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Rabies

Rabies is a viral disease caused by the rabies virus, primarily transmitted through animal bites, especially from dogs and bats. It is highly preventable with prompt medical care, including post-exposure prophylaxis, but is almost always fatal once clinical symptoms appear. The disease presents in two forms: encephalitic rabies, characterized by behavioral changes and paralysis, and paralytic rabies, which progresses to flaccid paralysis without early behavioral changes.

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Rabies

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Rabies

Straight to the point of care

Last updated: Jul 06, 2023

Table of Contents
Overview 3
Summary 3
Definition 3

Theory 4
Epidemiology 4
Aetiology 5
Pathophysiology 7
Classification 8
Case history 9

Diagnosis 10
Approach 10
History and exam 12
Risk factors 14
Investigations 15
Differentials 17
Criteria 18

Management 21
Approach 21
Treatment algorithm overview 23
Treatment algorithm 24
Emerging 30
Primary prevention 30
Secondary prevention 32
Patient discussions 32

Follow up 34
Complications 35
Prognosis 36

Guidelines 37
Diagnostic guidelines 37
Treatment guidelines 38

Online resources 40

References 41

Images 47

Disclaimer 51
Rabies Overview

Summary
Rabies is a notifiable disease in many countries.

Preventable through prompt medical care. Post-exposure prophylaxis with wound cleansing, immunisation,

OVERVIEW
and rabies immunoglobulin is highly effective at preventing the disease when given promptly and properly.

Symptoms begin with a non-specific prodromal illness. In encephalitic rabies, this is followed by early-onset
behavioural changes and late-onset paralysis. In the paralytic form, the behavioural changes are absent.

Almost always fatal following onset of clinical signs. The disease is rapidly progressive, leading to death
within 2 weeks in most cases. Some survivors have been reported.

Pre-exposure prophylaxis is recommended for certain people at high risk for exposure.

Definition
An acute viral encephalomyelitis caused by the rabies virus and other members of the Lyssavirus genus,
which is transmitted by animal bites, mainly dogs in developing countries and bats in other countries
including the US.

The World Health Organization (WHO) has set a global goal to achieve no human deaths from dog-
transmitted rabies by 2030.[1]

Epidemiology
Rabies is distributed worldwide. It is present in more than 150 countries and territories, and on all continents
except Antarctica. The main burden of disease is located in developing countries in Asia and Africa.[5] There
THEORY

has been a substantial reduction in the number of cases in Latin America and the Caribbean over the years.

Globally, about 59,000 people die from rabies every year, many of whom are children. Approximately 1-3
cases of rabies are reported in the US annually, but the main impact to the healthcare system is from the
thousands of exposures that require risk assessment and post-exposure prophylaxis every year.[6] [7]
Twenty-five human rabies cases were reported in the US between 2009-2019. Most of these cases were due
to transmission via bats. Between 1960-2018, 28% of cases were attributed to bats, and 28% were attributed
to dog bites during international travel.[8] Cases from organ transplantation have also been reported.[7]
Between September and November 2021, 3 people died from rabies in the US after direct contact with bats
in or around their homes, taking the total to 5 cases in 2021 (no cases were reported in the US in 2019, 2020
or 2022).[9] [10] Nineteen cases were reported in Latin American countries (Bolivia, Dominican Republic,
Guatemala, and Haiti only) in 2017.[11] Children account for 30% to 50% of rabies cases.[12] Approximately
50% of US cases occur between September and November.[13] [14] [15]

Human rabies is extremely rare in the UK. No human cases of rabies acquired from animals other than bats
have been reported in the UK since 1902. A single case of human rabies acquired from a bat was reported in
Scotland in 2002. Six cases of rabies associated with animal exposures abroad have been reported between
2000-2018, the most recent case being a UK resident who became infected and died following a cat bite
during a visit to Morocco.[16]

All mammals are susceptible to infection. The principal vector in developing countries is the dog. The
elimination of canine rabies has successfully eradicated rabies in some countries. Canine rabies has
been eliminated in the US, but other vectors exist, including bats, raccoons, skunks, foxes, jackals, and
mongooses.[17] Bats are now the major source of human rabies in the Americas. Infection of cats, dogs, and
other domestic animals occurs with some frequency and increases the exposure risk to humans.

In Western Europe, Brazil, and South Korea, rabies has also been maintained in nature by other vectors.
Many reservoirs are found in wild carnivora, including coyotes; red, arctic, and grey foxes; jackals;
mongooses; raccoons; skunks; and wolves.[18] Bats have also emerged as vectors in some Latin American
and European countries, parts of Africa, and in Australia. The main vector in Western Europe is the red fox.

4 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jul 06, 2023.
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Use of this content is subject to our) . © BMJ Publishing Group Ltd 2023. All rights reserved.
Rabies Theory

THEORY
A canine suspected of being rabid that had been exhibiting signs
of restlessness and overall uncharacteristic aggressive behaviour
Centers for Disease Control and Prevention

Aetiology
Rabies is caused by various negative-sense RNA viruses of the Lyssavirus genus, which belongs to the
Rhabdoviridae family. The genus is composed of 17 recognised species: rabies virus, Lagos bat virus,
Mokola virus, Duvenhage virus, Aravan virus, Irkut virus, Khujand virus, European bat lyssavirus types 1 and
2, West Caucasian bat virus, Australian bat lyssavirus type 1, Shimoni bat virus, Ikoma virus, Bokeloh bat
lyssavirus, Gannoruwa lyssavirus, Bat lyssavirus, and Taiwan bat lyssavirus.[19] [20] [21]

Rabies is usually transmitted to humans following a bite from an infected animal including bats, foxes,
raccoons, jackals, and mongooses. Dogs are the most common source globally, while bats are the major
source in the US and the Americas. Non-bite exposures are also possible and include being scratched, being
licked over an open wound or mucous membrane, or being exposed to infected brain tissue or CSF.

There are reported cases of rabies being transmitted by organ transplantation.[22] [23] [24] [25]

Rabies has been reported in an anteater (tamandua) which was translocated from Virginia to Tennessee. All
exposed people received post-exposure vaccination and no human cases occurred. This case demonstrates

Illustration of rabies virus in longitudinal section

Centers for Disease Control and Prevention

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Use of this content is subject to our) . © BMJ Publishing Group Ltd 2023. All rights reserved.
Rabies Theory

THEORY
Illustration of rabies virus in cross-section. Concentric layers: envelope
membrane bilayer, M protein, and tightly coiled encased RNA
Centers for Disease Control and Prevention

Pathophysiology
The incubation period is variable. It is usually 2 weeks to 3 months but with a range from 5 days to 7 years
(very rare). Shorter incubation periods are associated with severe bites and bites to the head and face.

The nicotinic acetylcholine receptor at the motor end plate mediates virus entry to myocytes where initial
replication takes place.[27] The virus enters the nervous system through unmyelinated sensory and motor
terminals and is transported by fast retrograde axonal transport, crossing new synapses roughly every 12
hours. Once the virus has entered the central nervous system, it is sequestered from the immune system
and immunisation will not be effective. In vitro studies have shown evidence of oxidative stress caused by
mitochondrial dysfunction in neurons and other cells of the CNS.[28] Clinical symptoms begin once the virus
infects the spinal cord and progress rapidly as the virus spreads through the CNS.[29] The rabies virus exits
the CNS through motor, sensory, and autonomic nerves, and replicates locally in salivary and lacrimal glands
in order to be transmitted to the next host.

Many aspects of rabies pathophysiology remain a mystery. It is unclear how rabies causes paralysis.[30] The
pathophysiological differences between the encephalitic and paralytic forms of rabies may involve differences
in the host inflammatory response.[31] The cause of death in rabies is unknown because wild-type viruses
are not cytopathic, apoptotic, or inflammatory.

This transmission electron micrograph reveals the presence of Lagos bat

virus virions and an intracytoplasmic inclusion body in this tissue sample
Centers for Disease Control and Prevention; Dr Fred Murphy; Sylvia Whitfield

Classification
Clinical classification
Encephalitic (furious) rabies

• A febrile prodrome is followed by behavioural changes, including alternating agitation and normalcy,
insomnia, and hallucinations. Paraesthesias and paralysis may occur. Coma and death follow.
Paralytic rabies

• A febrile prodrome is followed by rapid progression to flaccid paralysis. Behavioural changes occur
late.

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Rabies Theory

Case history
Case history #1

THEORY
An 11-year-old boy in the US presents to the emergency department with fever, sore throat, and
vomiting. The only known animal contacts are house pets. There is no history of travel abroad, but the
patient attended a summer camp in Alabama 2 months earlier. The patient has never received rabies
immunisation. Laboratory tests and CXR are unremarkable and he is sent home. He returns the same
day with additional symptoms of insomnia, urinary urgency, paraesthesias of the scalp and right arm,
dysphagia, disorientation, and ataxia. He deteriorates rapidly, with slurred speech, hallucinations, and
agitation requiring sedation and intubation. Tests for West Nile virus, HSV, and enterovirus were negative.
The patient progresses to coma over several days, and develops autonomic instability. He dies on the
14th day.

Case history #2
A 52-year-old man, recently arrived from India, presents after 3 days of restlessness and intermittent
abdominal pain. Examination shows only diaphoresis and mild distress. He is admitted for possible
bowel obstruction. Over 12 hours, he develops cardiac arrhythmia, fever, and increased diaphoresis.
He is unable to ingest liquids. The following day he exhibits strange behaviour and leg numbness. Later
he develops hallucinations, aggressive behaviour, hypersalivation, and cardiac arrest. The patient is
resuscitated and admitted to the ICU. He has tachycardia, muscular rigidity, and body tremor. An MRI of
the brain is unremarkable. A detailed history reveals that the patient had sustained bites from a puppy in
India to the right hand and leg 3 months ago and has never received a rabies immunisation. At this point,
rabies is suspected. The patient becomes comatose and dies 2 days later after another cardiac arrest.

