Etiology and reservoir of infection
The causative agent of rabies is an RNA-genomic neurotropic virus. It is thermolabile and lacks resistance to low temperatures.
The reservoir and source of infection in nature are wild animals (wolves, foxes, raccoons, bats) and domestic pets (dogs, cats). Dogs pose the greatest danger to humans—children are most frequently infected as a result of their bites. The infected human is a dead-end host and poses virtually no epidemiological risk.
It is important to remember the "infectiousness window": the animal begins excreting the virus with its saliva at the end of the incubation period—7–8 days before the appearance of the first visible clinical symptoms.
Mechanism of development (Pathogenesis)
Damaged skin serves as the port of entry for the infection. Once in the body, the virus travels strictly via a neurogenic pathway—along axon cylinders and perineural spaces toward the central nervous system at a rate of about 3 mm/h.
It is the location of the bite that determines the duration of incubation and prognosis: the closer the site of inoculation is to the brain, the faster the clinical picture will develop. Upon reaching the CNS, the virus begins active replication, causing edema, hemorrhages, and neuronal degeneration. Specific oxyphilic inclusions—Negri bodies—form in the cytoplasm of the affected cells.
Clinical presentation
The course of the disease is characterized by rapid progression and strict staging. Three clinical phases are distinguished:
- Prodromal stage (Initial). Characterized by inflammation in the area of the bite or scar (hyperemia, edema, itching, pain). A general infectious syndrome (cephalalgia, chills, sweating) and marked hyperesthesia develop.
- Encephalitic stage (Stage of excitation). Occurs in 2–3 days. Reflex excitability appears: painful muscle spasms in response to bright light, noise, or stuffiness. Psychomotor agitation, aggression, hallucinations, and fear of death develop. A pathognomonic triad is characteristic: hydrophobia (fear of water), profuse sweating, and hypersalivation (abundant foamy sputum). A fatal outcome is possible due to bulbar disorders.
- Terminal stage (Paralytic). Psychomotor agitation subsides, and a period of "false well-being" ensues. Flaccid paralysis of the limbs develops, and cranial nerves are affected. The outcome is sudden death without agony.
Features in children: the incubation period is significantly shorter, and the clinical presentation is often atypical (classic bouts of hydrophobia and pronounced agitation are absent).
Diagnostics and treatment
Diagnostics rely on clinical and epidemiological data (history of a bite, presence of hydrophobia, progressive course). In vivo laboratory diagnostics are difficult; rapid tests (IFAT) and serology (IHA, CFTest) are used. The "gold standard" is post-mortem histological examination of the brain for the presence of Negri bodies.
Treatment of the developed disease is exclusively palliative and symptomatic. The patient is transferred to mechanical ventilation and tube feeding, and infusion therapy is administered. Agitation and seizures are managed with sedatives, muscle relaxants, and narcotic analgesics.
Post-exposure prophylaxis
Emergency prophylaxis aims to induce immunity before the virus penetrates the CNS. It includes:
- Local wound care: immediate washing of the wound with warm soapy water, treatment of the edges with ethyl alcohol or a 5% iodine tincture, and application of a sterile bandage.
- Vaccination: the drug of choice is KOV (rabies vaccine). It is administered intramuscularly on days 0, 3, 7, 14, 30, and 90. If the animal is domestic and remains healthy after 10–15 days of veterinary observation, the course is discontinued.
- Passive immunization: in cases of dangerous localization (face, neck, hands) and deep/multiple wounds, rabies immunoglobulin (RIG) or rabies antiserum is additionally administered on day 0.
Triad of the excitation stage: Hydrophobia, Hypersalivation, Sweating.
Class and exam questions
Why does the location of the bite affect the severity of the disease?
The virus spreads along nerve trunks at a rate of about 3 mm/h. The closer the wound is to the brain (e.g., face or neck), the shorter the incubation period and the lower the chances of successful prophylaxis.
When does an animal start posing a danger?
The virus begins to be excreted in the animal's saliva 7–8 days before the appearance of the first clinical symptoms of the disease.
Can the course of rabies vaccinations be discontinued?
Yes, but only if the bite was inflicted by a known domestic animal (e.g., during play) that was under observation and remained completely healthy for 10–15 days.
What else to study on this topic
- Mechanisms of Negri body formation
- Pathogenesis of bulbar disorders and respiratory paralysis
- Differences in the clinical course of rabies in animals (vascular collapse)
- Regimen and rules for the administration of rabies immunoglobulin (RIG)
Master the entire topic in the Pediatrics course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Rabies" and 3,738 more pages of the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 71 video lessons on the subject
Other topics from the section «Chapter 12. Infectious and parasitic diseases»
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.