Histology · Year 1 · from Histology
Case 2: Rabies Encephalitis
Clinical Image
Source: Wikipedia - Rabies - CC BY-SA 3.0
Case Presentation
A 35-year-old man presents with agitation, confusion, and hydrophobia (fear of water with violent spasms when attempting to drink) three weeks after being bitten by a stray dog while traveling in Southeast Asia. He did not receive post-exposure prophylaxis. He develops hypersalivation, aerophobia (fear of air drafts), and fluctuating consciousness. Physical examination reveals autonomic instability with alternating periods of agitation and calm. The clinical presentation is classic for furious (encephalitic) rabies. Despite intensive care, he deteriorates and dies within one week. Autopsy reveals lymphocytic encephalitis affecting the brainstem and limbic system. Histologically, neurons contain pathognomonic Negri bodies - eosinophilic, round to oval cytoplasmic inclusions representing sites of viral replication, most prominent in hippocampal pyramidal neurons and cerebellar Purkinje cells. The pathophysiology involves rabies virus entering neurons at the bite site and traveling via retrograde axonal transport to reach the CNS.
Key Learning Points
- Rabies virus exploits retrograde axonal transport (dynein-mediated movement along microtubules) to travel from peripheral nerve endings to neuronal cell bodies
- The incubation period reflects the distance the virus must travel; bites closer to the CNS have shorter incubation
- Negri bodies are eosinophilic intracytoplasmic inclusions found in infected neurons, pathognomonic for rabies
- Neurons in the hippocampus (pyramidal cells) and cerebellum (Purkinje cells) are particularly affected
- Understanding axonal transport explains how peripheral infection reaches the CNS and why post-exposure prophylaxis must be given before virus reaches the CNS