Other presentations
Rabies is difficult to diagnose in the absence of identifiable rabies exposure. Clinically, rabies has 2
forms: encephalitic (furious) and paralytic. Both have non-specific prodromes of fever, chills, malaise, sore
throat, vomiting, headaches, and paraesthesias. Pain or paraesthesias at the site of the animal bite are
often present. In the encephalitic form, the prodrome is followed by symptoms of altered mental status,
agitation, hyperactivity, tremors, hypersalivation, mydriasis, dysphagia, hydrophobia, and aerophobia.
This is followed by paralysis with coma and death. In the paralytic form, there are no early changes
in mental status. Ascending weakness appears late in the infection and rapidly progresses to flaccid
paralysis, coma, and death. There is the suggestion that milder forms of rabies may exist.[2] [3] [4] With
better access to pre-mortem diagnostics, rare abortive cases, less severe forms, and spontaneous
recoveries have been identified.

Approach
Rabies should be suspected in any patient with a history of animal exposure who has an unexplained
encephalitis or myelitis. It is a rare cause of encephalitis in industrialised nations; therefore, more common
causes should be simultaneously considered and excluded. Symptoms of rabies progress rapidly over a
period of days. If this rapid progression does not occur, rabies infection is less likely.[13] [38] [39]

Rabies is a notifiable disease in many countries. Cases should be reported immediately to local health
authorities.

History
It is important to establish whether the patient has had a documented or likely exposure from a known
vector. Known vectors include dogs, bats, raccoons, skunks, foxes, jackals, and mongooses. Most
patients in the US contract rabies from bats.[17] A history of a bat bite or contact with a bite may be
present. Some patients may report finding a bat in the home. However, in many cases, there is no history
of contact with bats or any other vector, so the absence of an animal exposure history should not be used
to exclude rabies.

Dogs are the main vectors in most rabies-endemic developing countries. The red fox is the main vector
in Western Europe. Vectors in other countries include coyotes; red, arctic, and grey foxes; jackals;
mongooses; raccoons; skunks; and wolves.[18] In the UK, the UK Health Security Agency has also
issued information. [NaTHNaC/Travel Health Pro: rabies factsheet] (https://travelhealthpro.org.uk/
factsheet/20/rabies)

People at elevated risk for exposure to rabies include:[33]

• People working with live rabies virus in research or vaccine production facilities
• People performing diagnostic testing for rabies in laboratories
• People with frequent bat contact
• People who interact with animals who could be rabid
DIAGNOSIS

• People who perform animal necropsies

• People whose occupational or recreational activities typically involve animal contact
• Selected travellers (depending on occurrence of animal rabies in destination country, availability of
treatments, intended activities, and duration of stay).
Occupations at higher risk include animal handlers, field biologists, cavers, missionaries, veterinarians,
and some laboratory workers. Children are at highest risk of infection because of their height,
developmental skills, and proximity to dogs in the street.[33]

Clinically, rabies has 2 forms: encephalitic (furious) and paralytic. Both have non-specific prodromes of
fever, chills, malaise, sore throat, vomiting, headaches, and paraesthesias. Pain or paraesthesias at the
site of the animal bite are often present in both forms. Pruritus is another common presenting feature.

In the encephalitic form, the prodrome is followed by symptoms of altered mental status, agitation,
hyperactivity, tremors, hypersalivation, mydriasis, dysphagia, hydrophobia with hydrophobic spasms,
and aerophobia. The patient often maintains alertness and cognition at intervals. Hydrophobic spasms
may progress to cause seizures. The encephalitic symptoms are followed by paralysis. As paralysis
sets in, patients may have involvement of the bladder or bowel sphincters, leading to faecal or urinary
incontinence. Coma and death follow rapidly.

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Rabies Diagnosis
In the paralytic form, there are no early changes in mental status. Ascending weakness rapidly
progresses to flaccid paralysis, coma, and death.

There is the suggestion that milder forms of rabies may exist.[2] [3] [4]

Physical examination
Fever is a key sign of rabies, and the diagnosis of rabies is unlikely unless the patient is at least
intermittently febrile. Hydrophobia and aerophobia are the most specific signs. Severe laryngeal or
diaphragmatic spasms and a sensation of choking occur.

In rabies-endemic countries, offering a cup of water to elicit hydrophobia and fanning air at the face (or
placing nasal cannulae) to elicit aerophobia are common manoeuvres. The patient can have signs of
autonomic instability, including hypertension, profuse hypersalivation, marked tachycardia, priapism,
and hyperthermia. Signs of paralysis appear late in the disease course. Numbness and weakness
typically affect the same side of the body as the bite. Careful neurological examination excludes paresis
associated with conversion disorders.[39] [40]

Investigations to diagnose rabies

Diagnosis relies on viral antigen detection, viral antibody detection, viral RNA detection, or virus
isolation.[41] Establishing the diagnosis usually requires the simultaneous testing of saliva, a skin biopsy,
CSF, and serum. The virus is more likely to be detected at the beginning of the clinical course.

• Saliva is tested using PCR for rabies RNA. Most patients with rabies have a positive result with
repeated testing, as PCR testing is very sensitive. Viral culture can be used to isolate the virus if
the results of other tests are equivocal. A negative result in saliva alone does not exclude rabies. A
positive result is also an indication of the infectivity of patient and of the need for patient isolation
and prevention measures in healthcare personnel.
• A 5- to 6-mm skin biopsy is taken from the posterior region of the neck at the hairline. Rabies can
be detected by direct fluorescent antibodies against rabies antigens or PCR for rabies RNA. PCR
testing is very sensitive.

DIAGNOSIS
• CSF is examined microscopically and tested for biochemical markers and the presence of rabies
antibodies. A lymphocytic pleocytosis is detectable in 60% of patients in the first week and 85%
of patients in the second week. CSF protein levels may be mildly elevated (>0.5 g/dL [>50 mg/
dL]), with a low to normal glucose concentration. CSF quinolinic acid is high early on, and lactate
progressively increases over days. Rabies can be detected in CSF by detection of neutralising
antibodies.
• Serum and CSF are tested for the presence of neutralising antibodies but are rarely diagnostic at
presentation. Antibodies may not be detected at early stages of the disease, but serial tests will
demonstrate increase in antibody levels by day 14 of hospitalisation. A positive result in serum
indicates infection only in patients who have not been immunised; a positive result in CSF is always
diagnostic.
A negative result in any 1 sample alone does not exclude rabies. Results in saliva, skin biopsy, CSF,
and serum (in non-immunised patients) must all be negative. If the results are negative and the clinical
suspicion is high, the tests should be repeated.[38] [39] [42]

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Rabies Diagnosis
Investigations to exclude other causes
CSF should also be tested to exclude other treatable causes of encephalitis. CSF is usually sent to test
for HSV (using PCR), enterovirus (using PCR), and West Nile virus (detection of antibodies). Serological
tests for arboviruses, Bartonella , and rickettsial infection should also be considered. Testing for CSF N-
methyl-D-aspartate (NMDA) glutamate receptor antibodies is necessary to exclude this common mimic of
rabies.[43]

An MRI of the head may be performed to exclude other causes of neurological symptoms, and is
generally normal in the first week of rabies.[42]

History and exam

Key diagnostic factors
presence of risk factors (common)
• Key risk factors include a recent scratch or bite from a known vector in a rabies-endemic country,
recent contact with a bat, and occupational or recreational exposure.

hydrophobia (common)
• A classic sign of rabies that appears within a few days of disease onset and is identified in about one
third of the cases.
• Attempting to drink or being presented with liquid to drink produces severe laryngeal or diaphragmatic
spasms and a sensation of choking.
• Can be elicited by presenting a cup of water to the patient.
• One of the most specific signs of the disease.[13]

aerophobia (common)
• A classic sign of rabies that appears within a few days of disease onset.
DIAGNOSIS

• Air blown on the face produces severe laryngeal or diaphragmatic spasms and a sensation of choking.
• Can be elicited by fanning the face or placement of nasal cannulae.
• One of the most specific signs of the disease.[13]

limb numbness, pain, and paraesthesia (common)

• Occurs on the side of body where bite exposure occurred.[39] [40]

pruritus (common)
• A common presenting manifestation.[13] [39] [40]

dysphagia (common)
• Occurs in 41% of cases.[13]

fever (common)
• Always present in rabies infection and appears as part of the prodrome.
• The diagnosis of rabies is unlikely unless the patient is at least intermittently febrile.

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Rabies Diagnosis
change in behaviour (common)
• Frequently the first sign observed by the family.
• Rare in the paralytic form.

agitation and confusion (common)

• Usually relapsing/remitting over hours.[13]
• Rare in the paralytic form.

hallucination (common)
• Frequently seen in patients with encephalitic form.[44]

signs of autonomic instability (common)

• Consists of hypertension, hyperthermia, profuse hypersalivation, tachycardia, priapism, and
hyperventilation. Usually observed after first week of illness.[13] [38] [40]
• Rare in the paralytic form.

rapid progression of symptoms (common)

• Rabies progresses rapidly over a period of days.[39] If this progression does not occur, rabies is less
likely.

weakness and paralysis (common)

• Present in about 16% of cases.[13]
• The main feature of the paralytic form.

