household.

Symptoms of botulism

incubation period is counted from the moment of introduction of the pathogen to the first clinical manifestation.It lasts about one day, but can vary from 2-12 days and that is extremely rare and only happens when botulism and wound botulism infants.Penetrating through the digestive tract, the agent activates lecithinase and leykopenicheskuyu Activity (for more details in the description of the pathogen) - they facilitate the penetration of the pathogen in glublezhaschie tissue with parallel protection against phagocytosis.During the implementation phase starts acting toxin is due to activation of proteolytic enzymes in the digestive tract and, as soon as the toxin is activated, the symptoms appear.

cholinergic synapses - the target for botulinum toxin

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 of a general clinical symptoms (headache, dizziness, possible lifting of the body up to 38 ° C temperature)

• Symptoms of gastroenteritis in 90% of cases appear in the first place during the first days of the date of useThe affected products, manifested cramping pain in the epigastric area (approximately in the stomach), vomiting, diarrhea.

• Within a few hours, joined by neurological symptoms in the form of various combinations mionevrologicheskih syndromes:

  • oftalmoplegichesky syndrome;
  • bulbar syndrome as paresis pharyngoesophageal-lingual muscles in the defeat IX (glossopharyngeal), X (vagus), XII (hypoglossal) cranial nerves;
  • defeat parasimpatiki and change with the CCC;

neurological symptoms explains

  • tropic (selective loss) to the neurons of the medulla oblongata and the motor neurons of the spinal cord;
  • feature toxin action - increases the permeability of the targeted tissue;
  • primarily affects the muscles with high functional activity, those who are in constant tension / movement (oculomotor, pharyngeal muscles, etc.)

Sometimes, gastroenteritis symptoms may or may not be, and are the first manifestations of neurological symptoms.

• Oftalmoplegichesky syndrome:

  • mesh or mist before his eyes;
  • inability to read and see nearby objects, but maintaining good vision - this is due to paresis of the ciliary muscles, the ones that change the configuration of the lens as a result of their defeat, the lens is in a constant state of relaxed, which happens when focusing on distant objects;
  • strabismus (strobizm);
  • double vision (diplopia);
  • drooping eyelids (ptosis);
  • dilated pupils not reacting to light (mydriasis);
  • uneven pupils (anisocoria);
  • nystagmus (involuntary eye movement);
  • in severe cases can cause immobility of the eyeball.

• bulbar syndrome manifested aphonia and dysphagia.Aphonia: slurred speech, with a nasal tone, muscle paresis language, hoarseness.Dysphagia due to paresis of muscles of the pharynx, the epiglottis and soft palate, resulting in evident: in swallowing violation of both solid and liquid food, the latter flows through the nose, also note popёrhivanie when trying to swallow even saliva.

• Bilateral facial nerve paresis manifested "masklike face" due to violations of mimic muscles.

• paresis diaphragm and auxiliary respiratory muscles:

  • Mobility pulmonary region limitation arises from the intercostal muscle paralysis, patients complain of a feeling of compression "as if a hoop" of the chest;
  • fragmentation speech from a sense of lack of air;
  • tachypnea (↑ respiratory rate) and shallow breathing;
  • respiratory failure may increase gradually, and suddenly - there is a sudden cessation of breathing (apnea) and "death occurs on the floor of the word";
  • in the formation of respiratory failure, also contributes to bulbar syndrome.

• The defeat of the parasympathetic nervous system:

  • dryness of the skin and mucous membranes;
  • decrease salivation;
  • violation of the innervation of the gastrointestinal tract until the development of paralytic ileus;
  • violation of urodynamics in the form of acute urinary retention or incontinence.

• Changing the part of the cardiovascular system:

  • bradycardia (decreased heart rate) alternating with tachycardia (increase in heart rate);
  • tendency to raise blood pressure;
  • violation of excitement, with the emergence of atrioventricular block (AV-block);
  • increase in shortness of breath.

• In the course of the disease is increasing muscle weakness, at first it is most pronounced in the neck muscles so the head can hang down, trying to hold her patients.Muscle fatigue can persist for up to 6 months.

