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Детские инфекционные заболевания. Сибирская язва (конспект лекций)

Lecture notes, cheat sheets

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Lecture No. 13. Anthrax

Anthrax is a well-known animal disease that is transmitted to humans and proceeds as an acute infectious disease characterized by severe intoxication, damage to the skin and lymphatic apparatus. It got its name from the Greek word for "coal", by analogy with the black color of the scab that forms with the skin form.

Etiology. The causative agent of the disease, Bacillus anthracis, is a gram-positive, immobile rod with a capsule and spores formed under aerobic conditions, resistant to external influences and capable of surviving for years in soil and various products of animal origin.

Epidemiology. Human infection with anthrax is possible through contact, nutritional, aerogenic and transmissible routes. The incidence of anthrax in humans is predominantly sporadic; less often, group diseases may occur. School-age children, especially teenagers, mostly boys, are more likely to suffer from anthrax, which is associated with their participation in caring for animals.

The incidence of anthrax in people increases in the summer-autumn period.

Pathogenesis and pathomorphology. The cutaneous form of anthrax is caused by the introduction of pathogen spores into the subepidermal layer. The spores multiply and produce an exotoxin, which causes tissue necrosis and the formation of a black scab.

The pulmonary form of anthrax develops when spores are inhaled and enter the alveoli. Being phagocytosed, they are transported to regional lymph nodes, where they replicate and produce exotoxin. Subsequently, septicemia usually develops, sometimes meningitis, and death may occur. Intrathoracic lymph nodes are adematous, hemorrhages are observed in them, and due to their increase in size, the bronchi can be compressed. The action of anthrax exotoxin causes depression of the CNS function. Primary pneumonitis after inhalation of the pathogen rarely develops, but respiratory failure and death can occur due to extensive thrombosis of the lung capillaries.

The gastrointestinal form of anthrax develops when spores of the pathogen enter the stomach. This form of the disease is manifested by hemorrhages and necrosis of the terminal ileum and caecum as a result of the multiplication of bacteria and the production of a toxin by them.

Clinical manifestations. The incubation period for cutaneous anthrax is 2-5 days. Initially, a small spot appears at the site of spore penetration, quickly turning into a vesicle; as it increases in size, it becomes hemorrhagic, necrosis develops in its center, and a scab forms. Swelling and new blisters appear around the gradually enlarging scab.

Common manifestations of infection are a moderate increase in body temperature, a feeling of malaise, an increase in regional lymph nodes. Sometimes the only manifestations of diseases are atypical changes on the skin: dotted dark spots that do not transform into vesicles. The cutaneous form accounts for more than 90% of all anthrax cases. Lesions of the shoulders and forearm are more common than the fingers, on the legs they are very rare. The incubation period for the pulmonary form is 1-5 days. Initially, there is a general malaise, a moderate increase in body temperature, muscle pain. Then a dry cough may join, and wheezing begins to be heard.

After 2-4 days, a picture of severe respiratory failure develops. The pulse and respiration become more frequent, body temperature rises, shortness of breath and cyanosis increase. Wet rales are heard, pleurisy develops, and sometimes swelling of the subcutaneous tissue on the neck and chest. Death occurs within a day, usually due to severe respiratory failure.

The gastrointestinal form of infection most often occurs when eating the meat of sick animals. After an incubation period of 2-5 days, anorexia, nausea, vomiting appear, and body temperature rises. There may be bloody diarrhea and hematomesis. Shock quickly develops and death ensues.

Meningitis can develop with untreated cutaneous anthrax. More than half of all cases of meningitis are complications of the cutaneous form of the disease, although the latter may already subside by the time meningitis develops. The cerebrospinal fluid is usually hemorrhagic in nature, but may also be purulent. B. anthrasis is often found in it. Simultaneously with meningitis, patients often have signs of encephalomyelitis and hemorrhage in the cerebral cortex.

Diagnosis. Anthrax is diagnosed based on characteristic changes on the skin and history of exposure to infection. Isolation of the pathogen from a discharged vesicle or from a scab confirms the diagnosis. The pulmonary form is identified when the pathogen is determined in pleural effusion; it is rarely detected in sputum. Data on the consumption of meat from sick animals should lead to speculation about the gastrointestinal form of anthrax.

Differential diagnosis. The cutaneous form of anthrax must be differentiated from skin diseases caused by staphylococcal infection, tularemia, plague, infection caused by Pseudomonas aeruginosa, A hydrophila, and skin changes after vaccination.

Treatment. Penicillin is the drug of choice. In mild forms of the disease, patients can be treated with penicillin V; in severe and severe forms, patients should be treated with novocaine salt of penicillin. Skin lesions are sanitized and bandaged. Cutting them is not recommended due to the risk of progression of the process. For pulmonary and meningeal forms of anthrax, patients are treated with penicillin G, and in some cases a specific antitoxin is administered. Maintenance therapy is necessary.

Forecast. The mortality rate for anthrax meningitis, despite treatment, is 100%, and for pulmonary meningitis it exceeds 90%. The untreated cutaneous form of anthrax is fatal in 10-20% of cases, and with penicillin therapy it decreases to 1%. The gastrointestinal form of infection is fatal in 25-50% of cases.

Prevention. A vaccine has been created, the administration of which is recommended for persons whose occupation is at increased risk of this infection.

Author: Muradova E.O.

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