Topic
Rabies
Rabies: the prototype neurotropic zoonotic viral encephalomyelitis. Near-universal fatality once symptoms begin; fully preventable by timely post-exposure prophylaxis. The virus itself, the related lyssaviruses, and the operational South African prophylaxis framework.
Rabies is an acute viral encephalomyelitis transmitted by the bite of an infected mammal. Once neurological symptoms begin the disease is effectively 100% fatal, yet it is fully preventable by prompt wound care, vaccination and rabies immunoglobulin. That asymmetry between near-universal fatality after symptom onset and near-universal preventability before it defines the clinical and public-health response. The global burden is approximately 59,000 deaths annually, the great majority from rabid-dog exposure in low-income settings.
Human rabies is caused, in over 99% of cases worldwide, by the classical rabies virus (RABV), the type species of the genus Lyssavirus. Six other lyssaviruses have caused documented human disease, including Duvenhage and Mokola virus (both relevant in southern Africa), Australian bat lyssavirus, European bat lyssaviruses 1 and 2, and Irkut virus.
What makes rabies both so lethal and so preventable is its route to the brain. After a bite the virus replicates locally, then travels along peripheral nerves by retrograde axonal transport to the central nervous system, with no viraemia and little immune activation during an incubation that is usually one to three months. That long, immunologically silent window is when vaccine-induced or passively given antibody can still intercept the virus; once it reaches the brain and symptoms begin, no treatment reliably works.
Prevention rests on three measures applied together: immediate wound washing, the rabies vaccine, and, for the deepest exposures, rabies immunoglobulin. Given promptly and correctly, post-exposure prophylaxis is essentially 100% effective. Because bat teeth can leave no visible wound, any direct bat contact is treated as a Category III exposure.
In South Africa rabies is endemic, with approximately ten laboratory-confirmed human cases a year, almost all from domestic-dog exposure and concentrated in KwaZulu-Natal, the Eastern Cape, Mpumalanga, the Free State and Limpopo. It is an immediately notifiable condition, coordinated under a One-Health partnership between human and veterinary services. Since 2024 a first-of-its-kind outbreak in Cape fur seals has extended the local risk to the coastline. The global goal is zero human dog-mediated rabies deaths by 2030, pursued through mass dog vaccination.
The depth sits in two pages:
→ See Rabies virus for the profile: classification within Lyssavirus, genome and virion architecture, the receptors and retrograde axonal transport that explain why post-exposure prophylaxis works, the furious and paralytic clinical forms, ante-mortem and post-mortem diagnosis, and the related lyssaviruses.
→ See South African Rabies Guidelines for the operational framework: WHO Category I/II/III stratification, wound care, the vaccine and PrEP schedules, rabies immunoglobulin dosing and infiltration, the 10-day animal observation rule, special populations, specimen submission, and the South African epidemiology.
Key terms
The vocabulary that recurs across the topic, grouped by theme.
The virus and disease:
| Term | Definition |
|---|---|
| Lyssavirus | The genus of bullet-shaped, negative-sense RNA rhabdoviruses that cause rabies; RABV is the type species. |
| Phylogroup | An antigenic grouping of lyssaviruses that predicts vaccine cross-protection; standard biologics protect within Phylogroup 1 only. |
| Negri bodies | Eosinophilic cytoplasmic inclusions of viral nucleoprotein in infected neurons; pathognomonic but not fully sensitive. |
| Furious versus paralytic rabies | The two clinical forms: encephalitic with hydrophobia and aerophobia (~80%), or ascending flaccid paralysis (~20%). |
| Hydrophobia | Painful pharyngeal and inspiratory spasms triggered by swallowing or the sight of water; near-pathognomonic of furious rabies. |
Exposure and prophylaxis:
| Term | Definition |
|---|---|
| WHO exposure category | I, II or III by depth of skin breach; decides whether wound care alone, vaccine, or vaccine plus RIG is given. |
| Post-exposure prophylaxis (PEP) | Wound care, vaccine and (Category III) rabies immunoglobulin started after a potential exposure; essentially 100% effective if timely. |
| Pre-exposure prophylaxis (PrEP) | A two-dose vaccine course (days 0 and 7) for those at ongoing risk. |
| Rabies immunoglobulin (RIG) | Passive antibody (HRIG 20 IU/kg or ERIG 40 IU/kg) infiltrated into the wound, effective only within 7 days of the first vaccine dose. |
| 10-day observation rule | A biting dog, cat or ferret that stays healthy for 10 days could not have been shedding virus, so PEP may be stopped. |
Diagnosis:
| Term | Definition |
|---|---|
| Direct fluorescent antibody (DFA) | The post-mortem gold-standard test, performed on brain tissue. |
| Nuchal skin biopsy | A full-thickness biopsy from the nape including hair follicles, tested ante-mortem by DFA or RT-PCR. |
References and recommended reading
- National Department of Health, South Africa. National Guidelines for the Prevention of Rabies in Humans, South Africa. September 2021. The operational source for the prophylaxis framework.
- National Institute for Communicable Diseases. Human Rabies: Ante-mortem and Post-mortem Specimen Collection Guide. 2019 (republished 2021). The source for specimen submission.
- Jackson AC. Rhabdoviruses. In: Richman DD, Whitley RJ, Hayden FG, editors. Clinical Virology, 4th edition. ASM Press; 2017.
- Wallace RM, Shlim DR. Rabies. In: CDC Yellow Book: Health Information for International Travel, 2026 edition. US Centers for Disease Control and Prevention; 2025.