Anthrax

Anthrax

anthrax– an acute infectious disease from the group of bacterial zoonoses, occurring in the skin (with the formation of carbuncle and ulcers) or generalized form, depending on the place of introduction of the pathogen, due to the transmission of the infection. Etiology. The causative agent is a Gram-positive, immobile, spore-forming bacterium, Bacillus anthracis. When ingested by a human or animal, the spores turn into vegetative forms that can cause disease. Spores remain viable for several decades, withstand boiling for 1 hour, and are resistant to the action of sublimate, chlorine and other disinfectants. Vegetative forms of anthrax bacilli are resistant to low temperatures, quickly die under the influence of disinfectants and temperatures of 75-80 ° C, when heated to 50 ° C they die within 30 minutes. Epidemiology. Among animals, herbivores are the most susceptible, but cases of the disease have been noted among hares, cats and dogs. In humans, the disease is associated with a profession (agricultural workers, slaughterhouse workers, wool beaters and brush makers). Endemic areas are Asia, South Africa, South America and Australia. Sporadic cases are registered in Europe, the Russian Federation and the USA. Every year, anthrax affects about 1 million animals, and about 40,000 cases of the disease are recorded in humans. Animals become infected by ingesting spores during grazing or by eating contaminated feed. In animals, intestinal and septic forms of the disease predominate. Sick animals excrete anthrax in urine and feces. A person becomes infected through contact with infected material (caring for sick animals, processing wool, skins, bristles, skins and bones) or by eating the meat of diseased animals. Ways of infection – inhalation, ingestion or penetration through cuts and wounds of Bacillus anthracis spores. There are professional (agricultural, industrial) and non-professional (domestic, casual) risk groups. Animal burial grounds represent a significant epidemiological danger, especially if the corpses of animals that died from anthrax were buried without proper foresight. In rural areas, the incidence is seasonal (peak incidence is summer). A certain role in the spread of infection in the summer months belongs to blood-sucking insects – horseflies and stingers. Pathogenesis. Entrance gate – microtrauma of the skin and mucous membranes (conjunctiva, gastrointestinal tract, respiratory tract). Toxins and metabolites of the pathogen damage the endothelium of the lymphatic vessels with the development of serous-hemorrhagic inflammation, later leading to tissue necrosis. The manifestation of clinical signs of anthrax is mediated by the action of the toxin. Accumulation of the toxin in tissues and its effect on the central nervous system lead to death due to pulmonary insufficiency and hypoxia. The penetration of a large number of viruses into the blood causes anthrax sepsis. After the transferred disease, a persistent immunity to subsequent infections develops. The penetration of a large number of viruses into the blood causes anthrax sepsis. After the transferred disease, a persistent immunity to subsequent infections develops. The penetration of a large number of viruses into the blood causes anthrax sepsis. After the transferred disease, a persistent immunity to subsequent infections develops.