• have hypoxia (↓ O₂ in the peripheral blood) of various origins in exacerbating the symptoms of importance:

  • breathing (due to paresis of the diaphragm and auxiliary respiratory muscles);
  • toxic (direct and indirect effects of the toxin through the inhibition of enzymes of the pentose phosphate shunt and K-Na-pump);
  • circulatory (because of hemodynamic instability)

duration of the disease is on average 3 weeks, provided that treatment is carried out.Neurological symptoms were restored in the reverse order: first breath, and then swallowing.The remaining symptoms - headache, twang, oftalmoplegicheskie, parasympathetic, and other neurological symptoms - take place without a certain sequence, and can be stored for a long time (up to 1.5 months or more).We recover all the symptoms goes unnoticed and does not leave any disabling consequences.Without treatment, most possibly fatal.

Features wound and infant botulism:

  • long incubation period;Infection
  • not vegetative and spore forms;
  • No GI period;
  • Botulism newborns manifests in the form of lethargy, weakness, sucking or withdrawal, delayed stool, oftalmoplegicheskie symptoms, hoarse cry, the weakening of the swallowing or sucking reflex;
  • Children more often occurs as a complication of pneumonia and are more frequent deaths.

diagnosis of botulism

1. According to the data of the epidemic - the use of home-made preserves.

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

3. Laboratory diagnosis: focus on pathogen detection in food and biomaterials of the patient (blood, washings, feces and urine), with pH (neutralization reactions) and ELISA (enzyme-linked immunosorbent assay) - these results may be ready within 8hours.

botulism causative agent under the microscope (debate)

4. Determination of the level of cardiac enzymes to determine the extent of the heart and blood vessels compensation: MB-creatine, aspartic transaminase, hydroxybutyrate, tropanin.To do this, additional wires ECG.

Treatment of botulism

1. Antitoxic protivobotudinicheskaya horse serum mono / or polyvalent (in the case of an unknown type of botulinum toxin) or human immunoglobulin protivobotulinichesky.

2. Prednisolone is introduced in parallel with the therapeutic dose of serum to prevent anaphylactic shock.For the same reasons, the sample is carried out before the introduction of small doses of the serum and, if there is an allergic reaction, the dose prednezolona increase.

3. Iz-za paresis pharyngoesophageal-speaking muscles a high risk of aspiration (blockage of the airways) and iz-za paresis diaphragm and respiratory muscles formed respiratory failure - as a result of these two factors, life-threatening, patients transferred to enteral and parenteral nutrition, as wellalso connected to the ventilator.

4. With the defeat of the myocardium, appoint cytoprotectors.

5. When bacterial complications prescribe antibiotics with a broad spectrum of action.

6. In the early stages of the pathogen in the act and in the stomach, gastric lavage, and by setting cleansing enemas, and appoint sorbents.

Nutrition during and after illness

Therapeutic feeding provides an exception of dishes rich in extractive substances, spices and fatty foods.And also prescribe diet №10.Preferred translation mixture with a high energy activity.bed or polupostelny mode.

Complications Botulism

1. Specific: myositis (often affects the hip, occipital and calf muscles, it manifests itself in the form of swelling, pain and difficulty in movement) and the defeat of nervous knots of the heart with the subsequent formation of arrhythmias.

2. Secondary bacterial complications, pneumonia, atelectasis, traheobranhit purulent, pyelonephritis, sepsis.

3. Iatrogenic (post-treatment): serum sickness, hyperglycemia, hyperphosphatemia, atrophy of the intestine.

Prevention of botulism

1. Specific - antitoxic serum protivobotulinicheskaya polyvalent (A, B, E botulinum toxin type).
2. Non-specific:

strict adherence to the rules of preparation and storage of fish / meat / vegetable semis;

heat treatment before consumption of canned food by boiling in a water bath for 15 minutes, at the same time remind you that killing only vegetative forms and spores remain intact, so before use the remaining contents of the cans, should be boiled again to destroy the spores, which germinated invegetative form.

Medical consultation for Botulism:

Question: Does the patient Contagious?
answer is no

Question: Bombazhnye banks say about the presence of botulism?
answer unequivocally reject the affected products can not, because it does not manifest itself, and is ingrained myth of the "swelling caps, softening and unpleasant smell, a rancid taste", because it speaks only of the microflora fermentativnoaktivnoy more than causative agent of botulism(in particular Clostridium Perfringens - the causative agent of gas gangrene).The causative agent of botulism can only produce N₂S (hydrogen sulfide), which is a weak density gas, and it is certainly not the strength to create a high pressure inside the cans.

therapists Shabanova IECh.

infectious disease doctor Bykov NI