The epidemiological factor for botulism is. The causative agent of botulism
Ecology of clostridia.
Private microbiology
8. Clostridia(lat. Clostridium) is a genus of gram-positive, obligate anaerobic bacteria capable of producing endospores.
Clostridia are part of the normal flora of the gastrointestinal tract and female genital tract. Sometimes they are found in the mouth and on the skin.
Bacteria of the genus Clostridium produce the most powerful known poisons - botulinum toxin (C. botulinum), tetanospasmin (C. tetani), ε-toxin C. perf. and others.
Botulism (from botulus - sausage) is food poisoning that occurs in the form of a toxic infection and is accompanied by damage to the nuclei of the medulla oblongata.
Normally, they are part of the normal microflora of the gastrointestinal tract of animals (especially ruminants) and humans - they digest food, enhance peristalsis and at the same time produce toxins, which are immediately destroyed by juice proteases.
They are released into the environment with fecal matter and become spore-like, and remain there for decades. The reservoir of clostridia is the soil. Clostridial anaerobic infection has an exogenous origin - a wound infection. The entrance gate is a wound in which anaerobic favorable conditions are created for the transition of the spore form to the vegetative one.
Botulinum toxin is not destroyed by digestive tract enzymes. Its peculiarity is its absorption through the mucous membrane of the stomach and intestines, after which the latter is carried by the bloodstream throughout the body. The toxin selectively affects the cholinergic parts of the nervous system. The paralysis of various muscle groups characteristic of botulism is associated with the cessation of acetylcholine release at nerve synapses, while cholinesterase activity is not significantly impaired. Paralysis of the muscles of the larynx, pharynx and respiratory muscles leads to impaired swallowing and breathing, which contributes to the occurrence of aspiration pneumonia caused by secondary microflora. Patients usually die from respiratory paralysis or from a secondary infection of the respiratory system.
Specific treatment. The main thing in the specific treatment of botulism is the timely administration of anti-botulinum antitoxic serums in order to neutralize botulinum exotoxin. First, antitoxic serum of four serovars (A, B, C, E) is administered in equal doses, after establishing the serovar-serum of the corresponding serovar. At the same time, patients are injected with polyanatoxin (A, B, C and E) to stimulate the production of antibodies.
9. Corynebacteria(lat. corynebacterium) is a genus of gram-positive rod-shaped bacteria.
Corynebacterium diphtheriae is the causative agent of one of the most well-known human infections - diphtheria.
Corynebacteria are normally present in the human colon (Ardatskaya M.D., Minushkin O.N.).
general characteristics.
The causative agent of diphtheria - Corynebacterium diphteriae - is a rod located in a smear in pairs, in the shape of the letters V, Y, X.
At both ends of the diphtheria bacillus there are grains of volutin, which, when stained with alkaline methylene blue according to Leffler, are stained more intensely than the cytoplasm (the phenomenon of metachromasia), and according to Neisser - dark brown against the background of light yellow cytoplasm).
Grows on complex nutrient media, forming (virulent version) R-form colonies, similar to a daisy flower. Forms an exotoxin, which causes the development of diphtheria.
The content of the article
Botulism(synonyms for the disease: alantiasis, ichthyism) - a foodborne toxic infection that occurs as a result of consuming products infected with the botulism bacillus and its exotoxin; characterized by severe damage to the nervous system, predominantly cholinergic structures of the medulla oblongata and spinal cord, ophthalmoplegic, phonolaryngoplegic syndromes, paresis (paralysis) of the elms involved in the act of swallowing, breathing, general muscle (motor) weakness.Historical data of botulism
The name of the disease comes from Lat. botulus - sausage. The first reports of botulism as poisoning of people with blood sausage were made in 1817 by the doctor J. Kerner, who described in detail the epidemiology and clinical picture of the disease during its outbreak, when 122 people fell ill and 84 people died. Similar poisonings caused by eating smoked fish (hence the name “ichthyism”) were described in Russia in 1818 by Sengbusch, as well as by N.I. Pirogov, who studied pathomorphological changes in the human body during botulism.The causative agent of the disease was discovered in 1896 p. E. Van Ermengem, in his study of the spleen and colon in persons who died from botulism, and also isolated by him from the ham that caused the outbreak of the disease, was named Bacillus botulinus. A similar pathogen was isolated by V. S. Konstansov in 1903 while studying poisoning caused by red fish.
Etiology of botulism
The causative agent of botulism is Clostridium botulinum- belongs to the genus Clostridium, family Bacillaceae. Morphologically, it is a large, gram-positive rod with rounded ends, 4.5-8.5 µm in length and 0.3-1.2 µm in width, inactive, and has flagella. Forms spores in the external environment.There are 7 CI serovars. botulinum: A, B, C (Cu and C2), D, E, F, G. In patients with botulism, serovars A, B, E are more often isolated.
The causative agent of botulism- absolute anaerobe, optimal growth temperature and toxin formation is 25-37 ° C, at 6-10 ° C the formation of toxins is delayed. It grows on ordinary nutrient media; the pure culture has a pungent odor of rancid oil. Under conditions of sterilization with flowing steam at a temperature of 120 ° C, spores die within 10-20 minutes.
Vegetative forms of the pathogen are not resistant to environmental factors and quickly die when heated above 80 ° C, unlike spores, which can withstand boiling for 5-6 hours. The spores are relatively resistant to disinfectants. In a 5% formaldehyde solution they remain viable for 24 hours.
Clostridia botulism produces neurogropnium exotoxin of very strong strength, which belongs to the most powerful biological poisons. Botulinum exotoxin, unlike tetanus and diphtheria, is resistant to the action of gastric juice and is absorbed unchanged, and botulinum toxin serovar E is even activated by enzymes of gastric juice, as a result of which its biological activity in the intestine increases 10-100 times. The toxins of each serovar are neutralized only by homologous antibotulinum sera.
Botulinum toxin is heat labile. When boiled, it inactivates in 5-10 minutes. Large concentrations of table salt (more than 8%), sugar (more than 50%), as well as high acidity of the environment weaken the effect of botulinum toxin.
