Infectious diseases. Rabies. Etiology, epidemiology, clinic, diagnosis, treatment (lecture notes)

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Infectious diseases. Rabies. Etiology, epidemiology, clinic, diagnosis, treatment (lecture notes)

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LECTURE No. 18. Rabies. Etiology, epidemiology, clinic, diagnostics, treatment

Rabies is an acute viral disease that occurs after contact with the damaged skin of the saliva of an infected animal, is characterized by the development of damage to the central nervous system (encephalitis) with a fatal outcome.

Etiology. The causative agent - a neurotropic virus - belongs to the group of rhabdoviruses. It has a bullet shape, reaches a size of 80-180 nm. The nucleocapsid of the virus is a single-stranded RNA. The virus is unstable in the external environment, boiling kills it within 2 minutes, quickly dies in chloramine. The virus is resistant to low temperatures. The virus is dangerous for many warm-blooded animals, which, when infected, begin to secrete the virus with saliva 7-8 days before the onset of clinical symptoms.

Epidemiology. Rabies is a zoonotic infection. The main reservoir of the virus is carnivores (foxes, wolves, jackals, dogs, cats). The virus is excreted with saliva in the last 7-10 days of the incubation period and throughout the disease. Infection occurs when sick animals bite or saliva on damaged skin and less often mucous membranes. The virus is not transmitted from person to person. Susceptibility to rabies is universal. The highest incidence was noted in the summer-autumn period, due to more intensive contacts of people with wild animals.

Pathogenesis. After penetration through the damaged skin, the virus reaches the brain along the nerve trunks, where it is fixed and replicated in the neurons of the medulla oblongata, in the nodes of the base of the brain and in the lumbar part of the spinal cord, causing edema, hemorrhages, and degeneration of the nerve cells of the spinal cord. This leads to an increase in reflex excitability with the subsequent development of paralysis. The defeat of the higher autonomic centers in the hypothalamus, subcortical areas, in the medulla oblongata with an increase in their excitability causes convulsive contractions of the respiratory and swallowing muscles, hypersalivation, increased sweating, disorders of the cardiovascular system and respiratory activity characteristic of this disease. From the central nervous system, the virus enters various organs: the kidneys, lungs, liver, as well as the salivary glands and is released into the external environment with saliva.

Clinic. The incubation period ranges from 7 days to a year (usually 1-3 months). There are stages of premonitions, excitement and paralysis. During the prodromal period, a precursor stage is distinguished, which lasts 1-3 days. During this period, the patient is accompanied by unpleasant sensations in the area of the bite or salivation (burning, nagging pain, itching), despite the fact that the wound has already healed, causeless anxiety, depression, insomnia. The excitation stage is characterized by hydrophobia, aerophobia and increased sensitivity. Hydrophobia (phobia of water) manifests itself in the fact that when trying to drink, and then only when a glass of water approaches the lips, the patient is characterized by convulsive contraction of the muscles of the pharynx and larynx, breathing becomes noisy in the form of short convulsive breaths, and short-term cessation of breathing is possible. Convulsions may occur as a result of blowing a stream of air into the face (aerophobia). Body temperature is subfebrile. The skin is covered with cold, sticky sweat, the limbs are cold. Salivation is increased, the patient cannot swallow saliva and constantly spits it out. Excitement increases, visual and auditory hallucinations appear. Sometimes there are attacks of violence with aggressive actions. The paralytic period is characterized by mental calm. Fear and anxious melancholy mood disappear, attacks of hydro- and aerophobia stop, and after 2-3 days the excitement is replaced by paralysis of the muscles of the limbs, tongue, and face. Death occurs 12-20 hours after the onset of paralysis. The bulbar form with pronounced symptoms of damage to the medulla oblongata, paralytic (begins with paralysis, sometimes Landry type) and cerebellar with cerebellar disorders are considered to be variants of the course.

Diagnosis is based on the clinical picture. When examining a patient, attention is paid to the presence of scars from bites, salivation, sweating, the appearance of symptoms of mental disorders, etc.

Differential diagnosis is carried out by tetanus, encephalitis, encephalomyelitis, hysteria. After the death of patients, the diagnosis is confirmed by histological examination of the brain.

Treatment. There is no specific therapy for rabies. After the onset of clinical symptoms, it is not possible to save patients. Treatment is symptomatic and aimed at reducing the suffering of the patient. Patients are placed in a darkened soundproof room. Re-introduce pantopon, chlorpromazine, diphenhydramine.

Prevention. They combat rabies among animals and prevent rabies in people bitten by infected animals. In case of a bite, the wound is washed with soapy water and cauterized with tincture of iodine. Surgical excision of the wound edges and suturing in the first days should not be performed. At Pasteur stations, anti-rabies vaccinations and serotherapy are carried out according to a special scheme approved by the USSR Ministry of Health.

Author: Gavrilova N.V.

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