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Author's personal copy
Author's personal copy
R E V I E W / ABCD guidelines on feline rabies
The number of human rabies deaths is estimated at 40,000–100,000 worldwide
each year, and an estimated 10 million people receive post-exposure treatment.
Epidemiology
Developing countries
Organisation for Animal Health (OIE)
and the World Health Organization
(WHO) (Fig 1).1
The number of human rabies deaths is estimated at 40,000–100,000 worldwide each year,
and an estimated 10 million people receive postexposure treatment.2 Dog rabies is still important
in many parts of the world and is the principal
cause of human cases. Wildlife rabies has
increased in importance as a threat to domestic
animals and humans, and transmission by vampire bats is a significant issue in Latin America.
The red fox and the raccoon/skunk are the main
reservoir species for terrestrial rabies in Europe
and the Americas, respectively.
agencies cannot be afforded by many
developing countries, progress is being
made. For example, a substantial
decrease in the incidence of rabies has been
reported recently from China, Thailand and
Sri Lanka, after implementation of dog vaccination programmes and improved post-exposure prophylaxis of humans. Similarly, rabies
cases decreased in Latin America after the Pan
American Health Organization had implemented a vaccination programme to eliminate
urban dog rabies from the southern hemisphere.
A dreaded disease
In most countries of Asia, Latin America
Rabies is one of the oldest and
most dreaded diseases of humans and
Rabies occurs worldwide, with geoand Africa, dog rabies is endemic, causanimals – it was recognised in Egypt before
graphical exceptions. Large regions of
ing considerable mortality in domestic
2300 BC, and well described by Aristotle in
Europe are now free of terrestrial ancient
animals and man. Many people are
Greece. Rabies also has stimulated one
rabies as a result of wildlife vaccina- of the great early discoveries in biomedical vaccinated, and there is a continuing
tion programmes. The rabies situation science: in 1885, before the nature of viruses was need for comprehensive, professionaland the regulations are continuously understood, Louis Pasteur developed, tested and ly organised and publicly supported
updated on the websites of the World applied a rabies vaccine, thereby heralding the rabies control agencies. Though such
modern era of infectious disease prevention.
Rabies-free countries
Strictly enforced quarantine for dogs and cats
has kept rabies from entering Japan, the United
Kingdom (UK), Australia, New Zealand and
other islands. Rabies was never endemic in
wildlife in the UK and was eradicated in 1902,
and again in 1922 after it had become established in the dog population in 1918. Since then,
there has been no rabies in the UK. Isolated
reports of bats infected with EBL-2 have not
altered the terrestrial rabies-free status of the
UK. In contrast, rabies was not recognised in
Australia until the recent discovery of
Australian bat lyssavirus, which was subsequently found to be endemic in southeast
Australia.
a
586
FIG 1 Incidence maps
showing (a) terrestrial rabies
cases in 2008; and (b) bat
rabies cases between 1997
and 2008. Source WHO
b
JFMS CLINICAL PRACTICE
Industrialised countries
In most industrial countries, even in those
with a modest disease burden, publicly supported rabies control agencies undertake:
✜ Oral vaccination of wildlife – in Europe,
the red fox;
✜ Stray dog and cat removal and control of
pet movement (quarantine is used rarely
in epidemic circumstances);
✜ Immunisation of dogs and cats, to break
the chain of virus transmission;
✜ Laboratory diagnosis, to confirm clinical
observations and obtain accurate incidence
data;
✜ Surveillance, to measure the effectiveness
of all control measures;
✜ Public education programmes to assist
cooperation.
Author's personal copy
R E V I E W / ABCD guidelines on feline rabies
Though fewer persons obtain post-exposure
prophylaxis after cat bites, as compared with
dog bites, the treatment is justified more often.
The cat is considered as being a high-risk
species for rabies transmission to humans in
some European countries: of more than 20,000
inhabitants in Switzerland that had to be vaccinated after exposure to rabies between the
1960s and 1990s, around 70% had been either
bitten by, or in close contact with, cats.3 Even if
feline rabies is considered a ‘by-product’ of
canine or wildlife rabies, feline behavioural
characteristics and clinical aspects make it
important for public health reasons. In fact,
though fewer persons obtain post-exposure
prophylaxis after cat bites, as compared with
dog bites, the treatment is justified more often.4
Although unvaccinated cats may become
infected with rabies following contact with
rabid wildlife, such cases have become rare in
Western Europe. Instead, most recent cases of
terrestrial rabies have been traced to illegally
imported, infected pets from rabies-endemic
regions of Africa. Veterinary practitioners
should therefore remain alert for signs of
rabies in cats, even in rabies-free areas.