Epidemiology of botulism
There is no common idea about the source of infection for botulism. Most researchers classify the causative agent of botulism as ordinary soil saprophytes. The main reservoir of infection is warm-blooded herbivores, in whose intestines the microorganism multiplies and, with excrement, enters the soil in large quantities, where it can persist in the form of spores for a long time. From the soil, spores can land on food and, under favorable anaerobic conditions, germinate into vegetative forms to form a toxin.Transmission factors can be products contaminated with soil, in which toxin and living microorganisms accumulate, but most often the cause of the disease is the consumption of infected canned products (especially homemade): mushrooms, meat, vegetables, fruits, as well as sausages, ham, dried fish, etc. Reproduction of the pathogen does not change the taste of the product. The pathogen reproduces, as a rule, by nests in the thickness of sausage, balyk or other product, where anaerobic conditions are created. This explains isolated cases of botulism due to group consumption of the same product.
Canned goods infected with clostridia botulism usually swell (bombing), although the absence of bombing does not indicate the safety of the product.
Botulism is recorded in all countries of the world in the form of sporadic cases and cluster outbreaks. Susceptibility to botulism is high and does not depend on gender and age. Seasonality is autumn-winter due to the large consumption of canned foods during this period. A person with botulism is not dangerous to others.
After an illness, type-specific antitoxic and antibacterial immunity is formed. Repeated cases of botulism are known that were caused by other serotypes of clostridia.
Pathogenesis and pathomorphology of botulism
The disease develops as a result of penetration into the digestive canal along with food by vegetative forms of the pathogen and botulinum toxin, which is the main pathogenetic factor, although the role of the pathogen itself is undoubted in the pathogenesis of botulism. Infection is possible due to penetration of the toxin through the respiratory tract with dust or aerosols (bacteriological weapons), as well as in an experiment.Absorption of the toxin into the bloodstream begins in the oral cavity, but the main part of it is absorbed in the stomach and upper parts of the small intestine. Resorption of botulinum toxin causes a sharp spasm of blood vessels, which determines the clinical picture of the initial period of the disease (pallor of the skin, headache, dizziness, discomfort in the heart). With the blood, the toxin enters all tissues and organs. The motor neurons of the spinal cord and medulla oblongata are predominantly affected, the release of acetylcholine at neuromuscular synapses is inhibited, and the depolarization of muscle fibers is also disrupted, which causes the development of ophthalmological and bulbar disorders. In addition, botulinum toxin can suppress tissue respiration in the brain.
A variety of pathological changes that are caused by the influence of botulinum toxin indicate the leading role of hypoxia in the pathogenesis of botulism. All its types - hypoxic, histotoxic, hemic and circulatory - are caused both by the direct influence of botulinum toxin and indirect (catecholaminemia, acidosis, etc.), which leads to a complex of disorders that determine the clinical picture of the disease. It has been experimentally established that the simultaneous administration of several types of botulinum toxin results in additive toxic effects.
The infectious factor in botulism occurs when vegetative forms of the pathogen penetrate from the intestines into organs and tissues, where it multiplies and produces toxins, which is confirmed by the release of CI. botulinum from various organs (including the brain) when examining human corpses within 2 hours after death. This mechanism of disease development occurs if infected food products contain small doses of the toxin, but are significantly contaminated with spores of the pathogen. In this case, there is a long incubation period (about 10 days).
It has been proven that botulinum toxin suppresses the phagocytic activity of the immune system, increases tissue permeability to the pathogen, thereby creating conditions for the activation of clostridia in the body. Confirmation of the role of the pathogen in the pathogenesis of botulism, in addition to the long incubation period and the detection of clostridia in organs and tissues of the body, is the undulating course and relapses of the disease in individual patients, the presence of wound botulism, and the occurrence of botulism in newborns. Recently, cases of wound botulism, which develops when soil infected with spores enter a wound, have become more frequent.
Neonatal botulism is rarely reported.
Morphological changes in organs and tissues during botulism are not specific. They are caused primarily by the dissociation between the reduced supply of oxygen to the tissues against the background of an increased need for it, on the one hand, and a reduced possibility of its absorption, on the other. Characterized by severe hyperemia of internal organs, accompanied by multiple small and large hemorrhages. In addition to hemorrhages, in the brain tissue, degenerative-necrotic changes, damage to the vascular endothelium, and thrombosis are observed. The medulla oblongata and pons are more affected. In the digestive canal, hyperemia of the mucous membrane and hemorrhages are found throughout its entire length. The intestinal vessels are dilated, injekovani (“marble” pattern of the serous membrane). Changes in muscle tissue are significant. The muscles have a “cooked” appearance; upon microscopic examination, attention is drawn to the disappearance of the characteristic structure of striped muscle fibers, stasis in the capillaries, and hemorrhages.
Botulism Clinic
The incubation period for botulism lasts from 2 hours to 10 days (on average 6-24 hours). The duration of the incubation period depends on the dose of botulinum toxin that enters the body with food.Although the entrance gate of infection is predominantly the digestive canal, dyspeptic disorders are observed in only 1/3 of patients. In this case, the disease begins with nausea, abdominal pain (more in the epigastric region), short-term vomiting, flatulence, constipation, although diarrhea without pathological impurities is possible. Dyspeptic manifestations rarely last longer than 12 hours, and not only pass without a trace, but can also change to the opposite as the nervous system is damaged: diarrhea - constipation, vomiting - extinction of the gag reflex. Characterized by dryness of the oral mucosa and thirst.
Body temperature remains normal, rarely rising to low-grade fever. Patients complain of headache, dizziness and, typically, progressive muscle (motor) weakness (“wobbly” legs), as a result of which the patient sometimes cannot hold a glass in his hand.
After 4-6 hours from the onset of the disease, signs of damage to the nervous system appear, which can be combined into three main syndromes: ophthalmoplegic - visual impairment; phagoplegic - swallowing disorders; phonolaryngoplegic - speech disorders. Patients complain of deteriorating vision, “mesh”, “fog” before the eyes, double vision of objects. Due to accommodation paresis, reading ordinary text is difficult, letters “scatter” before the eyes. Convergence disorders, paralytic eyelid ptosis, mydriasis, anisocoria, and sluggish pupillary reflex are observed. Some patients may have strabismus (strabismus), nystagmus.
