Question
A 5-year-old boy was brought to pediatric casualty with irritability, agitation, abnormal behaviour, difficulty in swallowing liquids and fear of water. His mother informed that he had been bitten by a stray dog two months back. No medical help had been sought at that time.
- (a) What is the most probable clinical diagnosis 1 mark(s)
- (b) Draw a neat labelled diagram of the causative agent 2 mark(s)
- (c) Describe the pathogenesis of the condition 3 mark(s)
- (d) Describe the laboratory diagnosis e) Describe the risk categorization and recommended post exposure prophylaxis of this disease 4 mark(s)
Answer
(a) Most probable clinical diagnosis: Rabies (furious/encephalitic type) — irritability, agitation, abnormal behaviour, difficulty swallowing liquids, and hydrophobia, two months after an untreated dog bite, is the classical presentation.
(b) Causative agent — description (diagram in text form): the Rabies virus (genus Lyssavirus, family Rhabdoviridae) is a bullet-shaped (cylindrical with one flat and one rounded end), enveloped, single-stranded, negative-sense RNA virus. Its structure comprises: an outer lipid envelope studded with glycoprotein (G) spikes (responsible for host cell receptor attachment and eliciting neutralizing antibody); beneath the envelope, a matrix (M) protein layer; and internally, a helical ribonucleoprotein (RNP) core consisting of the single-stranded RNA genome tightly bound to nucleoprotein (N), along with the phosphoprotein (P) and RNA-dependent RNA polymerase (L protein). (A hand-drawn labelled diagram would depict this bullet-shaped virion with the 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. Within the CNS, extensive viral replication (particularly brainstem/limbic structures) causes severe encephalitis, and the virus then spreads centrifugally (anterogradely) to peripheral tissues including the salivary glands, facilitating transmission, and to structures governing swallowing/autonomic function, producing the characteristic hydrophobia and aerophobia.
(d) Laboratory diagnosis (antemortem): saliva (RT-PCR/virus isolation), nuchal skin biopsy (direct fluorescent antibody test/PCR on nerve twigs at hair follicle base), corneal impression smear (direct fluorescent antibody), 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) Risk categorization and post-exposure prophylaxis (WHO categories):
- Category I (touching/feeding animals, licks on intact skin) — no PEP required.
- Category II (nibbling of uncovered skin, minor scratches without bleeding) — wound care plus vaccination.
- Category III (single/multiple transdermal bites/scratches, licks on broken skin/mucous membrane, bat contact) — wound care, vaccination, plus Rabies Immunoglobulin (RIG) infiltrated around the wound. Given this child suffered a dog bite with no medical attention sought (likely Category III, given the eventual development of clinical rabies, implying an unaddressed significant exposure), the standard approach for such an exposure would have been: immediate, thorough wound washing with soap and water for 15 minutes; active vaccination via the intramuscular Essen regimen (days 0, 3, 7, 14, 28) or intradermal regimen (two sites on days 0, 3, 7, 28); and RIG infiltration around the wound for Category III exposures — unfortunately, since PEP was not administered in time in this case, the disease has now progressed to symptomatic, essentially untreatable rabies, which carries near-100% mortality once clinical symptoms appear.