Question
A 11-year-old girl, presented with history of agitation, delirium, abnormal behavior, hallucinations, difficulty in swallowing liquids and fear of water. Her parents reported that she was bitten by a stray dog on her right leg two months prior to presentation for which she had received only oral antibiotics and injection tetanus toxoid.
- (a) What is your clinical diagnosis and name the causative agent. 2 mark(s)
- (b) Draw a neat and labelled diagram of the causative agent. 2 mark(s)
- (c) Describe the pathogenesis. 3 mark(s)
- (d) Discuss the laboratory diagnosis in detail. e) Add a note on the prophylactic measures available for this disease. 4 mark(s)
Answer
(a) Clinical diagnosis and causative agent: Rabies (furious/encephalitic type), caused by the Rabies virus (genus Lyssavirus, family Rhabdoviridae) — agitation, delirium, abnormal behaviour, hallucinations, difficulty swallowing liquids, and hydrophobia, two months after a dog bite with inadequate management (only oral antibiotics and tetanus toxoid — notably, no rabies-specific post-exposure prophylaxis, vaccine, or immunoglobulin was given), is the classical presentation.
(b) Diagram description: rabies virus is bullet-shaped, an enveloped, single-stranded, negative-sense RNA virus. The outer lipid envelope is studded with glycoprotein (G) spikes (mediating host cell receptor attachment); beneath this lies the matrix (M) protein layer; internally, a helical ribonucleoprotein (RNP) core comprises the RNA genome tightly bound to nucleoprotein (N), along with phosphoprotein (P) and RNA-dependent RNA polymerase (L protein). (A hand-drawn labelled diagram would depict this bullet-shaped virion with envelope, glycoprotein spikes, matrix protein, and internal helical RNP core clearly labelled; described here in text form as diagrams cannot be rendered.)
(c) Pathogenesis: following inoculation via the bite, the virus replicates locally in muscle tissue, enters peripheral nerve endings, and travels retrograde (centripetally) along axons to the CNS — the variable incubation period (here, two months) reflects this neural transit time, influenced by bite site/severity. Within the CNS, extensive viral replication (particularly brainstem/limbic structures) causes severe encephalitis; the virus then spreads centrifugally (anterogradely) to peripheral tissues including salivary glands (facilitating onward transmission) and structures governing swallowing/autonomic function, producing hydrophobia and aerophobia.
(d) Laboratory diagnosis (antemortem): saliva (RT-PCR/virus isolation), nuchal skin biopsy (direct fluorescent antibody test/PCR on cutaneous nerve twigs at the hair follicle base), corneal impression smear (direct fluorescent antibody detection), CSF (antibody detection in an unvaccinated patient, RT-PCR), and serum (rabies-neutralizing antibody). (Postmortem: Negri bodies on brain histopathology and direct fluorescent antibody test on brain tissue, the definitive confirmatory method.)
(e) Prophylactic measures:
- Immediate, thorough wound washing with soap and running water for at least 15 minutes — the single most effective, immediately available intervention (which this patient did not appropriately receive).
- Category-based post-exposure prophylaxis (WHO categorization): Category I (no PEP), Category II (vaccination), Category III (vaccination plus Rabies Immunoglobulin, RIG, infiltrated around the wound) — a dog bite of this nature would typically warrant Category III management, which was clearly not administered here (only antibiotics and tetanus toxoid were given, entirely omitting rabies-specific prophylaxis).
- Active vaccination — modern cell-culture vaccines (PVRV, PCECV), via the intramuscular Essen regimen (days 0, 3, 7, 14, 28) or the dose-sparing intradermal regimen (two sites on days 0, 3, 7, 28).
- Pre-exposure prophylaxis — a vaccination series available for individuals at high occupational risk (veterinarians, animal handlers), reducing but not eliminating the need for post-exposure boosters if subsequently bitten.
- Animal control measures — vaccination of dogs, control of stray animal populations, and public health education on the critical importance of seeking immediate, complete rabies-specific PEP after any animal bite — this case illustrates the tragic consequence of incomplete/inappropriate post-exposure management.