Read the clinical history and answer the following questions:
A 27 years old male was admitted in intensive medical care unit with drooling of saliva
and fear for intake of liquids since morning. There was a past history of dog bite on
his right leg ten days back.
(a) What is the provisional diagnosis 1 mark(s)
(b) Discuss briefly about the pathogenesis of the above clinical condition. 3 mark(s)
(c) Describe the laboratory investigations to confirm the diagnosis 2 mark(s)
(d) Explain the prophylaxis of this condition 4 mark(s)
Q110 marksEssays
Answer
a) Provisional diagnosis: Rabies (furious/encephalitic form) — hydrophobia (fear of liquids), hypersalivation/drooling, and a history of a dog bite ~10 days earlier is classical.
b) Pathogenesis
Rabies virus (a rhabdovirus) is introduced into a bite wound in the saliva of an infected animal; the virus first replicates locally in muscle tissue near the inoculation site, then enters peripheral nerve endings and travels retrograde along axons (via fast axonal transport) toward the central nervous system — the interval before neural entry and the length of the neural pathway (distance from the bite site to the CNS) is a key determinant of the incubation period (bites closer to the head/face have shorter incubation, given the shorter neural distance). Once in the CNS, the virus replicates extensively in neurons (producing characteristic Negri bodies, intracytoplasmic inclusions in infected neurons, classically in hippocampal/Purkinje cells), causing severe encephalitis. From the CNS, the virus then spreads centrifugally via peripheral nerves to other tissues, notably the salivary glands (explaining infectivity of saliva and the basis for animal-to-human transmission via bite) and other highly innervated tissues (cornea, skin). The hydrophobia characteristic of furious rabies is thought to result from painful, violent spasm of the pharyngeal/laryngeal muscles triggered by attempts to swallow, itself due to viral involvement of brainstem swallowing centres and associated autonomic dysregulation.
c) Laboratory investigations
Direct Fluorescent Antibody (DFA) test — the gold-standard confirmatory test, on brain tissue (post-mortem) or, antemortem, on nuchal skin biopsy, corneal impression smear, or saliva.
Negri body demonstration — classical histopathological finding (eosinophilic intracytoplasmic inclusions) in brain tissue, though absence does not exclude rabies.
RT-PCR — highly sensitive molecular detection of viral RNA in saliva, CSF, or tissue.
Serology — detection of rabies-neutralizing antibody, useful in unvaccinated patients surviving long enough to mount a response, though generally unhelpful for early antemortem diagnosis.
d) Prophylaxis
Wound management: immediate, thorough washing with soap and water for at least 15 minutes, followed by a virucidal agent.
Category-based management (WHO exposure categories I–III): Category II (minor scratches) — vaccine alone; Category III (transdermal bites, deep scratches, mucous membrane exposure) — vaccine PLUS Rabies Immunoglobulin (RIG), infiltrated around the wound.
Active immunization: modern cell-culture-derived vaccines (HDCV, PCECV, PVRV) on a defined multi-dose schedule.
Passive immunization: RIG for Category III exposures, providing immediate neutralizing antibody while active immunity develops.
Pre-exposure prophylaxis: recommended for high-risk occupational groups.
General measures: animal (dog) vaccination programmes and public health education.