Clinical picture

    • The incubation period is from several hours to 8 days (approximately 2-3 days). There are skin and septic forms, in the aftermath it can proceed in the pulmonary or intestinal variant.
    • Cutaneous form of anthrax. Observed in 95% of patients. The skin of open parts of the body is affected more often than closed clothing. Shaving creates optimal conditions for infection (shaved areas are affected 2 times more often). Areas of skin with abundant fatty lubrication (for example, the skin of the nose), fingertips and nail beds are not affected. Most often the foci are localized on the upper limbs, head, neck. At the site of the entrance gate of infection, a reddish spot first appears, quickly transforming into a copper-red papule. From the very beginning, patients note itching, which increases in the dynamics of the disease. A few hours later, a vesicle 2-3 mm in diameter appears at the site of the papule, its content is first serous, then becomes dark, bloody (pustula maligna); due to severe itching, patients often tear off the vesicle, or it bursts itself, and in its place a scab appears, quickly blackening or increasing in volume. The formation of daughter pustules is characteristic, passing through all stages of development and merging into one brown-black scab with a hard, as if burnt, crust. The scab surrounds the infiltrate in the form of a purple shaft, as a rule, edema joins it, covering large areas. When struck with a percussion hammer in the area of ​​​​edema, gelatinous trembling is often observed (Stefanovsky’s sign). Body temperature is high. They note a combination of regional lymphadenitis with lymphangiitis, CCC disorders: tachycardia, a drop in blood pressure, etc. Nausea, vomiting and anorexia are often observed. With a favorable course, the temperature lasts 5-6 days, then drops critically. The formation of daughter pustules is characteristic, passing through all stages of development and merging into one brown-black scab with a hard, as if burnt, crust. The scab surrounds the infiltrate in the form of a purple shaft, as a rule, edema joins it, covering large areas. When struck with a percussion hammer in the area of ​​​​edema, gelatinous trembling is often observed (Stefanovsky’s sign). Body temperature is high. They note a combination of regional lymphadenitis with lymphangiitis, CCC disorders: tachycardia, a drop in blood pressure, etc. Nausea, vomiting and anorexia are often observed. With a favorable course, the temperature lasts 5-6 days, then drops critically. The formation of daughter pustules is characteristic, passing through all stages of development and merging into one brown-black scab with a hard, as if burnt, crust. The scab surrounds the infiltrate in the form of a purple shaft, as a rule, edema joins it, covering large areas. When struck with a percussion hammer in the area of ​​​​edema, gelatinous trembling is often observed (Stefanovsky’s sign). Body temperature is high. They note a combination of regional lymphadenitis with lymphangiitis, CCC disorders: tachycardia, a drop in blood pressure, etc. Nausea, vomiting and anorexia are often observed. With a favorable course, the temperature lasts 5-6 days, then drops critically. edema joins it, covering large areas. When struck with a percussion hammer in the area of ​​​​edema, gelatinous trembling is often observed (Stefanovsky’s sign). Body temperature is high. They note a combination of regional lymphadenitis with lymphangiitis, CCC disorders: tachycardia, a drop in blood pressure, etc. Nausea, vomiting and anorexia are often observed. With a favorable course, the temperature lasts 5-6 days, then drops critically. edema joins it, covering large areas. When struck with a percussion hammer in the area of ​​​​edema, gelatinous trembling is often observed (Stefanovsky’s sign). Body temperature is high. They note a combination of regional lymphadenitis with lymphangiitis, CCC disorders: tachycardia, a drop in blood pressure, etc. Nausea, vomiting and anorexia are often observed. With a favorable course, the temperature lasts 5-6 days, then drops critically.

At the same time, the healing of the local focus occurs: swelling gradually decreases, lymphadenitis and lymphangiitis disappear, the scab disappears, and after 2-4 weeks a dense white scar appears at the site of the healed ulcer. The following clinical variants are distinguished:

    • Carbunculous (typical) cutaneous anthrax
    • Edematous cutaneous anthrax: edema followed by necrosis and carbuncle formation
    • Bullous skin anthrax with the formation of several hemorrhagic blisters in place of the carbuncle. After opening, extensive erosions are formed in the latter, acquiring the appearance of a carbuncle.
    • Erysepeloid cutaneous anthrax. The appearance of a large number of blisters with the formation of ulcers during their opening is characteristic.
    • Septic form of anthrax. Skin lesions may be complicated by secondary septicemia. The body temperature again rises to 40-41 ° C, chills, sweating, severe headache, tachycardia, and profuse hemorrhagic rashes are found on the skin. Some patients observe vomiting of blood, frequent loose stools with blood. In debilitated patients, the generalization of the process quickly begins without previous local focal changes. The incubation period is reduced to several hours. The septic form of anthrax, as a rule, ends fatally in 2-3 days with symptoms of severe cardiovascular insufficiency. Conditionally allocate pulmonary and gastrointestinal forms.
    • Pulmonary anthrax (wool sorters’ disease) is caused by inhalation of spores and is extremely severe. After a short incubation period, along with severe intoxication, a feeling of tightness in the chest increases, a runny nose, cough, photophobia, severe chest pain, conjunctival hyperemia and lacrimation are found. A sharp rise in body temperature up to 40 ° C, tachycardia, shortness of breath, cyanosis, profuse sweating, delirium, convulsions, and a drop in blood pressure are noted. Later, pneumonia develops with signs of acute pulmonary edema and effusion pleurisy. In sputum (copious, frothy, bloody, such as raspberry jelly), a large number of anthrax bacilli are detected. With rapidly developing cardiovascular insufficiency, the death of the patient begins on 2-3 days,
    • The gastrointestinal form of anthrax is characterized by a diverse clinical picture: in some patients, symptoms of gastrointestinal damage dominate, in others, symptoms of intoxication. Common manifestations are an increase in body temperature, vomiting and diarrhea with blood, abdominal pain. Hemorrhagic rashes and secondary pustules are often found on the skin. Typically, the sudden onset of acute cutting pains in the abdomen, nausea, hematemesis with bile, diarrhea mixed with blood. In some cases, due to damage to the lymph nodes of the mesentery and intestinal paresis, intestinal obstruction begins. As a result of a specific lesion of the intestine, inflammation of the peritoneum develops, leading to the appearance of effusion, perforation of the intestinal wall and peritonitis. The death of the patient begins in 3-4 days with progressive heart failure.