The optic nerve is not affected, the fundus of the eye remains almost unchanged. Bulbar disorders due to damage to the nuclei of the IX and XII pairs of cranial nerves are characterized by impaired swallowing and speech. Patients are unable to swallow solid, and in severe cases, liquid food; coughing is observed due to the penetration of food particles into the respiratory tract. The voice becomes nasal, hoarse, weak, its pitch and timbre changes, speech is slurred, and aphonia often develops. In case of paresis of the muscles of the soft palate, liquid food is poured through the nose.
Main symptoms of the disease: deterioration of vision, swallowing and speech are sometimes combined into the “three D” syndrome - diplopia, dysphagia, dysarthria. Despite severe damage to the nervous system, the consciousness of patients with botulism is always preserved; the sensitive area, as a rule, is not impaired.
Dangerous manifestations of botulism can be disorders of the respiratory system, characterized by a decrease or disappearance of the cough reflex, paresis of the respiratory muscles of varying degrees and manifested by difficulty in diaphragmatic breathing, limited function of the intercostal muscles, and disturbance of the breathing rhythm until it stops (apnea). Patients complain of lack of air, shortness of breath, a feeling of heaviness in the chest, and quickly get tired during a conversation. The respiratory rate can reach 30-35 respiratory movements per minute or more. From the circulatory system, muffled heart sounds, expansion of the boundaries of relative dullness, systolic murmur over the apex of the heart, and tachycardia are observed. Blood pressure increases slightly due to the vasoconstrictor effect of the toxin. Neutrophilic leukocytosis with a shift in the leukocyte formula to the left and a slightly increased ESR are possible. The liver and spleen, as a rule, are not enlarged.
A mild form of botulism is characterized by the absence of damage to the central nervous system or progresses with a rapid reverse development of neurological symptoms in the form of minor visual and swallowing disorders, without breathing problems.
In the case of severe botulism, deep damage to the central and peripheral nervous system is observed. The incubation period is often reduced to 2-4 hours. The first symptoms of the disease are often bulbar disorders and visual impairment. Along with ophthalmoplegic syndrome, dysphagia, aphonia, and the inability to push the tip of the tongue beyond the edge of the teeth develop very quickly. Patients are sharply inhibited, have their eyes closed all the time as a result of ptosis, and, if necessary, open their eyes by lifting their eyelids with their fingers. The skin is pale, often with a cyanotic tint. Skeletal muscle tone is reduced. Heart sounds are sharply muffled, extrasystole and tachycardia are possible (about 130 beats per minute). Respiratory disorders develop quickly: tachypnea - 40 respiratory movements in 1 minute or more, shallow breathing, with the participation of auxiliary muscles. In the final phase of the disease, Cheyne-Stokes respiration develops. Death occurs from respiratory paralysis.
In case of recovery, the period of convalescence can be extended to 6-8 months. In some patients, disability persists for a year. The period of convalescence, as a rule, is characterized by asthenia and functional disorders in the circulatory organs and nervous system.
Complications of botulism
Due to swallowing disorders in patients with botulism, aspiration pneumonia is a common complication. Myocarditis develops less frequently, and myositis develops during the period of convalescence.The prognosis is always serious. With timely implementation of adequate treatment measures, it is possible to significantly reduce mortality, and if specific treatment is not carried out, mortality reaches 15-70%.
Diagnosis of botulism
The main symptoms of the clinical diagnosis of botulism are the acute onset of the disease with normal or subfebrile temperature, dyspeptic manifestations (nausea, pain in the epigastric region, short-term vomiting, dry mouth, flatulence, constipation), which are quickly joined by ophthalmoplegic and bulbar disorders - double vision, “mesh”, “fog” before the eyes, mydriasis, strabismus, disorders of swallowing, speech, breathing, progressive muscle (motor) weakness. It is necessary to take into account the data of the epidemiological anamnesis, the patient’s consumption of canned foods, sausages, smoked fish, especially homemade ones.Specific diagnostics is based on the identification of botulinum toxin or the causative agent of botulism in material obtained from the patient (blood, vomit, gastric lavage, food debris), as well as in products that could cause the disease.
To detect botulinum toxin in the blood, a neutralization reaction is used on white mice. For the study, blood in an amount of 5-10 ml is taken from a vein (before administering the therapeutic serum to the patient). Experimental mice are injected intraperitoneally with 0.5 ml of citrated blood (serum) of the patient, and animals in the control group are injected with polyvalent antibotulinum serum. If the experimental animals died, and the animals from the control group survived (neutralization of the toxin), the diagnosis of botulism can be considered confirmed. In the future, a similar study is carried out using monovalent antitoxic sera A, B and E to determine the type of pathogen. In a similar way, the toxin is detected in the filtrate of suspicious products, washing water, vomit, urine, and feces.
Bacteriological research is carried out by inoculating the test material on Hotinger broth or Kitt-Tarotsi medium and others. Cultivation of the pathogen is accompanied by gas formation. Identification of the pathogen is carried out by bacterioscopy, and its toxin - using a neutralization reaction on white mice.
Differential diagnosis of botulism
Differential diagnosis is carried out with food poisoning, encephalitis, bulbar form of poliomyelitis, diphtheria polyneuritis, poisoning with inedible mushrooms, methyl alcohol, belladonna, etc.Foodborne toxic infections are characterized by fever, vomiting, abdominal pain, diarrhea, sometimes with mucus in the stool, but, unlike botulism, ophthalmoplegic and boulevard disorders are not observed.
With stem encephalitis, as well as with the boulevard form of polio, there may be paresis of the soft palate, dysphagia, hoarseness, slurred speech, damage to cranial and other nerves. However, with botulism, ophthalmoplegia often develops, damage to the cranial and other nerves is usually symmetrical, there are no pathological reflexes, changes in the fundus of the eye, there are no disorders of consciousness, or changes in the cerebrospinal fluid. At the onset of the disease there is no fever, the necessary epidemiological anamnesis data.