Other diagnostic factors

urinary or faecal incontinence (common)
• Due to involvement of the bladder or bowel sphincters.[30] [40]

coma (common)

DIAGNOSIS
• Observed within 1 week after onset of symptoms.[44]

abdominal pain (uncommon)

• Reported in 20% of cases diagnosed antemortem. Can be confused with acute abdomen.[39]

insomnia (uncommon)
• A non-specific symptom.

seizures (uncommon)
• May be seen in pre-terminal phase.[40]

slurred or stut tered speech (uncommon)

• Due to neurological deficits.

ataxia (uncommon)
• May be accompanied by other motor deficits in atypical cases.[40]

Risk factors
Strong
recent scratch or bite from a known vector
• The principal vector in developing countries is the dog.
• In the US, vectors include bats, raccoons, skunks, foxes, and mongooses.[17] Bats are the major
source of infection in the US and the Americas. Over 95% of indigenously acquired cases in the US
are caused by bat viruses. Only 55% of patients with a bat rabies virus infection report an antecedent
bite from a bat or other physical contact with a bat.[13] About 10% of patients with a bat rabies
infection and no known history of bat contact have a recent history of finding bats in the home.[15] [32]
• In Western Europe, Brazil, and South Korea, rabies has also been maintained in nature by other
vectors. Many reservoirs are found in wild carnivora, including coyotes; red, arctic, and grey foxes;
jackals; mongooses; raccoons; skunks; and wolves.[18] Bats have also emerged as vectors in some
Latin American and European countries, parts of Africa, and Australia. The main vector in Western
Europe is the red fox.
• A case has been reported in a captive anteater (tamandua). This demonstrates the possibility of rabies
translocation by human movement of captive mammals, including species in which rabies has not
been previously reported.[26]

travel to/living in rabies-endemic country

• About 30% of cases in the US are foreign acquired. Nearly all imported cases are associated with dog
bites.[13] [14]

occupational or recreational exposure

• People at elevated risk for exposure to rabies include: people working with live rabies virus in research
or vaccine production facilities; people performing diagnostic testing for rabies in laboratories;
people with frequent bat contact; people who interact with animals who could be rabid; people who
perform animal necropsies; people whose occupational or recreational activities typically involve
DIAGNOSIS

animal contact; and selected travellers (depending on occurrence of animal rabies in destination
country, availability of treatments, intended activities, and duration of stay). Occupations at higher
risk include animal handlers, field biologists, cavers, missionaries, veterinarians, and some laboratory
workers.[33]

Weak
age <15 years
• A disproportionate number of dog bites and 30% to 50% of rabies cases occur in children.[12] Children
are also less likely to report contact with a bat or other wild animal.

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Rabies Diagnosis

Investigations
1st test to order

Test Result
saliva PCR and viral culture detection of rabies RNA;
isolation of rabies virus
• PCR detects rabies virus RNA.
• The virus is more likely to be detectable at the beginning of the
clinical course. Most patients with rabies have a positive result with
repeated testing, as PCR testing is very sensitive.
• Saliva, CSF, skin, and serum should be tested simultaneously for
accurate diagnosis. A negative result in saliva alone does not rule
out rabies. Results in saliva, skin biopsy, CSF, and serum (in non-
immunised patients) must all be negative.
• A positive saliva PCR or culture is also an indication of the infectivity
of patient and the need for patient isolation and prevention measures
in healthcare personnel.
• If the patient survives long enough, this test becomes negative,
indicating that the patient is no longer infectious.
skin biopsy (neck) with direct fluorescent antibody (DFA) and detection of rabies virus
PCR antigen by DFA; detection
of rabies RNA
• A 5- to 6-mm diameter section is taken from the posterior region of
the neck at the hairline. A good specimen contains a minimum of
10 hair follicles and is taken deep enough to include the cutaneous
nerves found at the base of hair follicles.
• DFA testing detects rabies antigens in the sample.
• PCR detects rabies virus RNA.
• The virus is more likely to be detectable at the beginning of the
clinical course.
• A negative result in skin biopsy alone does not rule out rabies.
Results in saliva, skin biopsy, CSF, and serum (in non-immunised
patients) must all be negative.

DIAGNOSIS
CSF cytology mild lymphocytic
pleocytosis
• Detectable in 60% of patients in the first week and 85% of patients in
the second week.
CSF biochemistry elevated protein; low or
normal glucose; high
• CSF protein levels may be mildly elevated (>0.5 g/dL [>50 mg/dL])),
quinolinic acid; high
with a low to normal glucose concentration. CSF quinolinic acid is
lactate
high early on, and lactate progressively increases over days.
CSF rabies neutralising antibody positive
• Indicates rabies infection.
• A negative result in CSF alone does not rule out rabies. Results in
saliva, skin biopsy, CSF, and serum (in non-immunised patients) must
all be negative.
serum rabies IgM or IgG positive
• Antibodies may not be detected at early stages of the disease;
serial tests will demonstrate increase in antibody levels by day 14
of hospitalisation. Previously immunised patients will have rabies

Test Result
antibodies, and this test cannot be used to detect infection in these
patients.
• A negative result in serum alone does not rule out rabies. Results in
saliva, skin biopsy, CSF, and serum (in non-immunised patients) must
all be negative.
CSF herpes simplex PCR negative
• Used to exclude herpes simplex encephalitis.
CSF enterovirus PCR negative
• Used to exclude enterovirus meningoencephalitis.
CSF West Nile virus IgM negative
• Used to exclude West Nile virus encephalitis.
serum N-methyl-D-aspartate (NMDA) glutamate receptor negative
antibodies
• Used to exclude common cause of limbic encephalitis.

Other tests to consider

Test Result
serum arbovirus antibodies negative
• Used to exclude arbovirus encephalitides.
serum Bartonella antibodies negative
• Used to exclude Bartonella infection.
serum Ricket tsia antibodies negative
• Used to exclude rickettsial infection.
head MRI normal in the first week of
infection
• Used to exclude acute disseminated encephalitis.
DIAGNOSIS

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Rabies Diagnosis

Differentials

Condition Differentiating signs / Differentiating tests

symptoms
Herpes simplex virus • Does not show the relapsing/ • HSV is detected in CSF by
infection remitting pattern of mental PCR with >95% sensitivity.
lucidity seen in rabies.

Enterovirus • May show similar profound • Enteroviruses are detected

meningoencephalitis dysautonomia with in CSF by PCR with >95%
cardiomyopathy. sensitivity.

West Nile virus • History of a mosquito bite. • West Nile virus-specific IgM
encephalitis • Generally shows more in CSF is diagnostic.
parkinsonian findings or
general body rigidity than
rabies.

Other arbovirus • History of a mosquito bite. • Serum anti-arboviral

encephalitides • Generally show more antibodies are positive.
parkinsonian findings or
general body rigidity than
rabies.

Rock y Mountain spot ted • Petechial rashes or eschars • WBC count usually low.
fever and ricket tsial are present. • Rocky Mountain spotted
encephalitis fever and other rickettsial
serologies are diagnostic.

Japanese encephalitis • Parkinsonian symptoms are • Presence of Japanese

common. encephalitis virus RNA in
• Patients develop tissue, blood, or CSF is
hyperreflexia. diagnostic.
• Japanese encephalitis virus

DIAGNOSIS
antibodies may be detected
in CSF or serum.

Zika virus infection • Mental status alterations, • RT-PCR testing in serum,

progression to coma. CSF, or urine positive for
Guillain-Barre syndrome is Zika virus; serology positive
strongly associated. for Zika virus antibodies.

Guillain-Barre syndrome • Acute flaccid paralysis is • CSF shows elevated

similar to paralysis seen in protein with a normal cell
rabies, especially paralytic count (albuminocytological
rabies. dissociation).
• Sphincter involvement is • Nerve conduction studies
rare. show slowing of nerve
• There is no fever. conduction velocities.

Limbic encephalitis • Features are very similar • Serum or CSF antibodies

to rabies. Seizures are to N-methyl-D-aspartate
common with limbic (NMDA) glutamate receptor
encephalitis with N-methyl- may be positive. Repeat
D-aspartate glutamate testing may be needed.

Condition Differentiating signs / Differentiating tests

symptoms
receptor (NMDAR)
antibodies.

Acute disseminated • Aerophobia and hydrophobia • Brain MRI shows white

encephalitis are absent, but other clinical matter lesions.
features are similar to rabies.

Tetanus • Aerophobia, hydrophobia, • Detection of tetanus toxin in

and mental state changes plasma or clostridial culture
are absent. from wound swab.
• The main sign is trismus • CSF is normal.
(which results in a grimace
described as 'risus
sardonicus' or sardonic
smile) associated with
muscle rigidity, spasms,
respiratory embarrassment,
dysphagia, or autonomic
dysfunction.

Bartonella encephalitis • Associated with • Bartonella serologies are

lymphadenitis. diagnostic.

Delirium tremens • History of chronic alcohol • The diagnosis is clinical.

use and either reduction or
cessation of drinking before
presentation.
• Prodromal illness is absent.
• Fever is rare.

Cocaine overdose • History of cocaine use. • Cocaine may be detected

in urine, blood, or gastric
contents. The half-life in
blood is short.
DIAGNOSIS

Amfetamine overdose • History of amfetamine • Urine is positive for

abuse. amfetamines.

Acute psychosis • Main symptoms are • No differentiating tests.

hallucinations, delusions,
and thought disorder,
possibly accompanied by
agitation. The prodrome and
physical manifestations of
rabies are absent.
• Other clinical features
depend on the cause.

