Rabies Virus: Symptoms, Transmission & Pathophysiology

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Questions and Answers

Why is a combination of tests required for antemortem rabies diagnosis rather than a single test?

  • No single test has sufficient sensitivity to reliably detect the virus before death. (correct)
  • The rabies virus mutates rapidly, and a single test may not be able to detect all variants.
  • The different tests detect different strains of the rabies virus. A combination of tests is needed to cover all possible strains.
  • Different tests are needed to differentiate rabies from other neurological diseases.

The rabies virus uses dynein to move within neurons. What is the significance of this mechanism in the context of rabies pathogenesis?

  • Dynein allows the virus to travel retrograde along peripheral nerves toward the central nervous system (CNS). (correct)
  • Dynein facilitates the rapid spread of the virus to different organs via the bloodstream.
  • Dynein enables the virus to travel anterograde, allowing the virus to leave the CNS and enter other tissues.
  • Dynein facilitates the virus's entry into muscle cells by binding to acetylcholine receptors.

Why is post-exposure prophylaxis (PEP) for rabies ineffective once symptoms appear?

  • Once symptoms develop, the virus has already reached the CNS, causing irreversible damage. (correct)
  • Antibodies from PEP can no longer cross the blood-brain barrier once the virus is in the brain.
  • PEP drugs interfere with the body's natural immune response, making the infection worse.
  • Once symptoms appear, the virus is no longer susceptible to the drugs used in PEP.

How does the rabies virus exploit the neuromuscular system to establish a CNS infection?

<p>The virus binds to acetylcholine receptors on muscle cells and then crosses the neuromuscular junction to enter motor neurons. (C)</p> Signup and view all the answers

What is the primary reason for the variable incubation period of the rabies virus?

<p>The distance the virus must travel from the entry site to the central nervous system (CNS). (C)</p> Signup and view all the answers

Why does rabies preferentially infect neurons over muscle cells, despite initially binding to receptors on muscle cells?

<p>Neurons offer a pathway to the CNS, facilitating the virus's pathogenic progression. (B)</p> Signup and view all the answers

How does the overactivity of the autonomic nervous system manifest in encephalitic (furious) rabies?

<p>Excessive saliva production, sweating, and dilated pupils. (A)</p> Signup and view all the answers

What is the significance of Negri bodies in the postmortem diagnosis of rabies?

<p>They are pathognomonic intracellular inclusions indicative of rabies infection. (A)</p> Signup and view all the answers

In developed countries, rabies transmission primarily occurs through wildlife such as bats, raccoons, skunks, and foxes. What preventative measure is MOST effective in reducing the risk of rabies transmission from these animals to humans and domestic pets?

<p>Administering routine rabies vaccinations to domestic animals. (B)</p> Signup and view all the answers

An individual who has been exposed to a potentially rabid animal receives post-exposure prophylaxis (PEP). Which of the following BEST describes the immunological mechanism by which human rabies immunoglobulin (HRIG) and the rabies vaccine work synergistically to prevent disease progression?

<p>HRIG directly neutralizes the rabies virus, while the vaccine stimulates the body to produce its own antibodies against the virus. (D)</p> Signup and view all the answers

Flashcards

Rabies Virus

Helical, enveloped, negative-sense, single-stranded RNA virus belonging to the Rhabdoviridae family.

Early Phase Rabies Symptoms

Malaise, headache, fever, and paresthesia (tingling, itching, or burning at the site of infection).

Encephalitic (Furious) Rabies

Fever, hydrophobia, foaming at the mouth, excessive saliva, agitation, aggression, potentially leading to coma.

Paralytic Rabies

Ascending paralysis that spreads up the body, potentially leading to respiratory failure.

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Rabies Neuroinvasion

The virus uses dynein to travel retrograde along peripheral nerves to the CNS.

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Negri Bodies

Intracellular sacs full of viral proteins found in CNS cells infected with rabies.

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RT-PCR for Rabies

Detects viral RNA in saliva.

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Immunofluorescent Staining

Detects viral antigen in cutaneous nerves of hair follicles from a skin biopsy.

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Post-Exposure Prophylaxis (PEP)

Must be given before symptoms appear, including wound cleaning, HRIG, and killed rabies vaccine.

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Passive Immunization for Rabies

Human rabies immunoglobulin (HRIG)

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Study Notes

  • Rabies virus is a helical, enveloped, negative-sense, single-stranded RNA virus.
  • It belongs to the Rhabdoviridae family.

Transmission

  • Transmitted via saliva from infected animals, such as dogs, skunks, raccoons, foxes, and bats.
  • In rare cases, it can be transmitted through airborne droplets, like in bat caves.

Early Phase (Prodromal Phase)

  • Symptoms include malaise, headache, fever, and paresthesia (tingling, itching, or burning sensation at the site of infection).

Clinical Phase: Encephalitic (Furious) Rabies

  • Most common presentation.
  • Symptoms: fever, hydrophobia (fear of water), foaming at the mouth (due to pharyngeal spasms), excessive saliva production, sweating, dilated pupils (due to autonomic nervous system overactivity), agitation, and aggression leading to coma.

Clinical Phase: Paralytic Rabies

  • Less common presentation.
  • Ascending paralysis that spreads up the body.
  • Leads to respiratory failure.

Pathophysiology

  • Glycoprotein spikes on the viral envelope bind to nicotinic acetylcholine receptors on muscle cells, facilitating entry.
  • Prefers neurons over muscle cells.
  • Crosses the neuromuscular junction and enters motor neurons to replicate.
  • Uses dynein (a motor protein) for retrograde transport along peripheral nerves toward the CNS (at a rate of a few millimeters per day).
  • Invades the brain and spreads to other structures, including the salivary glands.

Diagnosis: Antemortem (Before Death)

  • Requires multiple tests.
  • RT-PCR (Reverse Transcriptase Polymerase Chain Reaction) detects viral RNA in saliva.
  • Immunofluorescent staining on skin biopsy (from the back of the neck) detects viral antigen in cutaneous nerves of hair follicles.
  • Antibody detection in blood or cerebrospinal fluid (CSF).

Diagnosis: Postmortem (After Death)

  • Detecting Negri bodies in brain cells; intracellular sacs full of viral proteins.
  • Negri bodies are typically found in Purkinje cells (cerebellum) and pyramidal cells (hippocampus) and stain dark pink with eosin dye (eosinophilic).
  • Viral antigens in brain tissue.

Incubation Period

  • Typically 1–3 months.
  • Varies depending on the entry point; the farther from the CNS, the longer the incubation.

Treatment and Prevention: Post-Exposure Prophylaxis (PEP)

  • Must be administered before symptoms appear.
  • Includes wound cleaning.
  • Passive immunization with human rabies immunoglobulin (HRIG).
  • Active immunization with a killed rabies vaccine.

Pre-Exposure Vaccination

  • Given to high-risk groups.
  • Includes veterinarians and lab workers handling rabies virus.

Key Words

  • Negri bodies
  • Zoonotic disease
  • Hydrophobia
  • Bullet-shaped virus
  • Dog bite
  • Drooling/foaming at the mouth

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