Rabies
Rabies is an acute infectious disease caused by the neurotropic virus Rabies lyssavirus (family Rhabdoviridae). It is spread mainly through the saliva of infected animals, most often dogs, cats and bats, via bites, scratches or licks on tiny breaks in the skin. Once inside the body, the virus multiplies in the local muscle, then binds to nicotinic acetylcholine receptors at peripheral nerve endings and travels back along the nerves to the spinal cord and brain. Even when the original wound has healed, new tingling, burning or intense itching at the old bite site signals the prodromal stage of the disease. Once full-blown neurological symptoms appear (fear of water, fear of drafts, spasms of the breathing muscles or paralysis), the disease is almost always fatal.
At Haute-Derma, suspected rabies exposure is handled with a strict emergency protocol: high-pressure wound irrigation, grading of the exposure using WHO categories and urgent post-exposure prophylaxis (PEP). Once the infection risk has been ruled out, we follow up with cosmetic repair of the damaged skin.
Pathophysiology
Sources of Infection and Routes of Entry
- Animal hosts: Mammals. Domestic dogs are the main source (more than 95% of cases in developing countries), followed by cats, bats and wild animals.
- How the virus gets in: Virus in the saliva of an infected animal enters the dermis and subcutis directly through puncture bites, scratches that break the skin, or licks on grazed skin or mucous membranes.
The Virus's Path Along the Nerves and How It Destroys Cells
- Local replication and entry into nerve endings: The virus first multiplies in the skeletal muscle cells around the bite. It then binds to acetylcholine receptors (AChR) at the neuromuscular junction.
- Retrograde axonal transport: The virus travels backward along the axons of sensory and motor nerves toward the spinal cord at 12–100 mm per day.
- Central nervous system damage: Once it reaches the brain, the virus replicates explosively in neurons, causing acute gray-matter encephalitis and the characteristic Negri bodies in Purkinje cells and cortical neurons. This leads to diaphragmatic spasms, loss of autonomic control and death from respiratory and circulatory failure.
Clinical Stages of Rabies
Skin Symptoms and the Prodromal Stage
- Incubation period: Highly variable, typically 1–3 months. It can be under a week when the bite is in a nerve-rich area such as the head, face or neck, or it can stretch beyond a year.
- Telltale skin symptom: Abnormal sensations at the site of the healed bite: numbness, a crawling feeling, intense itching, burning pain or a feeling of heat. This is a very important clinical clue that the virus is invading and multiplying in the corresponding dorsal root ganglia.
- Mild general symptoms: Low-grade fever, tiredness, headache, and unexplained anxiety or restlessness.
The Acute Neurological Stage
- Furious (encephalitic) rabies – about 80% of cases:
- Hydrophobia: violent spasms of the larynx and breathing muscles, with overwhelming panic, when the patient tries to drink or even sees water.
- Aerophobia: even a light breeze on the skin can set off muscle spasms and convulsions.
- Excess salivation and drooling, agitation, hallucinations and autonomic instability.
- Paralytic rabies – about 20% of cases:
- Progressive paralysis that starts in the bitten limb and spreads throughout the body (much like Guillain–Barré syndrome), ending in respiratory muscle paralysis and coma.
Wound Care and Post-Exposure Prophylaxis at Haute-Derma
High-Pressure Wound Irrigation (the Most Important Step)
- Flush the wound continuously under running water with antiseptic soap for at least 15 minutes. This mechanically removes most of the virus-laden saliva from the wound.
- Then disinfect the wound with 10% povidone-iodine or 70% alcohol.
- Surgical caution: Bite wounds should not be closed with stitches straight away. Leave the wound open or delay closure so the virus is not pushed deeper into the tissue and nerves. If stitching cannot be avoided (a large or bleeding wound), rabies immune globulin should be infiltrated first and the wound closed loosely.
WHO Exposure Categories and PEP
- Category I (touching, or licks on intact skin): no prophylaxis needed; simply wash the exposed skin.
- Category II (nibbling of bare skin, minor scratches or abrasions without bleeding): start rabies vaccination immediately (Essen schedule on days 0, 3, 7, 14 and 28, or Zagreb 2-1-1 schedule with two doses on day 0 and one dose each on days 7 and 21).
- Category III (bites or scratches that break through the skin and bleed, licks on broken skin or mucous membranes, or any bite in a nerve-rich area such as the head, face, neck or fingertips):
- Rabies immune globulin (RIG) is essential: 20 IU/kg for human RIG or 40 IU/kg for equine RIG. As much of the dose as possible is infiltrated around and into the base of the wound, and any remainder is injected deep into a muscle away from the vaccine site.
- Plus a full course of rabies vaccine.
Cosmetic Repair of Bite Wounds at Haute-Derma Once Rabies Is Ruled Out
Preventing Bacterial Infection and Tetanus
- Tetanus vaccine and/or tetanus antitoxin (SAT) for Category II and III wounds.
- Amoxicillin-clavulanate 875/125 mg by mouth twice a day for 7 days to prevent secondary infection with bacteria from the animal's mouth (such as Pasteurella and anaerobes).
Rebuilding the Skin and Fading Bite Scars
- Once the animal observation period (10–14 days) is over and PEP has been completed safely:
- A topical solution containing epidermal growth factor (EGF), madecassoside and hyaluronic acid helps granulation tissue fill in the defect left by the bite.
- Fractional CO2 laser combined with light therapy smooths the scar edges, helps prevent hypertrophic or hardened scars and treats post-inflammatory hyperpigmentation (PIH).