Criteria
World Health Organization: case definition[41]
Clinical description:

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Rabies Diagnosis

• An acute neurological syndrome (i.e., encephalitis) dominated by forms of hyperactivity (furious rabies)
or paralytic syndromes (paralytic rabies) progressing towards coma and death, usually by cardiac or
respiratory failure, typically within 7–10 days of the first signs if no intensive care is instituted. These
may include any of the following:

• Aerophobia

• Hydrophobia

• Paraesthesia or localised pain

• Localised weakness

• Nausea or vomiting.

Laboratory criteria for diagnosis:

• One or more of the following laboratory criteria should be used to confirm a clinical case:

• Presence of viral antigens in samples (e.g., brain tissue, skin)

• Isolation of virus from samples in cell culture or in laboratory animals

• Presence of viral-specific antibodies in the cerebrospinal fluid (CSF) or serum of an

unvaccinated person; and/or

• Presence of viral nucleic acids in samples (e.g., brain tissue, skin, saliva, concentrated urine).

Case classification:

• Suspected: a case that is compatible with the clinical case definition

• Probable: a suspected case plus a reliable history of contact with a suspected, probable, or confirmed
rabid animal

DIAGNOSIS
• Confirmed: a suspected or probable case that is confirmed in the laboratory.

Centers for Disease Control and Prevention: 2011 case definition[45]

Clinical description:

• An acute encephalomyelitis that almost always progresses to coma or death within 10 days after the
first symptom.
Laboratory criteria for diagnosis:

• Detection of Lyssavirus antigens in a clinical specimen (preferably the brain or the nerves
surrounding hair follicles in the nape of the neck) by direct fluorescent antibody test; OR

• Isolation (in cell culture or in a laboratory animal) of a Lyssavirus from saliva or central nervous
system tissue; OR

• Identification of Lyssavirus specific antibody (i.e., by indirect fluorescent antibody [IFA] test or
complete rabies virus neutralisation at 1:5 dilution) in the CSF; OR

• Identification of Lyssavirus specific antibody (i.e., by IFA test or complete rabies virus neutralisation at
1:5 dilution) in the serum of an unvaccinated person; OR

• Detection of Lyssavirus viral RNA (using reverse transcriptase-polymerase chain reaction) in saliva,
CSF, or tissue.
Case classification:

• Confirmed case: a clinically compatible case that is laboratory confirmed by testing at a state or federal
public health laboratory.
DIAGNOSIS

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Rabies Management

Approach
The most commonly encountered clinical situation is an asymptomatic patient with potential rabies
exposure. The type of post-exposure prophylaxis (PEP) required depends on the type of exposure and the
immunisation status of the patient. PEP should be started immediately if rabies is suspected; laboratory
diagnosis is not required. Symptomatic rabies is rare, and almost always fatal. The treatment is either
palliative or supportive. Aggressive management protocols may be considered in exceptional circumstances;
however, they do not reliably result in survival without severe sequelae.[41] Effective antiviral agents do not
exist.

Management of rabies exposure

PEP consists of an effective rabies vaccine and administration of rabies immunoglobulin (if necessary)
after cleaning and disinfection of the wound. PEP is highly effective and should be given to any
asymptomatic patient with a documented or likely exposure, regardless of the time that has elapsed since
the exposure. However, PEP should not be given to symptomatic patients.[46]

In the US, the Advisory Committee on Immunization Practices (ACIP) defines exposures as bite or non-
bite.[46]

The World Health Organization (WHO) defines 3 categories of exposure:[34]

• Category I: touching or feeding of animals, or licks on intact skin (no risk of infection if the history is
reliable).
• Category II: nibbling of uncovered skin, or minor scratches or abrasions without bleeding (low risk
of infection).
• Category III: single or multiple transdermal bites or scratches, licks on broken skin, contamination
of mucous membrane with saliva from licks, or exposure to bat bites or scratches (high risk of
infection).
The PEP protocol depends on whether the patient has previously been immunised against rabies.
Pre-exposure rabies immunisation is reserved for people at increased risk of contracting rabies. See
Prevention .

If a non-immunised patient has had a bite or non-bite exposure as defined by ACIP criteria, or a category
II or III exposure as defined by WHO criteria, PEP is required, and consists of the following steps:[34] [46]

• The unclosed wound is immediately and thoroughly washed and flushed with soap and water (or
water alone) for 15 minutes, and disinfected with detergent, iodine, or ethanol.
• For bite or non-bite exposure (ACIP criteria) or category III (WHO criteria) exposure, human rabies
immune globulin (hRIG) is infiltrated into the wounds without primary closure (loose suturing
should be performed if necessary only after infiltration). It should be administered once as soon
as possible after the initiation of PEP, and not beyond day 7 after the first dose of vaccine. The full
dose should be given into the wound and surrounding area if anatomically feasible. If this is not
possible, ACIP recommend that any remaining hRIG should be given intramuscularly, although
MANAGEMENT

WHO guidance no longer supports this. The site used to give intramuscular hRIG must be remote
from the wound and from the site used to give the vaccine. The total dose should not be exceeded;
if the calculated dose is insufficient to infiltrate all wounds, sterile saline may be used to dilute the
hRIG to allow thorough infiltration. hRIG may not be available in developing countries, and equine

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21
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Rabies Management
rabies immune globulin (eRIG) may be used in these locations; both have shown similar clinical
outcomes in the prevention of rabies. eRIG is less costly than hRIG and can now be administered
without initial skin testing. In areas where RIG is limited, allocation should be prioritised for patients
with high-risk exposures (e.g., multiple bites, deep wounds).
• For bite or non-bite exposure (ACIP criteria) or category II and III exposures (WHO criteria), rabies
vaccination should be given:

• The ACIP recommends that the vaccine be given intramuscularly and must be given at the
correct site. In adults, this is the deltoid area. In children, the anterolateral aspect of the
thigh is acceptable. The gluteal area must never be used. The first dose is given as soon as
possible after the exposure. Further doses are given 3, 7, and 14 days after the initial dose
(an additional dose at 28 days is recommended if the patient is immunocompromised).
• The WHO recommends either an intradermal (3-dose) or intramuscular (4-dose or 2-1-1
dose) regimen. The intradermal regimen is preferred as it the most cost-, dose-, and time-
sparing regimen.

If a patient vaccinated against rabies has bite or non-bite exposure (ACIP criteria) or has a category II
or III exposure (WHO criteria), PEP is required, but the protocol is modified. Rabies immunoglobulin is
not recommended. The wound is cleansed and a 2-dose intradermal or intramuscular regimen is given
consisting of an immediate dose and a second dose 3 days later. The WHO also recommends a 1-
dose (4-site) intradermal regimen. If repeat exposure occurs within 3 months of PEP, further PEP is not
required.[34] [46]

In the UK, the UK Health Security Agency recommends using the combined country/animal risk and the
category of exposure to determine a composite rabies risk (designated as green, amber, or red). The
specific PEP regimen is based on the composite rabies risk, the immunisation status of the patient, and
whether the patient is immunosuppressed.[47]

[UKHSA: summary of rabies risk assessment and post-exposure treatment] (https://

assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/800038/
Rabies_summary_risk_assessment_treatment.pdf)

PEP does not have any contraindications if purified rabies immunoglobulin and vaccine are used. It is
recommended in children and pregnant women.

Other treatments may include antibiotics and tetanus prophylaxis depending on the presentation.

Management of symptomatic rabies

The patient should be isolated and standard precautions for infectious patients observed. Rabies
immunisation or immunoglobulin is contraindicated during active disease, as it confers no benefit and may
be harmful. Occasional rabies survivors are noted, but there is no recognised curative medical therapy.
Many experts recommend palliation. Given that spasms in rabies (hydrophobia and aerophobia) are
stimulus driven, standard therapies follow those for tetanus, which involve seclusion, room darkening, and
restraint. The only study of palliation in rabies recommends haloperidol.[48] [49] Other agents that may be
MANAGEMENT

used to relieve symptoms include opioid analgesics, anticonvulsants (for seizures), and neuromuscular
blockers.[50]

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Rabies Management

Treatment algorithm overview

Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

Initial ( summary )
asymptomatic with recent vector
exposure

unimmunised: non- 1st reassurance

bite exposure with no
infection risk

unimmunised: non- 1st wound cleansing

bite exposure with low
infection risk

plus multiple-dose immunisation protocol

adjunct rabies immunoglobulin

unimmunised: bite 1st wound cleansing

exposure, licks on
broken skin or mucous
membrane, or exposure to
bat bites or scratches

plus multiple-dose immunisation protocol

plus rabies immunoglobulin

immunised: any exposure 1st wound cleansing

with infection risk

plus multiple-dose immunisation protocol

Acute ( summary )
symptomatic rabies

1st palliative care

MANAGEMENT

Treatment algorithm
Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

Initial
asymptomatic with recent vector
exposure

unimmunised: non- 1st reassurance

bite exposure with no
infection risk » There is no risk of infection if the exposure
involves touching or feeding of animals, or
licks on intact skin. If the history is reliable, no
treatment is required.
unimmunised: non- 1st wound cleansing
bite exposure with low
infection risk » Nibbling of uncovered skin or minor scratches
or abrasions without bleeding carry a low risk
of infection, and post-exposure prophylaxis is
required.

