Rabies
Introduction
- Mostly bats in developed countries and dogs in developing
- Lyssavirus in Australia
Pathophysiology
- Infection of salivary gland is responsible for infectivity
- Can also spread via mucous membrane, aerosolised virus while in caves, lab exposure, infected organ transplant and improperly inactivated vaccine iatrogenic spread
- Virus remains close to bite site for 20-90 days (incubation)
- Binds to nicotinic Ach receptor in muscle on postsynaptic membrane of NMJ
- Spreads across motor end-plate, ascends and replicates in nervous axoplasm to the DRG, spinal cord and CNS
- Then spreads out from CNS to all peripheral nerves
- Negri bodies are eosinophilic intracellular lesions found in cerebral neurons = highly specific
Pre-exposure prophylaxis
| Risk Category | Nature of Risk | Typical Population | Recommendation |
| Continuous | Virus present continuously; specific exposure likely unrecognised | Rabies research labs | Primary course then serologic testing every 6 months with booster if titre level drops |
| Frequent | Episodic exposures but source may go unrecognised | Rabies diagnostic labs, cavers, vets, animal-control in rabies endemic region, regular bat-handlers | Primary course then serology every 2 years |
| Infrequent | Episodic and recognised | Animal handling in areas where rabies is rare | Primary course only |
| Rare | Always episodic | Population at large | No vaccination required |
Post-exposure prophylaxis
- Potential exposure
- Any bite or scratch from, or mucous membrane or broken skin contact with the saliva or neural tissue of a bat
- Even nibbling, minor abrasions should be considered potentially significant
- Touching, feeding, petting, licks to intact skin, exposure to blood/urine/faeces should not be considered at risk
- Wash all wounds for 5 minutes with soap and water then apply virucidal antiseptic (povidone-iodine or alcohol)
- Avoid suturing wounds at least until after PEP
PEP
- Group 1: No prior rabies vaccination
- HRIG 20IU/kg around wound + IM on ipsilateral deltoid or thigh if cannot fit all in wound
- Rabies vaccine IM contralateral deltoid or thigh (must be at different site)
- 4 doses on days 0, 3, 7 and 14 (+ day 28 if immunosuppressed)
- Follow-up serology 2 weeks after last dose
- Group 2: Previous rabies vaccination (documented)
- Rabies vaccine only on day 0 and 3
- Group 3: Post-exposure prophylaxis commenced overseas
- HRIG should NOT be given >7 days from first rabies vaccine dose as may suppress immune response to vaccination
Risk of rabies in absence of prophylaxis from exposure to rabid animal
- Multiple severe bites on face = 80-100%
- Single bite = 15-40%
- Superficial bite to extremity = 5%
- Contamination of recent wound by saliva = 0.1%
- Contamination of wound >24 hours old with saliva = 0%
- Transmission via fomites = theoretical
- Indirect e.g. raccoon saliva on dog = theoretical
Clinical rabies
- Acute encephalitis almost universally fatal
- Incubation 20-90 days (up to 5 years)
- Shorter incubation if bite on head
- Two clinical forms: Encephalitic (80%) vs. paralytic (20%)
- Encephalitic rabies causes episodes of generalised hyperexcitability, disorientation, hallucinations, bizarre behaviour with lucid intervals. Autonomic dysfunction with hypersalivation, hyperthermia, tachycardia, piloerection, cardiac arrhythmias and priapism are common
- Paralytic rabies begins with paresis of bitten extremity spreading to quadriparesis and bilateral facial weakness. Progresses to coma and organ failure with longer course than encephalitic
- 50% of patients have classic hydrophobia with spasm of pharynx, larynx and diaphragm when attempting to drink
- 7 patients have ever survived rabies and in all but one case, the patient received some form of pre- or post-exposure prophylaxis
Clinical rabies
| Clinical stage | Defining event | Duration | Common Sx |
| Prodrome | First symptom | 2-10 days | Pain/paraesthesia at bite site Malaise, lethargy, headache, fever, nausea, anxiety, agitation |
| Acute neurological phase | First neurological sign | 2-7 days | Anxiety, agitation, depression, hyperventilation, aphasia, incoordination, paresis, paralysis, hydrophobia, delirium, marked hyperactivity |
| Coma | Onset of coma | 0-14 days | Coma, pituitary hypofunction, cardiac arrhythmia |
| Death or recovery (rare) | Death or initiation of recovery | Months (recovery) | PTX, DVT, secondary infections |
Diagnosis and treatment
- Consider in differential for any unexplained acute, rapidly progressive encephalitis
- Especially if autonomic instability, dysphagia, hydrophobia, paraesthesia or paresis
- DDx includes tetanus, polio, GBS, botulism, tranverse myelitis, mass lesions, CVA, cholinergic delirium, viral encephalitis
- Important clues to diagnosis are history of animal bite/scratch and pathognomonic hydrophobia and aerophobia (grimacing with blowing air on face)
- During incubation period no diagnostic test is available
- Once symptoms arise, antigen and antibody testing of serum, CSF, skin and neural tissue can confirm diagnosis
- Steroids are contraindicated as shortens incubation period and increases mortality
- Treatment is aimed at complications as there is NO SPECIFIC THERAPY
Last Updated on October 2, 2020 by Andrew Crofton
Andrew Crofton
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