In patients with diphtheria polyneuritis, disturbances in accommodation, swallowing, paresis of the respiratory muscles, often with swelling of the subcutaneous cervical tissue, which are usually combined with myocarditis, are possible.
Methyl alcohol poisoning is accompanied by signs of ophthalmoplegia, nausea, vomiting, but intoxication, static disturbances, sweating, tonic convulsions, and damage to the optic nerve are also observed, which is not observed with botulism.
In case of belladonna poisoning, attention is drawn to nausea, vomiting, mydriasis, dry mucous membranes, but, unlike botulism, there are no characteristic excitations and disorders of consciousness (hallucinations, delirium), there is no ptosis.
Treatment of botulism
All patients with botulism are subject to mandatory hospitalization in an infectious diseases hospital; in case of breathing disorders - to the intensive care unit. The first-priority treatment measure is exclusively tube (!) Gastric lavage with a 5% sodium bicarbonate solution. Washing should be carried out with a large amount of solution (8-10 l) until the wash water is clean. After rinsing, it is advisable to introduce sorbents (activated carbon, aerosil) into the stomach, as well as perform a high cleansing siphon enema. The introduction of saline laxatives is not advisable due to partial or complete paresis of the intestines. Gastric and intestinal lavage is a mandatory procedure regardless of the duration of the illness.In order to neutralize the toxin circulating in the bloodstream, antibotulinum antitoxic serum is used. The effectiveness of serotherapy is highest in the early period of the disease, since the toxin freely circulating in the blood is quickly bound by body tissues. If the type of pathogen is unknown, a mixture of antitoxic sera of various types is administered. One therapeutic dose contains 10,000 AO serums of types A and E and 5000 AO serums of type B. In all cases, serums are administered according to the Bezredki method: 0.1 ml of diluted 1: 100 serum intradermally, after 20-30 minutes (if there is no reaction to administration) -0.1 ml of undiluted serum subcutaneously and after another 20-30 minutes (if there is no reaction to the injection) - the entire therapeutic dose, which is administered heated to 37 ° C only intramuscularly.
The duration of serotherapy should not exceed 2-3 days. Patients with severe forms of botulism are administered four therapeutic doses on the first day (the first administration is 2-3 doses and after 12 years - one dose). On the second day, two doses are administered with an interval of 12 hours. If necessary, one dose is administered on the 3-4th day. Patients with moderate forms of botulism are administered 1-2 doses of serum for three days. In case of mild botulism, one dose of serum is administered once.
Due to the toxic-infectious nature of the disease, to prevent the formation of vegetative forms of the pathogen in the body and further endogenous toxin formation, the use of antibacterial agents is mandatory. Prescribe chloramphenicol 0.5 g 4 times a day for 6-7 days, tetracycline 0.25 g 4 times a day for 6-8 days. In severe forms and the threat of developing pneumonia, antibiotics (semi-synthetic penicillins, cephalosporins, etc.) should be used.
Parenterally.
Since even high doses of botulinum toxin do not induce the production of antitoxic antibodies, some authors recommend administering a mixture of botulinum toxoids types A, B, E (100 units of each type) three times subcutaneously with an interval of 5 days to activate humoral immunity.
Along with specific treatment, nonspecific detoxification agents are used. Saline solutions, 5% glucose solution, and rheopolyglucin are administered intravenously. In case of dysfunction of the circulatory system (tachycardia, decreased AT), cardiac glycosides, camphor, sulfocamphocaine, and glycocorticosteroids are recommended. To restore the function of the nervous system, strychnine is prescribed, and during the period of convalescence - proserine, or galantamine; hyperbaric oxygen therapy (HBO). If breathing problems progress, the use of mechanical ventilation (ALV) may become necessary.
Indications for transfer to mechanical ventilation are:
a) apnea,
b) tachypnea over 40 respiratory movements per minute, increasing bulbar disorders,
c) progression of hypoxia, hypercapnia,
d) the need to ensure that the respiratory tract is cleared of mucus.
During the period of convalescence, the use of physiotherapeutic procedures is effective.
Prevention of botulism
The leading role in the prevention of botulism is played by strict adherence to sanitary and hygienic standards and rules in the production, transportation, and storage of food, especially canned food, sausages, salted and smoked fish. It is very important to prevent soil contamination of raw materials and finished products. Canned food must undergo long-term sterilization; bomb jars must be rejected. It is of great importance to explain to the population the rules of home canning.During group outbreaks of botulism, all persons who consumed a suspicious product are washed with their stomachs and intestines, and prophylactically administered with antibotulinum serum, 5000 AO of each type. Leftover food that causes illness is sent for bacteriological testing. For the purpose of specific prevention, risk groups (laboratory technicians, researchers working with botulinum toxin) are immunized with botulinum polyatoxin.
Botulism- an acute infectious disease that develops as a result of consumption of food products in which the neurotoxin Clostridium botulinum (botulinum toxin) has accumulated, occurring with damage to the nervous system and the development of flaccid paralysis of striated and smooth muscles.
Etiology: Clostridium botulinum - Gr+ rods, strict anaerobes that produce neurotoxin (botulinum toxin) - the most powerful toxin, 1 g of purified botulinum toxin - up to 1 million doses lethal for humans.
Epidemiology: food botulism is isolated - the result of eating foods in which a toxin has already accumulated (most often mushrooms, vegetables, fish and home-canned meat) and wound botulism - caused by a toxin that is formed under anaerobic conditions by contaminated Cl spores. botulinum wounds.
Pathogenesis: entry of a neurotoxin consisting of a heavy and light chain linked by a disulfide bond into the gastrointestinal tract (wound) and further into the blood --> binding of the heavy chain to receptors on the presynaptic membrane of motor neurons of the peripheral nervous system --> internalization of the active toxin in the form of an endosome - -> translocation of the toxin into the cytosol using the heavy chain --> enzymatic cleavage of target proteins (synaptobrevin and celubrevin) using the light chain --> disruption of Ca-dependent ACh release and nerve impulse transmission --> functional denervation of muscles --> bilateral descending flaccid muscle paralysis --> activation of the synthesis of neurotrophic factors --> development of additional axon processes that form new neuromuscular synapses (the reinnervation process takes several months, which explains the period of direct action of botulinum toxin); the effects of botulinum toxin are limited to the functional blockade of peripheral cholinergic nerve endings (neuromuscular junctions, postganglionic parasympathetic nerve endings, peripheral ganglia); adrenergic and sensory nerves are not involved.
