Rabies Virus

Categorization
Genome: RNA Virus, Negative ssRNA Virus Structure: Enveloped Virus, Helical Virus
Overview
  • Rabies Virus is the prototype member of the Rhabdovirus family and causes the syndrome of Rabies. The helical capsid of rabies virus gives the virion a characteristic "Bullet-shaped" profile on electron microscopy.
Transmission
  • Rabies is a zoonotic organism and infects a wide variety of mammalian species. While dogs were historically the main carriers, animal control measures have now largely relegated the disease to encounters with wild animals such as skunks, racoons, and foxes in the US. Human infection involves the bite of an infected animal and thus requires the inoculation of virus-laden animal saliva directly into a wound.
Pathogenesis
  • Following inoculation, rabies virus replicates within muscle or connective tissue at the wound site. The virus then binds local motor neurons at the neuromuscular junction and undergoes retrograde transport up the axon to the CNS. Replication within the CNS is extensive, causing neuronal derangement more than death, which results in the characteristic rabid syndrome. Remarkably, rabies virus then disseminates systemically by transport down peripheral nerves but especially concentrates in salivary glands which facilitates transmission to new hosts.
Pathology
  • Replication of rabies virus in neurons produces characteristic eosinophilic cytoplasmic inclusions termed "Negri Bodies" which represent aggregates of the viral capsid. The presence of Negri Bodies is pathognomonic of infection with Rabies Virus.
Clinical Consequences
  • Overview
    • The incubation period of rabies varies wildly from weeks to potentially decades. In part, this may reflect the distance the virus requires to travel to the CNS with inoculating wounds in the extrimities resulting in longer incubation periods than those in the face. *Once clinical disease becomes apparent it follows a sequence of prodromal signs, acute encephalitis, and then coma. Once clinical symptoms manifest the likelihood of recovery is essentially zero.
  • Prodrome
    • The prodrome of rabies infection includes constitutional symptoms and lasts several days. Pain or parasthesias may also be felt at the wound site.
  • Encephalitis
    • The acute encephalitic phase of rabies lasts several days and is characterized by a confusion, hallucinations, and potentially combative, bizarre behavior. Derangement of the brainstem can result in fear of water (Hydrophobia) and fear of breezes (Aerophobia). Dysphagia, due to extreme pain associated with swallowing, and hyper-salivation likely result in prototypical foaming at the mouth.
  • Coma
    • Coma rapidly follows the encephalitic phase and ultimately ends in death usually due to respiratory paralysis.
Treatment
  • Because there is no treatment for rabies once clinical signs manifest, clinical intervention is limited to post-exposure prophylaxis. Vaccination with inactivated virus usually allows patients to develop protective humoral immunity during the incubation period. Patients are also injected with protective anti-rabies virus antibody for the rare possibility that the incubation period might be shorter than development of humoral immunity.