» The wound should be thoroughly washed and

flushed with soap and water (or water alone) for
15 minutes, and disinfected immediately with
detergent, iodine, or ethanol.
plus multiple-dose immunisation protocol
Treatment recommended for ALL patients in
selected patient group
Primary options
WHO protocols
» rabies vaccine: 0.1 mL intradermally
(divided between 2 sites) on days 0, 3, and
7; 1 dose intramuscularly (1-site) on days
0, 3, 7, and between days 14-28; 2 doses
intramuscularly (2-sites) on day 0, followed by
an additional dose (1-site) on days 7 and 21

ACIP protocol
» rabies vaccine: 1 mL intramuscularly
on days 0, 3, 7, and 14 (and 28 in
immunocompromised patients)

» The World Health Organization (WHO)

recommends either an intradermal (3-dose) or
MANAGEMENT

intramuscular (4-dose or 2-1-1 dose) regimen.

The intradermal regimen is preferred as it is the
most cost-, dose-, and time-sparing regimen.[34]

» The US protocol (recommended by the

Advisory Committee on Immunization Practices

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Rabies Management

Initial
[ACIP]) involves intramuscular injection into
the deltoid area (in adults) or anterolateral
aspect of the thigh (in children). The first dose
is given as soon as possible after the exposure
(day 0). Further doses are given 3, 7, and 14
days after the initial dose (an additional dose
at 28 days is recommended if the patient is
immunocompromised).[46] There are 2 vaccines
available in the US: human diploid cell vaccine
and purified chick embryo cell vaccine. Purified
vero cell vaccine and purified duck embryo
vaccine are other vaccines that are available
internationally and pre-qualified by the WHO.

» Immunisation protocols vary; consult local

guidance for regimens. For example, in the UK,
the specific post-exposure prophylaxis regimen
is based on the composite rabies risk, the
immunisation status of the patient, and whether
the patient is immunosuppressed.[47]
adjunct rabies immunoglobulin
Treatment recommended for SOME patients in
selected patient group
Primary options

» rabies immunoglobulin (human): 20 units/

kg (maximum) as a single dose infiltrated into
the wound and surrounding tissue
The dose of eRIG is 40 units/kg (maximum)
as a single dose.

» The World Health Organization (WHO)

recommends use in these types of exposures
if the patient is immunosuppressed. Individuals
with immunodeficiency should be evaluated on a
case-by-case basis.[34] ACIP recommends use
in all patients with non-bite exposure.[46]

» Human rabies immune globulin (hRIG) is

infiltrated into the wound(s) without primary
closure. The full dose should be given into the
wound(s) and surrounding area if anatomically
feasible (loose suturing should be performed if
necessary only after infiltration).

» If this is not possible, US guidelines

recommend any remaining hRIG should be given
intramuscularly, although WHO guidance no
longer supports this.[34] [46] The site used to
give intramuscular hRIG must be remote from
MANAGEMENT

the site used to give the vaccine. The total dose

should not be exceeded; if the calculated dose is
insufficient to infiltrate all wounds, sterile saline
may be used to dilute the hRIG to allow thorough
infiltration.

Initial
» Use of rabies immune globulin may be delayed
by up to 7 days from the first vaccine dose if
necessary (e.g., it is not available).

» Equine rabies immune globulin (eRIG) may

be used in developing countries if hRIG is not
available (note: the dose differs to hRIG). Both
have shown similar clinical outcomes in the
prevention of rabies. eRIG is less costly than
hRIG and can now be administered without initial
skin testing.[34]

» In areas where RIG is limited, allocation

should be prioritised for patients with high-
risk exposures (e.g., multiple bites, deep
wounds).[34]
unimmunised: bite 1st wound cleansing
exposure, licks on
broken skin or mucous » Single or multiple transdermal bites or
membrane, or exposure to scratches, licks on broken skin, contamination
bat bites or scratches of mucous membrane with saliva from licks, or
exposure to bat bites or scratches carry a high
risk of infection, and post-exposure prophylaxis
is required.

» The wound should be thoroughly washed and

ACIP protocol
» rabies vaccine: 1 mL intramuscularly
on days 0, 3, 7, and 14 (and 28 in
immunocompromised patients)

» The World Health Organization (WHO)

MANAGEMENT

recommends either an intradermal (3-dose) or

intramuscular (4-dose or 2-1-1 dose) regimen.
The intradermal regimen is preferred as it
is the most cost-, dose-, and time-sparing
regimen.[34]

26 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jul 06, 2023.
BMJ Best Practice topics are regularly updated and the most recent version of the topics
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Rabies Management

Initial
» The US protocol (recommended by the
Advisory Committee on Immunization Practices
[ACIP]) involves intramuscular injection into
the deltoid area (in adults) or anterolateral
aspect of the thigh (in children). The first dose
is given as soon as possible after the exposure
(day 0). Further doses are given 3, 7, and 14
days after the initial dose (an additional dose
at 28 days is recommended if the patient is
immunocompromised).[46] There are 2 vaccines
available in the US: human diploid cell vaccine
and purified chick embryo cell vaccine. Purified
vero cell vaccine and purified duck embryo
vaccine are other vaccines that are available
internationally and pre-qualified by the WHO.

» Immunisation protocols vary; consult local

guidance for regimens. For example, in the UK,
the specific post-exposure prophylaxis regimen
is based on the composite rabies risk, the
immunisation status of the patient, and whether
the patient is immunosuppressed.[47]
plus rabies immunoglobulin
Treatment recommended for ALL patients in
selected patient group
Primary options

» rabies immunoglobulin (human): 20 units/

kg (maximum) as a single dose infiltrated into
the wound and surrounding tissue
The dose of eRIG is 40 units/kg (maximum)
as a single dose.

» Human rabies immune globulin (hRIG) is

» If this is not possible, US guidelines

recommend any remaining hRIG should be given
intramuscularly, although WHO guidance no
longer supports this.[34] [46] The site used to
give intramuscular hRIG must be remote from
the site used to give the vaccine. The total dose
should not be exceeded; if the calculated dose is
insufficient to infiltrate all wounds, sterile saline
may be used to dilute the hRIG to allow thorough
infiltration.
MANAGEMENT

» Use of rabies immune globulin may be delayed

by up to 7 days from the first vaccine dose if
necessary (e.g., it is not available).

Initial
» Equine rabies immune globulin (eRIG) may
be used in developing countries if hRIG is not
available (note: the dose differs to hRIG). Both
have shown similar clinical outcomes in the
prevention of rabies. eRIG is less costly than
hRIG and can now be administered without initial
skin testing.[34]

» In areas where RIG is limited, allocation

should be prioritised for patients with high-
risk exposures (e.g., multiple bites, deep
wounds).[34]
immunised: any exposure 1st wound cleansing
with infection risk
» The wound should be thoroughly washed and
flushed with soap and water (or water alone) for
15 minutes, and disinfected immediately with
detergent, iodine, or ethanol.

» Rabies immunoglobulin is not required in these

patients.
plus multiple-dose immunisation protocol
Treatment recommended for ALL patients in
selected patient group
Primary options
WHO protocols
» rabies vaccine: one dose intradermally/
intramuscularly on days 0 and 3; 0.1 mL
intradermally injected four times (equally
distributed over left and right deltoids, thigh,
or suprascapular areas)

ACIP protocol
» rabies vaccine: 1 mL intramuscularly on
days 0 and 3

» The World Health Organization (WHO)

recommends either intradermal or intramuscular
administration on days 0 and 3, or a 4-site
intradermal regimen (four 0.1 mL injections
equally distributed over left and right deltoids,
thigh, or suprascapular areas during a single
visit). The intradermal regimens are preferred as
they are the most cost-, dose-, and time-sparing
regimens.[34]

» The US protocol, recommended by the

MANAGEMENT

Advisory Committee on Immunization Practices

(ACIP), involves intramuscular injection into the
deltoid area (in adults) or anterolateral aspect
of the thigh (in children). The first dose is given
as soon as possible after the exposure (day 0),

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Rabies Management

Initial
with a second dose on day 3.[46] There are 2
vaccines available in the US: human diploid cell
vaccine and purified chick embryo cell vaccine.
Purified vero cell vaccine and purified duck
embryo vaccine are other vaccines that are
available internationally and pre-qualified by the
WHO.

» Immunisation protocols vary; consult local

Acute
symptomatic rabies

1st palliative care

Primary options

» haloperidol: 0.5 to 10 mg orally every 1-4

hours initially, titrate according to response,
maximum 100 mg/day

» Occasional rabies survivors are noted, but

there is no recognised curative medical therapy.

» The patient should be isolated to minimise

the number of medical staff who might need
later prophylaxis. Standard precautions are
recommended (e.g., masks, gloves, eye/face
protection, gowns).

» Rabies immunisation or immunoglobulin is

contraindicated during active disease, as it
confers no benefit and may be harmful.

» Many experts recommend palliation. Given that

spasms in rabies (hydrophobia and aerophobia)
are stimulus driven, recommendations include
seclusion, room darkening, and restraint.

» The only study of palliation in rabies

recommends haloperidol.[48] [49]

» Other agents that may be used to relieve

symptoms include opioid analgesics,
anticonvulsants (for seizures), and
neuromuscular blockers.[50]
MANAGEMENT

Emerging
Milwaukee protocol
This is a detailed protocol for the treatment of symptomatic rabies.[51] The intent is to avoid fatal
dysautonomia through deep, non-barbiturate sedation pending immune clearance. Active drugs, including
ketamine and nimodipine for prophylaxis against generalised basal artery spasm, are theoretically
neuroprotective. Prerequisites for the use of this protocol include good logistics and access to a rabies
reference laboratory and rehabilitation facilities.[52] [53] The protocol requires further evaluation to establish
its efficacy, as data relate to a limited number of cases. Occasional survivors were reported.

