botulism infectious disease

1. Botulism Presentation by

2. Botulism Definition Severe toxic-infectious disease characterized by botulinum toxin damage to the nervous system, mainly the medulla oblongata and the spinal cord, with a predominance of ophthalmoplegic and bulbar syndromes

3. Etiology - Large rods (4-9 microns) with rounded ends. - Disputes are located subterminally, giving the appearance of a tennis racket. • Mobile due to availability peritrichium • Gram positive • The capsule is not formed • Strict anaerobic The causative agents of botulism are widespread in nature and live in the soil. Optimal conditions for the growth of vegetative forms -extremely low residual pressure oxygen(0.40-1.33 kPa) and temperature mode within 28-35 ° C

4. Intestine of Animals, birds, molluscs, carcasses of dead animals (saprozoonosis); in hot countries, spores grow in vegetative forms and actively reproduce in soil, silt of water bodies etc. Spores are able to survive for several hours at a temperature of 100 ° C, and when they get into a favorable environment, they turn into vegetative forms. source of infection and transmission

5. Transmission factors - products that create anaerobic conditions at a sufficiently high temperature Sausages Canned meat smoked products special, cooked in home conditions Dried, smoked fish Canned fish Canned caviar CANNED CRABS Canned squid

6. Transmission factors - products that create anaerobic conditions at a sufficiently high temperature CANNED FOOD, ESPECIALLY Home made from mushrooms, cucumbers,beans and honey based products

7. Antigenic properties • C. botulinum forms exotoxins differing in antigenic properties and on this basis subdivided into serotypes • 7 antigenic variants of botulinum toxin are known: A, B, C (subtypes C1 and C2), D, E, F, G. • In addition to neurotoxic effects, botulinum toxin possesses leukotoxic, hemolytic and lecithinase activity

8. absorbed starting from the mouth and intestine, where it is partially activated by proteolytic enzymes --- attaches to epithelial cells and is absorbed by pinocytosis Pathogenesis into lymphatic vessels into the blood and then the blood-brain barrier toxin affects the motor neurons of the spinal motor centers, the medulla oblongata and the peripheral nervous system

9. The mechanism of action of the toxin • In the body, the toxin breaks down into 2 subcomponents: L-light and H-heavy • The H-subcomponent binds to gangliosidespresynaptic membranes motoneurons... L-subcomponent, acting as endoprotease, blocks secretion acetylcholine at synaptic gap *, thereby interrupting the nerve impulses coming from motor neuron to the muscle, leading to the development of flaccid paralysis • Death from hypoxia, less often from cardiac arrest • * at on average, 10 molecules are enough to block one synapse botulinum toxin

10. Pathogenesis:- Causes of hypoxia • Hypoxic - inhibition of the activity of large motoneurons anterior horns of the spinal cord, innervating the respiratory muscles + obturation bronchi with aspiration vomit, saliva and food due to paresis of the muscles of the larynx, pharynx and epiglottis • Histotoxic - emerging acidosis • Hemic - suppression of enzymes pentose phosphate cycle, inhibition K-Na pump • Circulatory - constriction of capillaries

11. Classification (WHO) • food botulism (the disease occurs after consumption in food products containing accumulated botulinum toxin); • wound botulism (develops when contaminated soil contect with wounds • childhood botulism (occurs in children mainly up to 6 months, when they become infected with spores of Clostridium botulinum); • botulism of unspecified nature (it is not possible to establish any connection of the disease that has arisen with the food product). According to the severity, there are mild, moderate and severe forms With a mild course in patients, paralytic syndrome is limited to damage to the oculomotor muscles; with moderate severity, the muscles of the pharynx and larynx are also affected. severe course is characterized by respiratory failure and severe bulbar disorders.

12. Incubation period • From 2-12 hours to 7 days, on average 18-24 hours MAIN SYNDROMES • Paralytic • Gastrointestinal • intoxicating

13. Pathogenesis of certain symptoms and syndromes in botulism • Breathing disorder (frequent, superficial) - Paresis of the muscles of the diaphragm, abdominal muscles, intercostal muscles, hypoxia • Muscle weakness, paresis, paralysis - Impaired transmission of nerve impulses, hypoxia, metabolic disorders • tachycardia, increased blood pressure - hypoxia, increased activity of the sympathetic-adrenal system (increased content of catecholamines) • dry mouth (occurs in 100%) , impaired swallowing, nasal voice, restriction of tongue movement - Damage to the nuclei of the V, IX, XII cranial nerves • Convergence disorder, ptosis, diplopia - Damage to the nuclei of the III, IV cranial nerves • Wide pupils, visual impairment, accommodation - Defeat nmciliares • Amimia - Damage to the facial nerve NEUROLOGICAL DISORDERS ARE ALWAYS SYMMETRIC. NO SENSITIVITY DISTURBANCES, seizures, mental disorders, no spastic paralysis, no intoxication with advanced neurological symptoms

14. Pathogenesis of certain symptoms and syndromes in botulism. • Bloating, constipation - suppression of the function of the vagus nerve, an increase in the content of catecholamines • Vomiting, one or two loosening of the stool in the initial period - Local action botulinum toxin, act other flora contained in the product (Cl.perfringens, Cl.aedematies) • Initial temperature is the effect of other flora contained in the product (Cl.perfringens, Cl.aedematies) • urinary retention - Damage to the autonomic nervous system, predominance of sympathetic activity, decreased bladder tone • Pale skin - Narrowing of skin capillaries • THE EFFECT OF BOTULOTOXIN IS FULLY REVERSIBLE

15. Complications • Aspiration pneumonia, atelectasis, secondary infection associated with invasive methods of therapy (mechanical ventilation, bladder catheterization) • Mumps (due to a secondary infection, due to hyposalivation) • Serum sickness • Botulinum myositis is a specific complication of a severe course - at 2-3 weeks of the disease, painful manifestations in the muscles appear, resembling ordinary myositis. Calf muscles are often affected

16. Diagnostics Clinical picture Isolation of botulinum toxin and the causative agent of botulism from the patient (gastric lavage, intestines, vomit, feces, blood - from a vein 8-10 ml before serum injection) and from the product that the patient consumed. Sowing on Kitt-Tarozzi media , casein-mushroom, Hottinger's broth, etc. Then neutralization of the toxin in mice by injecting different types of serum

17. Differential diagnosis Most often, • food toxic infection, • violation of cerebral circulation, • hypertensive crisis, • encephalitis, • mushroom poisoning, • myasthenia gravis

18. Treatment • Gastric lavage to remove residual toxin from the stomach (first with boiled water to collect material - then 2-5% solution of soda); introduction of enterosorbents through the probe. ENZYMES DO NOT GIVE! • intestinal dialysis (2-5% solution soda); • antitoxic serum (type A, C, E each 10,000 ME, type B 5,000 ME, type F - 3 thousand); in severe cases, a double dose. Coverglucocorticoids... i / m or i /v by frequently • parenteral administration of infusion media for the purpose of detoxification, correction of water-electrolyte and protein disorders; • antibiotic therapy (chloramphenicol,; • hyperbaric oxygenation as a remedy hypoxia; • treatment of complications Promising - homologous plasma and human anti-botulinum immunoglobulin

19. prevention • Compliance with sanitary and hygienic measures • Boiling canned food for 10-15 minutes