Clinical picture of food botulism:
Incubation period 18-36 hours (from 6 hours to 10 days)
The onset of the disease can be acute or gradual, the course is mild or fatal on the 1st day of the disease
Common cardiac signs of botulism:
1) absence of fever (or it may be caused by other pathogens and combined with the syndromes of acute gastritis, gastroenteritis or gastroenterocolitis)
2) symmetry of neurological symptoms
3) preservation of consciousness (unless severe respiratory failure has occurred)
4) absence of sensory disorders
In the clinic neurological symptoms prevail as progressive descending weakness or paralysis primarily of the muscles innervated by the cranial nerves, followed by involvement of the muscles of the neck, upper extremities, trunk and lower extremities
The earliest complaints are dry mouth, difficulty examining nearby objects, when reading regular font (haze or grid before the eyes), double vision (diplopia), then dysphonia (change in voice, its roughness, hoarseness), dysarthria (unclear speech) appears , blurred, often with a nasal tint), dysphagia (feeling of a lump in the throat, liquid food being thrown into the nasopharynx) and severe muscle weakness; with severe intoxication bulbar palsy syndrome and ophthalmoplegic syndrome can reach maximum manifestations with the development of aspiration of food, water, saliva
Difficulties in defecation and urination are characteristic (due to paralysis of the smooth muscles of the gastrointestinal tract and bladder)
On examination, patients are conscious, adynamic, have a hypomimic, mask-like face, characterized by bilateral ptosis, dilated pupils, sluggish or unresponsive to light, sometimes strabismus (strobism), nystagmus; the mucous membrane of the oropharynx is dry, hyperemic; paresis of the soft palate is noted, the reflex from the soft palate is weakened or absent
Due to weakness of skeletal muscles, patients are inactive and unsteady when walking; tendon reflexes are reduced or absent
Breathing is frequent, shallow, respiratory sounds are weakened; involvement of the respiratory muscles leads to progressive respiratory failure with terminal outcome without mechanical ventilation
Characterized by severe paresis of the gastrointestinal tract, manifested by moderate bloating and a sharp weakening of peristaltic sounds
Features of wound botulism: incubation period about 10 days; neurological symptoms are the same as with foodborne botulism, with the exception of gastrointestinal syndrome; with a mixed microbial wound process, fever is possible.
Diagnosis of botulism:
1) epidemiological history (consumption of foods that may be a factor in the transmission of botulism)
2) detection and identification of botulinum toxin in the blood serum of patients, vomit or gastric lavage, in food products, the consumption of which could cause poisoning, by means of a biological test on mice (mice are injected intraperitoneally with the material and observed for 4 days; control mice are injected with neutralizing serum types A, B, C and E; signs of intoxication in animals are recorded after 6-24 hours) followed by determination of the type of toxin in RA with monovalent anti-botulinum sera of types A, B, C and E.
Differential diagnosis of botulism:
a) with poisoning from poisonous mushrooms– only diarrhea is common with botulism; a pronounced gastrointestinal syndrome is characteristic with uncontrollable vomiting, bloody diarrhea, abdominal pain (in case of poisoning with toadstool) or repeated vomiting and diarrhea (in case of poisoning with fly agarics, strings, morels)
b) with toxic stem encephalitis– characterized by severe fever, general cerebral symptoms (disorders of consciousness, generalized convulsions), asymmetric localization of focal lesions (paresis, paralysis), absence of paresis of the ciliary muscle innervated by the parasympathetic nerve
c) with methyl alcohol poisoning– nausea, abdominal pain, dizziness, blurred vision, diplopia, mydriasis are observed, but unlike botulism, confusion, hypertonicity of the occipital and limb muscles, convulsions, irreversible blindness, acute heart failure are characteristic
d) with the bulbar form of poliomyelitis– characterized by an acute onset with high fever, catarrhal symptoms, absence of dyspeptic manifestations, salivation is not impaired, developing paresis and paralysis are often asymmetrical, accompanied by the disappearance of tendon reflexes, there are changes in the cerebrospinal fluid
Treatment of botulism:
1. Mandatory hospitalization, strict bed rest (due to the risk of orthostatic collapse), constant monitoring of the patient with readiness for immediate respiratory resuscitation
2. Mechanical removal or neutralization of the toxin in the gastrointestinal tract: very thorough, until the water is clean, tube gastric lavage (especially indicated if no more than 72 hours have passed since the absorption of the toxin with food), first with boiled water to obtain material for laboratory research, and then 2-5% sodium bicarbonate solution to simultaneously neutralize the toxin; if swallowing is impaired, instead of a thick gastric tube, use a thin or nasogastric tube + high siphon enemas with 5% sodium bicarbonate solution (also after sampling for laboratory tests). After gastric lavage, patients are administered enterosorbents (polyphepan, enterodes), and also given one dose of anti-botulinum serum orally (to neutralize the remaining part of the botulinum toxin in the stomach)
3. Etiotropic therapy - administration of antitoxic antibotulinum serum
NB! Because the antitoxin neutralizes only the toxin freely circulating in the blood, which has not yet contacted the nerve endings, delay is unacceptable!
Principle of administration of anti-botulinum serum:
1) use heterologous (horse) antitoxic monovalent serums (one therapeutic dose - 10 thousand ME of antitoxins of types A and E, 5 thousand ME of type B antitoxin); before establishing the type of toxin, a mixture of monovalent serums (A+B+E, i.e. 25,000 IU) is administered; if the type of toxin is known, the appropriate serum is used
2) before the introduction of serum, a test is carried out to identify sensitivity to a foreign protein according to Bezredko A.M.: intracutaneous injection of 0.1 ml of horse serum diluted 1:100 --> no local allergic reaction, negative intradermal test (papule diameter not > 0.9 cm, limited hyperemia) --> subcutaneous injection after 20 min 0, 1 ml of undiluted anti-botulinum serum --> absence of general allergic reactions --> administration of the entire therapeutic dose after 30 minutes
With a positive intradermal test antitoxic serum is administered for health reasons(severe course of the disease, moderate forms and even mild ones, but with an increase in neurological symptoms) after desensitization by subcutaneous administration of diluted horse serum at intervals of 20 minutes in doses of 0.5-2.0-5.0 ml and under cover desensitizing agents (glucocorticoids, antihistamines).