Monoclonal antibodies
The World Health Organization (WHO) is undertaking a project to develop a cocktail of unique combinations
of monoclonal antibodies capable of neutralising a diverse range of rabies isolates. Products such as CL184,
RMAb, Rabimabs, and SYN023 are undergoing clinical trials.[54]SII RMAb has been shown to be safe and
non-inferior to human rabies immunoglobulin for post-exposure prophylaxis.[55]

Antivirals
Favipiravir has shown efficacy against rabies virus in vitro and in vivo. One study found that early
administration reduced the morbidity and mortality associated with rabies virus infection in mice.[56] Ribavirin
has also shown in vitro activity against rabies virus but has not been effective in animal studies.[50] [57]

PIKA® vaccine
The PIKA® rabies vaccine contains a novel adjuvant, a synthetic analog of double-strand RNA and a refined
form of polyinosinic-polycytidylic acid stabilised with kanamycin and calcium, as well as the inactivated and
purified rabies virus. It acts as an agonist at toll-like receptor-3 (TLR-3) and is capable of inducing nonspecific
immunity. A phase II, randomised study in healthy adults found that an accelerated regimen using the PIKA®
vaccine was well tolerated and demonstrated non-inferior immunogenicity compared to the classic vaccine
regimen using Rabipur®.[58] Phase 3 trials are due to commence in some countries in 2023. The PIKA®
vaccine was granted orphan drug designation by the US Food and Drug Administration in 2016.

Primary prevention
Rabies is 100% preventable through prompt medical care. Dogs are the most important global source of
rabies in humans; therefore, vaccination of pets and reducing pet exposure to wildlife in rabies-endemic
countries is recommended. Children are often at risk of dog bites, so education about avoiding stray or
unknown dogs (as well as other wildlife) is important. Wild animals should also be avoided, particularly bats.
Animal control should be contacted to remove bats from homes. Travellers to enzootic areas should avoid
contact with all wild or domestic animals including stray dogs or cats.

Rabies vaccination is recommended for pre-exposure or post-exposure prophylaxis. Two modern cell culture
vaccines are generally available in most countries: a human diploid cell vaccine, and a purified chick embryo
cell vaccine. Embryonated egg-based rabies vaccines may also be available. Choice of vaccine depends on
local availability.

Pre-exposure prophylaxis (PrEP)

MANAGEMENT

• Pre-exposure rabies immunisation is generally reserved for people at increased risk of contracting
rabies.
• Vaccine dose schedules and recommendations for who should receive PrEP may vary, and local
guidelines should be consulted.

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Rabies Management
• The World Health Organization (WHO) recommends PrEP for people at high risk of rabies virus
exposure (including sub-populations in highly endemic settings with limited access to timely and
adequate post-exposure prophylaxis), people at occupational risk, and travellers who may be at risk
of exposure. PrEP should also be considered in populations living in rabies endemic areas where the
dog bite incidence is >5% per year or vampire bat rabies is known to be present. Two different dose
schedules are recommended:[34]

• An intradermal dose (2-site) on days 0 and 7; or

• An intramuscular dose (1-site) on days 0 and 7 (deltoid muscle for adults and anterolateral area
of thigh in children <2 years).
• In the US, the Centers for Disease Control and Prevention (CDC) recommends a 2-dose intramuscular
regimen (days 0 and 7). Further recommendations depend on the person’s specific risk for being
exposed to rabies.[35]

• Risk category 1 (highest risk; people who work with live rabies virus in research or vaccine
production facilities, or people who perform testing for rabies in diagnostic laboratories): 2-dose
schedule (days 0 and 7), then check rabies antibody titre every 6 months (give booster if titre
<0.5 IU/mL).
• Risk category 2 (people who frequently handle or have contact with bats, enter high-density bat
environments such as caves, or perform animal necropsies): 2-dose schedule (days 0 and 7),
then check rabies antibody titre every 2 years (give booster if titre <0.5 IU/mL).
• Risk category 3 (risk duration >3 years after they receive primary 2-dose PrEP vaccination
series and: people who interact with animals that could be rabid such as veterinarians,
technicians, animal control officers; people who handle wildlife reservoir species; spelunkers;
and selected travellers): 2-dose schedule (days 0 and 7) plus either: a one-time rabies antibody
titre check after 1 year and up to 3 years following the vaccination series (give booster if titre
<0.5 IU/mL); or a one-time booster dose between 3 weeks and 3 years following the first
vaccination series.
• Risk category 4 (same population as category 3 above, but risk duration ≤3 years after they
receive primary 2-dose PrEP vaccination series): 2-dose schedule (days 0 and 7).
• Risk category 5 (lowest risk; general population): none.
• In the UK, the UK Health Security Agency (UKHSA) recommends a 3-dose intramuscular regimen
(days 0, 7, and 28). The third dose can be given from day 21 if there is insufficient time before travel.
An accelerated regimen may be given if there is insufficient time to complete the 21-28 day course,
with 3 doses given on days 0, 3, and 7 and an additional dose at one year if they continue to travel to
high-risk areas. PrEP is recommended in the following people:[36]

• Laboratory staff routinely working with rabies virus

• Workers at DEFRA-authorised quarantine premises and carriers
• Those who regularly handle bats (including on a voluntary basis) in the UK
• Veterinary and technical staff who encounter enhanced risk
• Travellers to rabies enzootic areas, especially if post-exposure medical care and rabies biologics
are lacking or are in short supply at the destination, or the person is undertaking higher-risk
activities (e.g., cycling, running), or they are living/staying in the area for ≥1 month
• Animal control and wildlife workers, veterinary staff, or zoologists who regularly work in rabies
MANAGEMENT

enzootic areas.
• Response to vaccination may be sub-optimal in immunocompromised people.

• The WHO recommends that immunocompromised people should be assessed on a case-by-

case basis and receive an additional third dose between days 21 to 28.[34]

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jul 06, 2023.
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31
can be found on bestpractice.bmj.com . Use of this content is subject to our disclaimer (.
Use of this content is subject to our) . © BMJ Publishing Group Ltd 2023. All rights reserved.
Rabies Management
• The CDC recommends checking that the person’s rabies antibody titre is >0.5 IU/mL at least
1 week (preferably 2 to 4 weeks) after completion of the vaccine series and all booster doses.
If the titre is <0.5 IU/mL, a booster dose should be administered, followed by a subsequent
titre check. If two booster doses fail to elicit an acceptable antibody titre, local public health
authorities should be consulted. If the patient has a temporary immunocompromising condition,
vaccination can be delayed until after the condition has resolved or immunosuppressive
medications can be withheld.[35]
• Concomitant administration of chloroquine or hydroxychloroquine (commonly used antimalarial drugs)
may result in a significant reduction in rabies antibody titre.

• The WHO recommends that while there is no contraindication to vaccination for people
receiving treatment with chloroquine or hydroxychloroquine, PrEP should be completed before
chloroquine or hydroxychloroquine treatment is initiated, if possible.[34]
• The CDC recommends considering avoiding the use of chloroquine when rabies vaccine is
being administered, or if it cannot be avoided, confirming the patient’s rabies antibody titre is
>0.5 IU/mL at least 1 week (preferably 2 to 4 weeks) after completion of the vaccine series.[35]
• PrEP Has been shown to be safe and immunogenic.[37]
Post-exposure prophylaxis (PEP)

• Consists of an effective rabies vaccine and administration of rabies immunoglobulin (if necessary)
after cleaning and disinfection of the wound. It is highly effective and should be given to any
asymptomatic patient with a documented or likely exposure, regardless of the time that has elapsed
since the exposure.
• PEP protocols vary; see Treatment algorithm .

Secondary prevention
Rabies is a notifiable disease in many countries. Cases should be reported immediately to local health
authorities. Centers for Disease Control and Prevention laboratory confirmation is required for antemortem
or postmortem suspected cases in the US. No cases of person-to-person spread to hospital or autopsy
personnel have ever been reported. However, relatives, healthcare workers, and others who may have
been exposed to direct contact to saliva or body fluids of the patient should be assessed for rabies risk to
determine need for rabies post-exposure prophylaxis.

Patient discussions
Travellers to rabies-enzootic countries should be advised to:

• Avoid contact with animals, especially dogs or bats

• Avoid entering caves where bats may be found
• Thoroughly wash animal bite or scratch wounds with lots of soap and water and apply an antiseptic
(e.g., povidone-iodine)
• Seek medical attention immediately if bitten or scratched by an animal that may have rabies
(particularly in countries where rabies is enzootic).
MANAGEMENT

Children should also be educated about the risks.

Pre-exposure vaccination may be recommended in some travellers.

32 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jul 06, 2023.
BMJ Best Practice topics are regularly updated and the most recent version of the topics
can be found on bestpractice.bmj.com . Use of this content is subject to our disclaimer (.
Use of this content is subject to our) . © BMJ Publishing Group Ltd 2023. All rights reserved.
Rabies Management
The World Health Organization and the Centers for Disease Control and Prevention provide useful
information resources for patients:

[WHO: rabies fact sheet] (http://www.who.int/mediacentre/factsheets/fs099/en)

[CDC: rabies] (http://www.cdc.gov/rabies)

MANAGEMENT

34 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jul 06, 2023.
BMJ Best Practice topics are regularly updated and the most recent version of the topics
can be found on bestpractice.bmj.com . Use of this content is subject to our disclaimer (.
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Rabies Follow up

Complications

Complications Timeframe Likelihood

FOLLOW UP
respiratory failure short term high

A common cause of death in patients with rabies.

poikilothermia short term high

The patient loses the ability to control body temperature, and the paralysed body adopts the temperature
of the local environment. Control of ambient temperature is required to control body temperature. This
condition does not respond to antipyretics.

