Etiology and reservoirs of infection
The causative agent of the disease is a neurotropic RNA-containing rhabdovirus (RABV). Its virion has a characteristic bullet-like shape and is covered by a bilayer lipoprotein envelope with spikes. A key pathogenicity factor is glycoprotein G, which is responsible for virus adsorption, cell entry, and exhibits an affinity for nicotinic acetylcholine receptors (nAChRs) of nerve and muscle cells.
In nature, the "wild" (street) variant of the virus circulates. The true reservoirs of infection are small mammals (e.g., mice and rats), which carry the infection asymptomatically and shed the virus in their saliva for life. Predators (foxes, wolves, raccoon dogs, and in anthropurgic foci, stray dogs and cats) act as the main vectors. The disease deprives them of caution, increases aggressiveness, and causes them to bite other animals and humans.
Transmission mechanism and susceptibility
Infection occurs via the contact mechanism (through wounds). The virus present in the saliva of an infected animal enters the human body through bites or when saliva contacts microlesions of the skin, conjunctiva, and mucous membranes. The virus appears in the animal's saliva 7–10 days before clinical manifestations.
Susceptibility to rabies is universal, but not all bitten individuals develop the disease (on average 15–30% without prophylaxis). The probability of developing the disease directly depends on the site of the wound: the risk is 99% for a face bite, 63% for hand bites, and almost 100% if saliva contacts the conjunctiva.
Pathogenesis: how the virus invades the CNS
The incubation period consists of a stage of viral latency and transportation of the virus to the brain:
- Primary replication: upon entering the wound, the virus invades striated muscles and replicates in myocytes. This latency phase can last from several weeks to months.
- Retrograde axonal transport: the virus binds to nAChRs, enters synapses, and moves centripetally along motor neuron axons at a speed of 8–12 cm per day. Transport is carried out via dynein proteins.
- CNS involvement: upon reaching the spinal cord and brain, RABV actively replicates in neuron cell bodies, forming specific eosinophilic inclusions—Negri bodies. The infection inhibits neurotransmitter synthesis and disrupts synaptic transmission.
- Centrifugal dissemination: from the brain, the virus spreads via efferent pathways to internal organs, concentrating primarily in the salivary glands for subsequent transmission.
Feature: the virus hides behind the blood-brain barrier without immediately destroying host cells. Consequently, specific antibodies appear in the blood fatally late, when CNS damage is already irreversible.
Clinical Forms
The disease proceeds as severe brainstem encephalitis. Two main forms are distinguished:
- "Furious" form (classic): Attacks of severe psychomotor agitation predominate. The main symptom is hydrophobia (spasmodic, extremely painful contractions of the swallowing muscles and inspiratory dyspnea upon attempting to drink, seeing, or even mentioning water). Aero-, photo-, and acoustico-phobias are also typical. The patient suffers from profuse salivation (sialorrhea), severe sweating, and hyperpyrexia (up to 43°C). Death occurs in 2–3 days from respiratory arrest or heart failure against the background of cerebral edema.
- Paralytic form: Characterized by the sequential development of flaccid paralysis, starting from the bitten limb and progressing to quadriplegia. The manifest period lasts longer (up to 30 days), but invariably ends in death.
Prevention and management tactics
Upon the appearance of the first symptoms, the prognosis is utterly unfavorable, and patients are doomed. The only chance for life is an immediate full course of anti-rabies vaccinations during the early stages of the incubation period.
The foundations of this specific prophylaxis were laid by Louis Pasteur, who created a vaccine strain—fixed virus (virus fixe), which lacks pathogenicity for humans. When a patient presents with suspected contact with a rabid animal, emergency post-exposure prophylaxis is mandatory, along with hospitalization in a specialized department once the clinical picture is developed (with medical personnel observing personal protective measures).
Briefly: answers to topical questions
What are the timelines for emergency vaccination and the administration schedule of the anti-rabies vaccine?
Emergency vaccination is effective if started no later than the 14th day after contact. The vaccine is administered intramuscularly at a dose of 1 ml according to a strict schedule (an unconditional course of 6 injections):
- Injection schedule — on days 0, 3, 7, 14, 30, and 90 after the bite.
- Injection site — in adults, into the deltoid muscle of the shoulder; in children under 5 years old, into the upper anterolateral thigh.
If the animal in question remains healthy during 10 days of observation, the vaccination course is discontinued after the third injection.
In which cases is the administration of rabies immunoglobulin (RIG) indicated?
The administration of rabies immunoglobulin (RIG) is indicated on day zero for severe injuries and contacts. Such cases include:
- Dangerous localization — any bites to the face, head, neck, hands, fingers and toes, genitals, and perineum.
- Severe injuries — single or multiple deep lacerated wounds, as well as transdermal bites and scratches with bleeding.
- Mucosal contact — any salivation of mucous membranes or damaged skin.
- High risk from the animal — injuries inflicted by wild carnivores, bats, rodents, as well as farm animals.
To easily remember the key seizure triggers ("phobias") in rabies, use the mnemonic PHGA: Photophobia (light), Hyperacusis/Acousticophobia (sound), Hydrophobia (water), Aerophobia (air).
Class and exam questions
Why do profuse salivation and aquaphobia occur in rabies?
The virus descends centrifugally from the brain into the salivary glands. Aquaphobia (the inability to swallow due to painful spasm) and sialorrhea ensure the accumulation of a huge amount of infected saliva in the mouth, which is evolutionarily advantageous for the virus to transmit via a bite.
Why don't antibodies destroy the virus before symptoms develop?
The rabies virus exhibits strict neurotropism. It replicates inside neurons behind the blood-brain barrier without inducing rapid apoptosis. The immune system "does not see" the pathogen, and protective antibodies appear far too late—when the brain has already been critically damaged.
What determines the duration of the incubation period?
The incubation period depends on the distance from the bite site to the brain and the volume of innervation in the wound. The virus travels along axons at a fixed speed (8–12 cm per day); therefore, a face bite results in the shortest incubation period, while a foot bite results in the longest.
What else to study on this topic
- The mechanism of competitive blockade of nerve growth factor (NGF) by the virus
- Properties of Pasteur's fixed virus (virus fixe) and principles of vaccine development
- Differential diagnosis of rabies from delirium tremens and Brunner's tetanus
- Features of viral survival in the external environment (temperatures, putrefaction, UV)
- Pathophysiology of inspiratory dyspnea and the development of cerebral edema in infection
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