3) the serum is heated to a temperature of 37°C and administered intravenously one dose regardless of the severity of the disease
4. Pathogenetic therapy: infusion-detoxification therapy (5% glucose, saline solution with the addition of diuretics), proserin 1 ml of 0.05% solution 1-2 times/day subcutaneously to reduce intestinal and urinary atony bubble
5. Considering the complex nature of developing hypoxia, hyperbaric oxygenation can be used; if there is a threat of asphyxia, it is necessary to transfer the patient to controlled breathing (tracheal intubation and mechanical ventilation)
6. If there is a risk of secondary infectious complications - AB, with the exception of drugs that disrupt the conduction of nerve impulses (streptomycin, aminoglycosides, tetracyclines).
Prevention of botulism: strict adherence to the production technology of canned products; storing home-canned products in refrigerators and heat treatment for 20 minutes before consumption.
Botulism is an infectious disease, which occurs under the influence of a specific protein neurotoxin produced by microorganisms - Clostridium botueinum. Now there are 3 fundamentally different forms of the disease: food-borne, the most common, and rare forms - wound and neonatal botulism.
Relevance.
Botulism is an endemic pathology, which occurs annually on the territory of Belarus, often leading to death.
Characteristics of the pathogen.
Clostridium botulinum an anaerobic, mobile, spore-forming rod capable of producing the most powerful toxin known to science. A rod with rounded edges, 5-10 µm long, 0.3-0.4 µm wide, with 3-20 flagella. According to the antigenic properties that are inherent in both the pathogen and the toxin, 7 types of pathogen are known: A, B, C, Cp, D, E, F, G.
Optimal conditions for the growth of vegetative forms-- extremely low residual oxygen pressure and temperature conditions within 28-35°C, except for type “E” - 3°C refrigerator conditions. At the same time, heating at 80°C for 30 minutes causes their death.
In unfavorable conditions, vegetative forms of botulism pathogens form spores. They are extremely resistant to various physical and chemical factors, can withstand boiling for 4-5 hours, exposure to various disinfectants in high concentrations, and are preserved in products containing up to 18% table salt. Of interest is the phenomenon of the formation of so-called “dormant spores” from vegetative forms of Clostridium bolulinum, when they are not warmed up sufficiently, capable of germination only after 6 months. Spores are resistant to freezing and drying, and to direct ultraviolet irradiation.
In anaerobic or similar conditions, the causative agents of botulism produce a specific lethal neurotoxin, which is the only pathogenicity factor of exceptional strength. Botulinum toxins of a protein nature under normal environmental conditions persist for up to a year in canned foods - for years. They are stable in an acidic environment and are not inactivated by enzymes of the digestive tract. The toxic properties of botulinum toxin E under the influence of trypsin can increase hundreds of times. Botulinum toxins can withstand high concentrations (up to 18%) of table salt and are not destroyed in products containing various spices. Toxins are relatively quickly inactivated under the influence of alkalis; when boiled, they completely lose their toxic properties within a few minutes, and under the influence of small concentrations of potassium permanganate, chlorine or iodine - within 15-20 minutes. The presence of botulinum toxin in food products does not change their organoleptic properties.
The main manifestations of the epidemic process.
The causative agents of botulism are widespread in nature. Vegetative forms and spores are found in the intestines of various domestic and, especially, wild animals, waterfowl, and fish. Once in the external environment, they accumulate and remain in a spore-like state for a long time. However, the disease can only occur when consuming those that were stored in anaerobic or similar conditions without sufficient heat treatment. This can be canned food, especially home-made, smoked, dried meat and fish products, as well as other products in which there are conditions for the development of vegetative forms of microbes and toxin formation. More often, group, “family” outbreaks of diseases occur. If the contaminated product is solid-phase (sausage, smoked meat, fish), then “clustered” damage to the products is possible. Currently, diseases caused by poisoning are more often recordedtoxins A, B and E. Thus, the source of infection for botulism is objects of living and non-living nature in which conditions for toxin formation are created.
Wound botulism and neonatal botulism are much less common. Their peculiarity is that infection occurs due to entry into the wound or gastrointestinal tract of infants vegetative forms or spores of botulism pathogens. In the crushedIn necrotic tissues deprived of oxygen, conditions close to anaerobic are created, under which vegetative forms sprout from spores and produce botulinum toxin. Botulism in infants occurs when spores enter their gastrointestinal tract along with complementary feeding or supplementary feeding. When investigating cases of infant botulism, spores were isolated from honey included in artificial nutritional mixtures, or were found in the child’s environment (dust, soil).
Features of the epidemiology of botulism:
The toxin plays a leading role in the pathogenesis of botulism. The following stages are distinguished:
- absorption of the toxin through the mucous membranes of the initial sections of the gastrointestinal tract (with normal infection, it enters the body along with food that also contains vegetative forms of pathogens that produce poison; absorption of botulinum toxin occurs through the mucous membrane of the proximal sections of the gastrointestinal tract, starting from the oral cavity; absorption of botulinum toxin from the respiratory mucosa is possible, as evidenced by both experimental data and clinical observations);
- lymphogenous drift (the most significant entry of the toxin is from the mucous membrane of the stomach and small intestine, from where it enters the lymph);
- hematogenous drift (enters the blood and spreads throughout the body);
- fixation on nerve structures (the toxin is firmly bound to nerve cells; motor neurons of the anterior horns of the spinal cord and nerve endings are affected; action on the cholinergic parts of the nervous system, cessation of the release of acetylcholine into the synaptic cleft, disruption of neuromuscular transmission, development of paresis and paralysis);
- penetration through the blood-brain barrier into the central nervous system (suppression of the respiratory center).