CSF lactic acidosis short term high

Progressive CSF lactic acidosis has been seen in the few patients where this has been measured,
independent of non-invasive measures of cerebral perfusion.

coma short term high

Coma occurs in all patients in the late stages of infection. The diagnosis of brain death poses particular
challenges in these patients. Rabies can mimic brainstem death by causing denervation in the presence
of ongoing electrical activity. Clinical brain-death criteria do not apply; electrical activity and cerebral
perfusion studies are more reliable to confirm brain death.[13] [44]

cardiac arrhythmias short term medium

These occur within the first 10 days of symptomatic infection. Arrhythmias include tachycardia or
supraventricular tachycardia, which occur with hypertension, or bradycardia and asystole. Bradycardia
or asystole lead to death in some patients. Arrhythmias usually respond to increased sedation but may
require cardiac pacing. Bradycardia is often unresponsive to anticholinergics.

hypotension short term medium

Can occur at any time from the onset of symptoms. Produced by dehydration, and may also be related to
insufficiency of adrenal medulla from tetrahydrobiopterin (BH4) deficiency.

hypersalivation short term medium

Secretions may be viscous and cause aspiration. Some patients may require intubation. Aspiration may
require bronchoscopy for adequate clearance.

ileus short term medium

Typically occurs during the second week after symptoms begin and lasts 5 to 7 days. Nasojejunal feedings
are recommended.

Complications Timeframe Likelihood

diabetes insipidus short term medium
FOLLOW UP

The onset is in the second week. Can be confused with salt-wasting syndrome. Monitoring of urine output
and serum glucose and electrolytes is required. Diuretics should be avoided.

cerebral oedema short term medium

Onset in second week, concurrent with onset of immune response (possibly in bat rabies only). Appears
to be related to the presence of high rabies antibody titres in the CSF (>10 U/mL). This antibody response
can be halted by methylprednisolone pulse therapy.

hyponatraemia short term medium

Occurs at presentation, originating from dehydration or salt wasting rather than SIADH. Monitoring of
serum sodium and urine output is required.

urinary retention short term low

Occurs before the onset of paralysis. May cause reflex dysautonomia.

myocarditis short term low

Heart failure can occur at any time during the symptomatic infection, and is possibly related to myocarditis
or catecholamine stunning.

Prognosis

Rabies is a fatal illness. Typically, patients with rabies do not survive more than 18 days from the onset of
symptoms even with modern critical care.[53] Approximately 15 survivors have been reported worldwide, all
with moderate-to-severe neurological sequelae.[59]

Fatal breakthrough infections can very rarely occur in people who have started post-exposure prophylaxis
(PEP) after a zoonotic exposure. The median time from exposure to symptom onset in patients with
breakthrough infections was 20 days. Most patients received PEP within 2 days of an exposure, and severe
wounds were common. Adherence to core practices (i.e., wound cleaning and vaccine administration)
is important, as deviations from core practices were reported in 56% of patients with breakthrough
infections.[60]

36 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jul 06, 2023.
BMJ Best Practice topics are regularly updated and the most recent version of the topics
can be found on bestpractice.bmj.com . Use of this content is subject to our disclaimer (.
Use of this content is subject to our) . © BMJ Publishing Group Ltd 2023. All rights reserved.
Rabies Guidelines

Diagnostic guidelines

United Kingdom

Rabies risks in terrestrial animals by country (ht tps://www.gov.uk/

government/publications/rabies-risks-by-country)
Published by: UK Health Security Agency Last published: 2023

Rabies: risk assessment, post-exposure treatment, management (ht tps://

www.gov.uk/government/collections/rabies-risk-assessment-post-exposure-
treatment-management)
Published by: UK Health Security Agency Last published: 2023

Guidelines on managing rabies post-exposure (ht tps://www.gov.uk/

government/publications/rabies-post-exposure-prophylaxis-management-
guidelines)

GUIDELINES
Published by: UK Health Security Agency Last published: 2023

International

WHO expert consultation on rabies: third report (ht tps://apps.who.int/iris/

handle/10665/272364)
Published by: World Health Organization Last published: 2018

North America

CDC Yellow Book: health information for international travel - rabies (ht tps://
wwwnc.cdc.gov/travel/page/yellowbook-home)
Published by: Centers for Disease Control and Prevention Last published: 2020

Oceania

Rabies and other lyssaviruses (including Australian bat lyssavirus) (ht tps://
immunisationhandbook.health.gov.au/vaccine-preventable-diseases)
Published by: Australian Government Department of Health Last published: 2018

Treatment guidelines

United Kingdom

Rabies: risk assessment, post-exposure treatment, management (ht tps://

www.gov.uk/government/collections/rabies-risk-assessment-post-exposure-
treatment-management)
Published by: UK Health Security Agency Last published: 2023

Europe

Rabies prevention and control guidance (ht tps://www.hpsc.ie/A-Z/Zoonotic/

Rabies/Guidance)
Published by: National Zoonoses Committee; The Health Protection Last published: 2015
Surveillance Centre (HPSC) - Ireland
GUIDELINES

International

WHO expert consultation on rabies: third report (ht tps://apps.who.int/iris/

handle/10665/272364)
Published by: World Health Organization Last published: 2018

38 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jul 06, 2023.
BMJ Best Practice topics are regularly updated and the most recent version of the topics
can be found on bestpractice.bmj.com . Use of this content is subject to our disclaimer (.
Use of this content is subject to our) . © BMJ Publishing Group Ltd 2023. All rights reserved.
Rabies Guidelines

North America

Use of a modified preexposure prophylaxis vaccination schedule to prevent

human rabies (ht tps://www.cdc.gov/mmwr/volumes/71/wr/mm7118a2.htm?
s_cid=mm7118a2_w)
Published by: Advisory Committee on Immunization Practices; Centers Last published: 2022
for Disease Control and Prevention

Compendium of animal rabies prevention and control, 2016 (ht tp://

www.nasphv.org/documentsCompendia.html)
Published by: National Association of State Public Health Veterinarians; Last published: 2016
Compendium of Animal Rabies Prevention and Control Committee

GUIDELINES
Canadian immunization guide part 4, active vaccines: rabies vaccine (ht tps://
www.canada.ca/en/public-health/services/publications/healthy-living/
canadian-immunization-guide-part-4-active-vaccines.html)
Published by: National Advisory Committee on Immunization, Canada Last published: 2015

Use of a reduced (4-dose) vaccine schedule for postexposure prophylaxis

to prevent human rabies (ht tps://www.cdc.gov/rabies/resources/
acip_recommendations.html)
Published by: Advisory Committee on Immunization Practices; Centers Last published: 2010
for Disease Control and Prevention

Oceania

Online resources
1. NaTHNaC/Travel Health Pro: rabies factsheet (https://travelhealthpro.org.uk/factsheet/20/rabies)
(external link)

2. UKHSA: summary of rabies risk assessment and post-exposure treatment (https://

assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/800038/
Rabies_summary_risk_assessment_treatment.pdf) (external link)

3. WHO: rabies fact sheet (http://www.who.int/mediacentre/factsheets/fs099/en) (external link)

4. CDC: rabies (http://www.cdc.gov/rabies) (external link)

ONLINE RESOURCES

40 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jul 06, 2023.
BMJ Best Practice topics are regularly updated and the most recent version of the topics
can be found on bestpractice.bmj.com . Use of this content is subject to our disclaimer (.
Use of this content is subject to our) . © BMJ Publishing Group Ltd 2023. All rights reserved.
Rabies References

Key articles
• World Health Organization. Weekly epidemiological record. Rabies vaccines: WHO position paper.

REFERENCES
April 2018 [internet publication]. Full text (http://apps.who.int/iris/bitstream/handle/10665/272371/
WER9316.pdf?ua=1)

• Centers for Disease Control and Prevention. Use of a modified preexposure prophylaxis vaccination
schedule to prevent human rabies: recommendations of the Advisory Committee on Immunization
Practices - United States, 2022. May 2022 [internet publication]. Full text (https://www.cdc.gov/mmwr/
volumes/71/wr/mm7118a2.htm?s_cid=mm7118a2_w)

• World Health Organization. WHO expert consultation on rabies: WHO TRS N°1012 (third report). April
2018 [internet publication]. Full text (https://apps.who.int/iris/handle/10665/272364)

• Rupprecht CE, Briggs D, Brown CM, et al; Centers for Disease Control and Prevention. Use of
a reduced (4-dose) vaccine schedule for postexposure prophylaxis to prevent human rabies:
recommendations of the Advisory Committee on Immunization Practices. MMWR Recomm Rep.
2010;59:1-9. Full text (http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5902a1.htm) Abstract (http://
www.ncbi.nlm.nih.gov/pubmed/20300058?tool=bestpractice.bmj.com)

• Willoughby RE Jr, Tieves KS, Hoffman GM, et al. Survival after treatment of rabies with
induction of coma. N Engl J Med. 2005;352:2508-2514. Full text (http://www.nejm.org/doi/
full/10.1056/NEJMoa050382#t=article) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/15958806?
tool=bestpractice.bmj.com)

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42 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jul 06, 2023.
BMJ Best Practice topics are regularly updated and the most recent version of the topics
can be found on bestpractice.bmj.com . Use of this content is subject to our disclaimer (.
Use of this content is subject to our) . © BMJ Publishing Group Ltd 2023. All rights reserved.
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news-room/fact-sheets/detail/rabies)