Research methods

    • Isolation of the pathogen is carried out by inoculation on conventional nutrient media, determination of mobility, staining according to Thunder and the study of biochemical features. Growing on media containing penicillin leads to the manifestation of the pearl necklace phenomenon. Materials for laboratory research: contents of pustules, purulent discharge of carbuncles, blood, urine, sputum, feces and vomit. During pathological and anatomical examination, pieces or whole organs are taken. All samples are placed in sealed vessels and transported sealed in sealed bixes or wooden boxes.
    • Express diagnostics by microscopy of smears of clinical material stained by Grom
    • Infection of laboratory animals for the final clarification of the diagnosis
    • Serological studies: RSK, RIGA, ELISA
    • For retrospective diagnosis in epidemiological studies, skin tests are performed (delayed-type hypersensitivity reaction) by intradermal injection of 0.1 ml of a bacterial allergen (anthraxin). The reaction is considered positive if, after 24 hours, hyperemia and an infiltrate of at least 3 cm in size are detected at the injection site.
    • The Ascoli reaction makes it possible to identify the pathogen Ag in case of negative results of bacteriological studies. For life-time diagnosis of this reaction, it has no advantages over the above bacteriological and serological methods.
    • Conducting differential diagnosis using bacteriophages VA-9n Saratov.

Differential Diagnosis

    • Furunculosis and carbunculosis of staphylococcal etiology
    • Plague
    • Tularemia.

Treatment

    • Antibiotics – benzylpenicillin sodium salt, 4 million units every 4 hours for 7-10 days, with intolerance to penicillins – tetracycline or chloramphenicol.
    • In combination with antibiotic therapy, a specific y-globulin is administered 20 ml (for mild form), 30-40 ml (for moderate), 60 ml (for severe) intramuscularly. With a very severe form of the disease, the dose is increased to 450 ml.
    • Anthrax serum 50-200 ml intramuscularly or intravenously (depending on the severity of the process, after a preliminary test according to Bezredka) – for all forms of the disease. Re-introduction of serum is acceptable after 1-2 days.
    • Detoxification therapy: 5-10% glucose solution, gemodez, polyglucin.
    • To accelerate reparative processes, locally apply dressings with boric acid or penicillin ointment, chipping the lesion with penicillin (3,000 IU per 0.5% solution of novocaine).

Prevention

    • Active immunization of persons belonging to risk groups is carried out with protective antigen of the pathogen (STI vaccine), which does not cause pronounced adverse reactions.
    • Veterinary and sanitary measures: isolation of diseased and suspicious animals, burning of the corpses of dead animals and infected objects (litter, manure), disinfection of sick animals’ campsites, cleaning of watering places, drainage of wetlands (plowing, chlorination). If the burning of corpses is improbable, they are buried in remote dry and desert areas, the depth of the pit should not be less than 2 m, the corpse is placed on a thick layer of bleach and covered with it from above (with a layer of up to 10 cm). All disposal activities must be carried out in compliance with sanitary standards.
    • Sanitary supervision of enterprises engaged in the processing of animal raw materials. All incoming raw materials are tested in the Ascoli thermoprecipitation reaction. Fur products are made only from raw materials that gave negative results in the Ascoli reaction.

ICD. A22 Anthrax

See also fig. 4-16

Literature

    • 129: 225—229
    • Anthrax. Ipatenko NG, Gavrilov VA et al. M.: Kolos, 1996

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