Paresis or paralysis of the intercostal muscles, diaphragms lead to acute ventilation respiratory failure with the development of hypoxia and respiratory acidosis. Inhibition of pulmonary ventilation is facilitated by dysfunction of the muscles of the pharynx and larynx, accumulation of thick mucus in the supra- and subglottic space, aspiration of vomit, food, and water. With botulism, due to the indirect or direct action of the toxin, all types of hypoxia develop: hypoxic. histotoxic, hemic and circulatory. Ultimately, it determines the course and outcome of the disease. At the same time, the role of such secondary changes associated with impaired innervation as aspiration pneumonia and atelectasis is also significant. Due to hyposalivation, the mucous membrane of the oropharynx becomes inflamed, and purulent parotitis may develop as a consequence of an ascending infection. The death of patients usually occurs from ventilation respiratory failure and very rarely from sudden cardiac arrest. The nervous system is not the only target for botulinum toxin.
Clinic.
The incubation period for botulism lasts up to a day, less often up to 2-3 days and very rarely (in single descriptions) up to 9 and even 12 days. A shorter incubation period corresponds, although not always, to a more severe course of the disease. Alcohol intake, as a rule, does not affect the course of the disease, and intoxication can obscure the first manifestations of botulism, preventing its timely diagnosis.
The leading clinical syndromes are:
- general intoxication;
- gastrointestinal;
- paralytic.
The latter is specific and decisive in diagnosis. The first two are starting, first and, as a rule, not taken into account by specialists in the initial stages of the disease.
The key clinical signs of botulism are various neurological symptoms, the totality of which can vary over a wide range and varying degrees of severity. However, in approximately every second patient, the first manifestations of botulism may be short-term symptoms of acute gastroenteritis and general intoxication. Typically, patients in such cases first complain of acute pain in the abdomen, mainly in the epigastric region, after which repeated vomiting and loose stools without pathological impurities appear, no more than 10 times a day, more often 3-5 times. Sometimes, against this background, headaches, malaise appear, and there is an increase in body temperature to subfebrile levels. By the end of the day, hypermotility of the gastrointestinal tract is replaced by persistent atony, body temperature becomes normal. The main neurological signs of the disease begin to appear. In rare cases, between gastrointestinal and neurological syndromes, the patient’s state of health may remain quite satisfactory and only with a targeted examination can signs of damage to the nervous system be identified.
The disease usually begins suddenly. The most typical early signs of botulism are manifestations of ophthalmoplegic syndrome: impaired visual acuity, “fog in the eyes”, “mesh in front of the eyes”, patients have difficulty distinguishing nearby objects, cannot read first regular print, and then large print. Double vision appears. Ptosis of varying severity develops. Further, sometimes in parallel, a dysphonic syndrome (aphonic) develops: the pitch and timbre of the voice changes, sometimes nasality is noted. As the disease progresses, the voice becomes hoarse, and hoarseness can turn into aphonia. One of the first to occur is dysphagic syndrome, up to aphagia: there is a sensation of a foreign body in the throat (“unswallowed tablet”), choking, difficulty swallowing first solid and then liquid food and water. In severe cases, complete aphagia occurs. When trying to swallow water, the latter pours out through the nose. During this period, aspiration of food, water, and saliva is possible with the development of aspiration pneumonia and purulent tracheobronchitis. All of the above neurological symptoms appear in various combinations, sequences and degrees of severity. Some of them may be missing. However, the obligatory background for them is a violation of salivation (dry mouth), progressive muscle weakness and persistent constipation.
Muscle weakness gradually increases- total myoplegia syndrome. Muscle weakness increases according to the severity of the disease. Initially, it is most pronounced in the occipital muscles, as a result of which in such patients the head may hang down and they are forced to support it with their hands. Due to the weakness of the intercostal muscles, breathing becomes shallow and barely noticeable. With complete paralysis of the intercostal muscles, patients feel compression of the chest “as if by a hoop.”
When examined at the height of the disease, patients are lethargic and adynamic. The epithelium is mask-like, one or more often bilateral ptosis. The pupils are dilated, sluggish or do not react to light at all; nystagmus, strabismus are possible, convergence and accommodation are impaired. Protrusion of the tongue occurs with difficulty, sometimes with jerks. Articulation deteriorates. The mucous membrane of the oropharynx is dry, the pharynx is bright red. In the supraglottic space there may be an accumulation of thick, viscous mucus, initially transparent and then cloudy. There is paresis of the soft palate, muscles of the pharynx and epiglottis, vocal cords, and the glottis is widened. Due to paresis or paralysis of the diaphragm muscles, expectoration of mucus is impaired, which accumulates in the subglottic space. A thick, viscous, mucous “film” in the supraglottic and subglottal space can lead to asphyxia. Patients are inactive due to weakness of skeletal muscles. A mask-like frozen face, shallow breathing, and aphonia may suggest loss of consciousness.
A sign of severe botulism is the appearance of respiratory distress syndrome. When examining the respiratory organs, attention is paid to shallow breathing. There is no cough, respiratory sounds are weakened, and auscultatory phenomena of pneumonia may not be audible. Changes in the cardiovascular system are detected mainly in moderate and severe disease: tachycardia, arterial hypotension, and sometimes hypertension, signs of metabolic changes on the ECG.
The full clinical picture of botulism is characterized by severe paresis of the gastrointestinal tract, manifested by moderate bloating, a sharp weakening of peristaltic bowel sounds, persistent and prolonged constipation. There are no changes typical for botulism in other organs and systems. Sometimes there may be urinary retention.
Peripheral blood tests do not reveal any significant abnormalities, with the exception of monocytosis, which also does not always occur. Leukocytosis, neutrophilia, accelerated ESR should alert you to a possible purulent complication of botulism.
Complications. There are two groups of complications: specific - due to the direct action of the toxin: botulinum carditis, myositis, etc. and nonspecific (iatrogenic) i.e. secondary microbial complications: pneumonia, including aspiration, atelectasis, etc. Iatrogenic complications: drug allergies, serum sickness, dysbacteriosis, “resuscitation” pneumonia, post-injection abscesses, cystitis, bedsores, sepsis.