19. Gunawardena PS, Marston DA, Ellis RJ, et al. Lyssavirus in Indian Flying Foxes, Sri Lanka. Emerg
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20. Aréchiga Ceballos N, Vázquez Morón S, Berciano JM, et al. Novel lyssavirus in bat, Spain. Emerg
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21. Hu SC, Hsu CL, Lee MS, et al. Lyssavirus in Japanese Pipistrelle, Taiwan. Emerg Infect Dis. 2018
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22. Vora NM, Basavaraju SV, Feldman KA, et al; Transplant-Associated Rabies Virus Transmission
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35. Centers for Disease Control and Prevention. Use of a modified preexposure prophylaxis vaccination
schedule to prevent human rabies: recommendations of the Advisory Committee on Immunization
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volumes/71/wr/mm7118a2.htm?s_cid=mm7118a2_w)

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44 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jul 06, 2023.
BMJ Best Practice topics are regularly updated and the most recent version of the topics
can be found on bestpractice.bmj.com . Use of this content is subject to our disclaimer (.
Use of this content is subject to our) . © BMJ Publishing Group Ltd 2023. All rights reserved.
Rabies References
40. Hemachudha T, Laothmatas J, Rupprecht CE. Human rabies: a disease of complex
neuropathogenetic mechanisms and diagnostic challenges. Lancet. 2002;2:101-109. Abstract (http://
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2018 [internet publication]. Full text (https://apps.who.int/iris/handle/10665/272364)

42. Laothamatas J, Hemachudha T, Mitrabhakdi E, et al. MR imaging in human rabies. AJNR Am J

Neuroradiol. 2003;24:1102-1109. Full text (http://www.ajnr.org/content/24/6/1102.full) Abstract (http://
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43. Gable MS, Sheriff H, Dalmau J, et al. The frequency of autoimmune N-methyl-D-aspartate receptor
encephalitis surpasses that of individual viral etiologies in young individuals enrolled in the California
Encephalitis Project. Clin Infect Dis. 2012;54:899-904. Abstract (http://www.ncbi.nlm.nih.gov/
pubmed/22281844?tool=bestpractice.bmj.com)

44. Hantson P, Guerit JM, de Tourtchaninoff M, et al. Rabies encephalitis mimicking the
electrophysiological pattern of brain death. Eur Neurol. 1993;33:212-217. Abstract (http://
www.ncbi.nlm.nih.gov/pubmed/8043086?tool=bestpractice.bmj.com)

45. Centers for Disease Control and Prevention. Rabies, human: 2011 case definition. 2011 [internet
publication]. Full text (https://wwwn.cdc.gov/nndss/conditions/rabies-human/case-definition/2011)

46. Rupprecht CE, Briggs D, Brown CM, et al; Centers for Disease Control and Prevention. Use of
a reduced (4-dose) vaccine schedule for postexposure prophylaxis to prevent human rabies:
recommendations of the Advisory Committee on Immunization Practices. MMWR Recomm Rep.
2010;59:1-9. Full text (http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5902a1.htm) Abstract (http://
www.ncbi.nlm.nih.gov/pubmed/20300058?tool=bestpractice.bmj.com)

47. UK Health Security Agency. Guidelines on managing rabies post-exposure. Jan 2023 [internet
publication]. Full text (https://www.gov.uk/government/publications/rabies-post-exposure-prophylaxis-
management-guidelines)

48. Willoughby RE Jr, Opladen T, Maier T, et al. Tetrahydrobiopterin deficiency in human rabies. J
Inherit Metab Dis. 2008;32:65-68. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/18949578?
tool=bestpractice.bmj.com)

49. Marsden SC, Cabanban CR. Rabies: a significant palliative care issue. Prog Palliat Care.
2006;14:62-67.

50. Jackson AC, Warrell MJ, Rupprecht CE, et al. Management of rabies in humans. Clin Infect Dis.
2003;36:60-63. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/12491203?tool=bestpractice.bmj.com)

51. Medical College of Wisconsin. Milwaukee rabies protocol, version 6. Nov 2018 [internet publication].
Full text (https://www.mcw.edu/-/media/MCW/Departments/Pediatrics/Infectious-Diseases/
Milwaukee_protocol.pdf)

52. Willoughby RE Jr, Tieves KS, Hoffman GM, et al. Survival after treatment of rabies with
induction of coma. N Engl J Med. 2005;352:2508-2514. Full text (http://www.nejm.org/doi/

53. Willoughby RE, Roy-Burman A, Martin KW, et al. Generalized cranial artery spasm in human rabies.
Dev Biol (Basel). 2008;131:367-375. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/18634498?
tool=bestpractice.bmj.com)

54. World Health Organization. Rabies monoclonal antibodies post exposure prophylaxis. December
2016 [internet publication]. Full text (http://www.who.int/rabies/resources/Summary-rabies-mAbs-for-
Web_Dec2016.pdf?ua=1)

55. Gogtay NJ, Munshi R, Ashwath Narayana DH, et al. Comparison of a novel human rabies monoclonal
antibody to human rabies immunoglobulin for postexposure prophylaxis: a phase 2/3, randomized,
single-blind, noninferiority, controlled study. Clin Infect Dis. 2018 Jan 18;66(3):387-395. Abstract
(http://www.ncbi.nlm.nih.gov/pubmed/29020321?tool=bestpractice.bmj.com)

56. Yamada K, Noguchi K, Komeno T, et al. Efficacy of favipiravir (T-705) in rabies postexposure
prophylaxis. J Infect Dis. 2016;213:1253-1261. Full text (https://www.ncbi.nlm.nih.gov/pmc/articles/
PMC4799667) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/26655300?tool=bestpractice.bmj.com)

57. Bussereau F, Picard M, Blancou J, et al. Treatment of rabies in mice and foxes with antiviral
compounds. Acta Virol. 1988;32:33-49. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/2897770?
tool=bestpractice.bmj.com)

58. Kalimuddin S, Wijaya L, Chan YFZ, et al. A phase II randomized study to determine the safety
and immunogenicity of the novel PIKA rabies vaccine containing the PIKA adjuvant using an
accelerated regimen. Vaccine. 2017 Nov 22;35(51):7127-32. Full text (https://www.doi.org/10.1016/
j.vaccine.2017.10.097) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/29174316?
tool=bestpractice.bmj.com)

59. Mani RS, Anand AM, Madhusudana SN. Human rabies in India: an audit from a rabies diagnostic
laboratory. Trop Med Int Health. 2016 Apr;21(4):556-63. Full text (http://onlinelibrary.wiley.com/
doi/10.1111/tmi.12669/full) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/26799375?
tool=bestpractice.bmj.com)

60. Whitehouse ER, Mandra A, Bonwitt J, et al. Human rabies despite post-exposure prophylaxis:
a systematic review of fatal breakthrough infections after zoonotic exposures. Lancet Infect
Dis. 2023 May;23(5):e167-74. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/36535276?
tool=bestpractice.bmj.com)

46 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jul 06, 2023.
BMJ Best Practice topics are regularly updated and the most recent version of the topics
can be found on bestpractice.bmj.com . Use of this content is subject to our disclaimer (.
Use of this content is subject to our) . © BMJ Publishing Group Ltd 2023. All rights reserved.
Rabies Images

Images

IMAGES
Figure 1: A canine suspected of being rabid that had been exhibiting signs of restlessness and overall
uncharacteristic aggressive behaviour
Centers for Disease Control and Prevention

Figure 2: Illustration of rabies virus in longitudinal section

Centers for Disease Control and Prevention

48 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jul 06, 2023.
BMJ Best Practice topics are regularly updated and the most recent version of the topics
can be found on bestpractice.bmj.com . Use of this content is subject to our disclaimer (.
Use of this content is subject to our) . © BMJ Publishing Group Ltd 2023. All rights reserved.
Rabies Images

IMAGES
Figure 3: Illustration of rabies virus in cross-section. Concentric layers: envelope membrane bilayer, M
protein, and tightly coiled encased RNA
Centers for Disease Control and Prevention

Figure 4: This transmission electron micrograph reveals the presence of Lagos bat virus virions and an
intracytoplasmic inclusion body in this tissue sample
Centers for Disease Control and Prevention; Dr Fred Murphy; Sylvia Whitfield

50 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jul 06, 2023.
BMJ Best Practice topics are regularly updated and the most recent version of the topics
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52 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jul 06, 2023.
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Contributors:

// Authors:

Sergio Recuenco, MD, MPH, DrPH

Associate Professor
Faculty of Medicine Sa Fernando, National University of San Marcos, Lima, Peru
DISCLOSURES: SR declares that he has no competing interests.

Rodney Willoughby, MD
Professor
Pediatrics, Medical College of Wisconsin, Milwaukee, WI
DISCLOSURES: RW is an author of a number references cited in this topic.

// Acknowledgements:
Dr Sergio Recuenco and Dr Rodney Willoughby would like to gratefully acknowledge Dr Kis Robertson, a
previous contributor to this topic.
DISCLOSURES: KR declares that she has no competing interests.

// Peer Reviewers:

Peter Leggat, MD
Head
School of Public Health, Tropical Medicine and Rehabilitation Sciences, Faculty of Medicine, Health and
Molecular Sciences, James Cook University, Townsville, Queensland, Australia
DISCLOSURES: PL is a member of the Australian Travel Health Advisory Group that is supported by a
grant from GlaxoSmithKline. PL has received travel grants from GlaxoSmithKline to attend travel medical
conferences in the last 5 years.

Allan Grill, MD, CCFP, MPH

Assistant Professor
Department of Family and Community Medicine, Dalla Lana School of Public Health, University of Toronto,
Toronto, Ontario, Canada
DISCLOSURES: AG declares that he has no competing interests.

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