Pathogenesis
Rabid animals are the only source of infection.
Virus is shed in the saliva some days before the
onset of clinical signs and transmitted through
a bite or a scratch to the skin or mucous membranes (eyes, nose, mouth). Rabid
animals are not viraemic, and their
Why is the incubation
blood is not infectious. The averperiod so variable?
age incubation period in cats is
The variability in the incubation period
2 months, but may vary from
is explained by the pathogenic behaviour of
2 weeks to several months, or
the virus, which moves along peripheral nerves,
with the normal axoplasmic flow, from the inocueven years, depending on
the transmitted virus dose, lation site to the central nervous system (CNS). The
greater the distance from the CNS, the longer the
the severity of the wound incubation period; and the greater the density of
and its localisation.5,6 This innervation of the inoculated tissue, the shorter the
must be taken into account incubation period.7 Very long incubation periods
observed in some experimental
when evaluating the wound have been
cases.8
history, especially when freeroaming cats exhibit sudden
behavioural changes and/or
signs of motor neuron dysfunction
that may herald the clinical phase.
The virus replicates in striated muscle and
connective tissue at the site of inoculation,
and from there enters the peripheral nerves
through the neuromuscular junction.9
Alternatively, it can infect peripheral nerves
directly, spreading to the CNS via the axonal
route. It then travels via the retrograde axonal
route to reach the salivary glands, at which
time the animal becomes infectious,
usually about 3 days before clinical signs
appear. Virus becomes widely disseminated
throughout the organs. In most cases,
death occurs within 5 days – an infected cat
will therefore be shedding the virus in saliva
for about 8 days in total. Most of the clinical
signs are related to central and peripheral
nervous system dysfunction, and abnormalities in neurotransmission, rather than to
neuronal death.5
Immunity
Passive immunity acquired via colostrum
Kittens from vaccinated queens obtain maternally derived antibodies (MDA) via the
colostrum, their titres depending on both the
antibody titre of the queen and the amount of
colostrum ingested during the first day of life.
In most kittens, MDA will not persist for
longer than 12 weeks.
Maternally derived antibodies may neutralise vaccine antigens, thereby inhibiting
adaptive immunoglobulin production and
interfering with the immunisation process
during the first weeks of life. It is therefore
recommended that vaccination of kittens
should not start before 12 weeks of age.
Active immune response
Rabies virus antigens are highly immunogenic and can elicit the full spectrum of protective immune responses. However, the
virus is not very cytopathic – cell lysis hardly
occurs during replication and maturation,
and little antigen is therefore presented to the
immune system. Neither humoral nor cellmediated responses can be detected during
the early stages of viral movement from the
site of the bite to the CNS.10 Hence, infection
of naive animals with rabies virus invariably
results in death. Fortunately, this can be
averted by prompt post-exposure immunisation, because anti-rabies viral immunity
before extensive infection of neurons is
protective.
Most recent cases of terrestrial rabies in Western Europe have been traced
to illegally imported, infected pets from rabies-endemic regions of Africa.
Veterinary practitioners should therefore remain alert for signs of rabies in cats,
even in rabies-free areas.