Botulism in infants (up to 1 year), first described in 1976 (Piquet). The proof was the identification of the toxin and vegetative forms of the pathogen in the feces of children. It is considered the result of the penetration of spores with milk into the gastrointestinal tract of children, which has characteristics and differences from adults (intestinal microflora, acidity), as well as conditions for anaerobic reproduction of the pathogen.
Wound botulism- 10-13% of household wounds are infected with clostridia; they are not found in pus. It occurs more often in spring and autumn, boys are more often affected, and isolated cases have been reported. In the wound, in the presence of deep necrosis, conditions are created for toxic formation. This is supported by the length of the incubation period - up to 2 weeks.
Diagnostics.
Clinical, anamnestic and laboratory methods are used in diagnosis. The clinical method must necessarily take into account the peculiarities of the manifestation of botulism - general intoxication and gastrointestinal syndromes. The mistake of doctors in the polyclinic network is to ignore the first symptoms of an intestinal infection, when only the phenomena of paralytic syndrome are taken as a basis and the patient is referred (appeals) to an ophthalmologist, JIOP doctor, therapist or neurologist.
Specific diagnosis is based on identifying the pathogen or its toxin. A reliable sign: growth of the pathogen on Kitt-Tarozzi and Gibler media, detection and identification of the toxin. The pathogen can be found in blood serum, washing water, food residues, and feces. To detect the toxin, 15-20 ml of blood is taken to administer botulinum serum. Detection method - biological test and toxin identification (neutralization reaction in mice). 0.2 ml serum and antitoxic serum are mixed and administered to mice after 40-45 minutes.
Methods for detecting antibodies and antitoxin are ring precipitation reactions, RSK, RNGA, enzyme-labeled antibody reaction.
Treatment.
Treatment for botulism should be urgent in all cases., and monitoring of patients is constant, ensuring the prevention of complications and readiness for immediate transfer to mechanical ventilation.
All patients, regardless of the duration of the disease, are indicated for gastric lavage already at the prehospital stage. It is carried out first with boiled water to obtain material for laboratory research, and then with a 2-5% solution of sodium bicarbonate in order to simultaneously neutralize the toxin. For gastric lavage, a thick gastric or nasogastric tube is used, and if swallowing is impaired, a thin gastric or nasogastric tube is used. The procedure is continued until clean wash water is obtained. If swallowing is not impaired and the gag reflex is preserved, then evacuation of the stomach contents is achieved by inducing vomiting mechanically. All patients are given cleansing enemas.
Etiotropic treatment.
Simultaneously with attempts to mechanically remove or neutralize botulinum toxin, an antitoxic anti-botulinum serum is administered. For specific antitoxic therapy, heterologous (horse) antitoxic monovalent sera are usually used, one therapeutic dose of which is 10 thousand IU of antitoxins of types A, C and E, 5 thousand IU of type B and 3 thousand IU of type F. To establish the type of toxin a mixture of monovalent sera (A, B and E) is administered in 1 therapeutic dose in cases of mild or moderate disease and 2 therapeutic doses in patients with a severe clinical picture of the disease. The serum is heated to a temperature of 37°C and administered intramuscularly or intravenously, depending on the severity of the disease.
For mild forms of botulism, the serum is administered 1 time for 1-2 days, for moderate cases - 2-3 days. In cases of severe disease, repeated administration of serums is possible after 6-8 hours in the absence of a positive effect, and the duration of specific antitoxic therapy is 3-4 days with an administration interval first after 6 hours and then after 12-24 hours.
The serum is administered strictly according to the instructions attached to this immune preparation.
Before administering the serum, it is necessary to lavage the stomach and collect the necessary material. for research. In the past, when there was only one manufacturer of anti-botulinum serum (USSR), an intradermal test was required to determine sensitivity to a heterogeneous (horse) protein. First, 0.1 ml of horse serum diluted 1:100 is injected intradermally. In the absence of an allergic reaction, a negative intradermal test (the diameter of the papule does not exceed 0.9 cm, and the redness is limited), 0.1 ml of undiluted anti-botulinum serum is injected subcutaneously after 20 minutes. If there is no reaction, the entire therapeutic dose is administered after 30 minutes.
If the intradermal test is positive, antitoxic serum is administered according to vital indications after desensitization (according to Urbach) by subcutaneous administration of diluted horse serum at intervals of 20 minutes in doses of 0.5-2.0-5.0 ml and under the cover of desensitizing agents (glucocorticoids, antihistamines).
For the purpose of nonspecific detoxification, enterosorbents are prescribed orally(polyphepan, enterodes, etc.), carry out infusion and detoxification therapy. To do this, 400 ml of hemodez are administered intravenously daily (no more than four days), lactasol, glucose solutions with simultaneous stimulation of diuresis (furosemide, lasix 20-40 mg).
Guanidine can be used to improve synaptic conduction hydrochloride 15-35 mg/kg/day.
For all patients to suppress the vital activity of botulism pathogens in the gastrointestinal tract and the possible formation of a toxin, chloramphenicol is prescribed 0.5 g 4 times a day for 5 days. Instead of chloramphenicol, you can use ampicillin 0.75-1.0 g per day, tetracyclines in average therapeutic doses. In case of purulent complications, appropriate antibacterial therapy is carried out.
Prevention and measures in the outbreak.
Prevention of botulism is based on strict adherence to the rules for the preparation and storage of semi-finished fish and meat products, canned foods, smoked meats, etc. Therefore, before consuming such products, it is advisable to boil them for 10-15 minutes, which ensures complete neutralization of botulinum toxins.
If cases of the disease are detected, suspicious products are subject to seizure and laboratory control, and those who consumed them together with the sick - medical supervision for 10-12 days. It is advisable to intramuscularly administer 2000 IU of antitoxic antibotulinum serums A, B and E, and prescribe enterosorbents. Active immunization is carried out only to persons who have or may have contact with botulinum toxins. Vaccinations are carried out with polyanatoxin three times with intervals of 45 days between the 1st and 2nd and 60 days between the 2nd and 3rd vaccinations. In the prevention of botulism, sanitary education of the population regarding the preparation of food products, which can cause botulinum toxin poisoning, is essential.
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