Rabies is a viral disease that affects the central nervous system and is almost always fatal once symptoms appear. It is transmitted most often through the bites of rabid animals like dogs. The rabies virus travels from the site of exposure along motor neurons until reaching the brain. There are two clinical forms - furious rabies which causes agitation, hallucinations and hydrophobia, and paralytic rabies which causes muscle weakness and paralysis. Testing of saliva, CSF or brain tissue can detect the virus. Post-exposure prophylaxis including wound cleaning and a vaccine series is highly effective if administered promptly.

1. RABIES
DR ZULU

2. INTRODUCTION
 Rabies is a zoonotic viral disease that affects the CNS
 Caused by a virus of the family Rhabdoviridae, genus Lyssavirus, subgroup rabies
virus
 Rabies is present on all continents except Antartica, with over 95% of human
death occurring in Asia and Africa
 It is one of the neglected tropical disease that predominantly affects already
marginalized, poor and vulnerable populations
 Once clinical symptoms appear, rabies is virtually 100% fatal.

4. TRANSMISION
 Through deep bite or scratch from an animal with rabies, usually a dog
 Transmission can also occur if saliva of infected animals comes into direct contact
with mucosa (e.g eyes or mouth) or fresh skin wounds.
 Wildlife vectors and / or reservoirs include cats, wolves, foxes, jackals, skunks,
mongooses, raccoons, vampire bats, and fruit and insect eating bats.
 Human to human transmission has been documented only through infected
corneal and solid organ grafts from unsuspected rabies infected donors.

5. PATHOPHYSIOLOGY
 Inoculation into muscle
 Endogenous muscle micro-RNA bind to viral transcripts and limit both replication
and viral protein production , such that the virus is able to evade detection by
antigen presenting cells
 Once enough virus replicates, it binds motor neuron junctions at postsynaptic
nicotinic acetylcholine receptors, which initiates uptake into the motor endplate.
 The virus then rapidly propagates across motor axons and chemical synapses in
retrograde fashion toward the ganglia and nerve roots.
 The rabies virus travels along these axons at a rate of 12-24mm/day to enter the
spinal ganglion.
 At this point the prodromal symptoms of neuralgia and hypoesthesia may begin,
in addition to fever and flulike illness

6.  Once reaching the CNS, it spreads throughout
 Anterograde spread of rabies virus via sensory and autonomic pathways from CNS
to salivary glands and other viscera
 Throughout propagation of the virus along motor pathways, the virus elicits little
inflammation
 Rabies does not damage neurons
 Neuronal morphology and lifespan is normal throughout the cause of the
 Death occurs from global neurotransmitter blockade and widespread
dysfunction

7.  The virion acts in the synaptic space, where homology in amino acid sequences
between neurotransmitter receptors for acetylcholine, GABA, and glycine may
afford a mechanism for viral binding of these receptors. Thus its action is
neurotoxic rather than cytotoxic
 Characterized by the presence of negri

8. PATHOPHYSIOLOGY

9. INCUBATION PERIOD
 Average duration of incubation is 20-90 days
 In more than 90% of cases, incubation is less than 1year
 A person whose inoculum occurs with a scratch on the hand may take longer to
develop symptoms of rabies than a person who receives a bite to the head
 The incubation period is less than 50days if the patient is bitten on the head or
neck or if a heavy inoculum is transferred through multiple bites, deep wounds, or
large wounds.
 Infected patients may not recall exposure because of the prolonged incubation
period

10. CLINICAL FEATURES
 Two forms of rabies
- Furious rabies
- Paralytic rabies
FURIOUS RABIES
Most common presentation and the duration of this period is 2-10days
 Headache
 Fevers, flu like symptoms
 Confusion
 Fluctuating periods of excitement with hallucinations
 Hydrophobia

11.  Insomnia
 Depression
 Diarrhea and vomiting
 Pain or intense itching at the inoculation site
-After several hours to days, this becomes episodic and interspersed with calm,
cooperative, lucid periods
-Furious episodes last less than 5min
Episodes may be triggered by visual, auditory or tactile stimuli or may be
spontaneous
- This phase may end in cardiorespiratory arrest or may progress to paralysis

12. PARALYTIC RABIES
-Associated with objective signs of developing CNS disease, however consciousness
remains unaffected until the onset of coma.
-Patient is relatively quiet compared with a person with the furious form.
-The duration is 2-7days.
 Muscle fasciculation
 Priapism
 Focal or generalized convulsions
 Paralysis (ascending paralysis)

13. INVESTIGATIONS
 Viral cultures and polymerase chain reaction (PCR) assay;
- Saliva
- CSF
- Brain tissue
 Blood gas analysis
 FBC/DC
 CXR
 EEG,ECG
 Skin biopsy (most reliable test of rabies infection during the first week)

14. MANAGEMENT
 Wound should be cleaned immediately with soap and water, flushing it thoroughly
to remove saliva.
 Debridement and careful exploration for foreign body
 Leave wounds to heal by secondary intention to permit drainage of wound fluids
and prevent infection
 Antibiotic prophylaxis
 Anti rabies on day 0,3,7,14 and 28

15. REFERENCES
 Zandi F, Goshadrou F, Meyfour A, Vaziri B. Rabies Infection: An Overview of
Lyssavirus-Host Protein Interactions. Iran Biomed J. 2021 Jul 1. 25 (4):226-42
 WHO. Rabies. World Health Organization. Available at
http://www.who.int/mediacentre/factsheets/fs099/en/. 21 May 2019; Accessed: 1
Jun 2019.
 Liu C, Cahill JD. Epidemiology of Rabies and Current US Vaccine Guidelines. R I
Med J (2013). 2020 Aug 3. 103 (6):51-53.