JFMS CLINICAL PRACTICE
587
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R E V I E W / ABCD guidelines on feline rabies
Virus neutralising antibody is crucial in this
immunity. Rabies is an example of a ‘Th-2
healing disease’ in which activation of B
lymphocytes, with the help of CD4 T cells,
mediates protection.11 When activated, primarily by the nucleocapsid (N) protein, CD4 T
cells produce cytokines that stimulate B cells
to produce antibodies. In contrast, rabiesspecific CD8 T cells cause neuronal damage
when a Th-1 response predominates.12,13
However, vaccinated animals without
detectable virus neutralising antibody
did survive a challenge infection,
which hints at still other protective
mechanisms.14,15
After intramuscular infection, the
virus replicates locally in the myocytes
or nervous tissue. In vaccinated cats,
the invading virus is neutralised early
during the incubation period, whereas
unvaccinated cats may produce an
antiviral immune response, but too late
to prevent disease. Laboratory experiments have shown that protection
early after infection is provided by the
native immune system, with interferon
playing a critical role.16 It is not clear
how effective these mechanisms are
Clinical signs
Typical clinical picture for rabid cats
infected with rabies virus
History and clinical signs reported by the owner
✜ Dramatic changes from normal behaviour
✜ Very aggressive: biting people and/or
animals with no apparent reason
General appearance and clinical signs at presentation
✜ 90% of rabid cats show clinical signs of the furious form
✜ Thin body condition (the cat does not eat)
✜ Ruffled and dirty coat (the cat does not clean itself)
✜ Mucous membranes, tongue, nose and footpads are
reddish pink (high fever)
✜ The chin and front legs are wet from salivation
✜ Perpetual movement and excitement (restlessness)
✜ Imbalanced gait due to paresis of the hind legs
✜ Pupil dilation unresponsive to light
✜ Abnormal water uptake (water runs back out of mouth)
Courtesy of Veera Tepsumethanon
a
FIG 2 Any aggressive behaviour expressed by a cat should
lead to a suspicion of rabies. Courtesy of (a) Andy Sparkes;
(b) AFSSA/ERZ
b
in naturally exposed naive cats. Morbiditydetermining factors include the amount of
virus transmitted, the strain, and the age and
immunocompetence of the cat. A young,
unvaccinated animal that has been bitten
severely in the head, with a large saliva
deposit in the wound, has a higher risk of
developing rabies (with a shorter incubation
period) than an adult cat bitten in a limb,
especially after extensive bleeding.17
In natural infections, neutralising antibody
usually appears after the virus has entered the
CNS. Hence, once symptoms are evident,
recovery is exceedingly rare.18 However, antibodies to lyssaviruses have been detected
occasionally in domestic and wild cats with
no history of vaccination, consistent with a
non-fatal disease or subclinical infection.19
Clinical signs
Any unexplained aggressive behaviour or
sudden behavioural change in cats should be
considered suspicious (Fig 2). Rabies should
be suspected not only when there has been a
recent history of a bite or exposure to a rabid
animal, but also where a cat has had contact
with wildlife, particularly bats. Indeed, a cat
in France died of rabies as the result of
an infection with bat lyssavirus. However,
Rabies should be suspected not only when there has been a
recent history of a bite or exposure to a rabid animal, but also where a cat
has had contact with wildlife, particularly bats.
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JFMS CLINICAL PRACTICE
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R E V I E W / ABCD guidelines on feline rabies
a
b
c
FIG 3 Cats in the paralytic phase of rabies. Note the anisocoria. Courtesy of (a) Artur Borkowski; (b) AFSSA/ERZ; (c) Merial
although rabid bats have been reported in
the UK, and the Mammal Society has estimated that British cats kill about 230,000 bats a
year, no cases of cat rabies are on record.20,21
These findings indicate a low risk of cats
becoming infected with lyssaviruses from
bats.
Two disease manifestations have been identified in cats: the furious and the dumb form.
The furious form has three clinical phases
(prodromal, mad or psychotic, and paralytic)
but these are not always distinct in cats. In the
dumb form, the ‘mad’ phase is lacking.
During the short (12–48 h) prodromal phases
of both forms, non-specific clinical signs
(fever, anorexia, vomiting, diarrhoea) occur,
sometimes accompanied by neurological
signs. Behavioural changes may be the first to
be noticed, such as unusually friendly manners, a shy or irritated conduct, or increased
vocalisation. These indicate forebrain involvement and are later associated with other neurological signs. Cranial nerve involvement may
produce depressed or absent reflexes (palpebral, corneal, pupillary), strabism, dropped
jaw, inability to move whiskers
forward,
dysphagia,
laryngeal paralysis,
voice change and
tongue paralysis
(Fig 3). Forebrain
Minimising public health risks
involvement is
The substantial public health risk (particularly for
veterinarians) requires that the differential diagnoses for
responsible for
seizures, mus- CNS diseases characterised by sudden-onset and rapidly
evolving clinical signs should always include rabies for freecular twitch- roaming, unvaccinated cats living or travelling in endemic
ing or tremors, areas. Indeed, rabies should be included in the differential
aimless pac- diagnosis for any cat with suspected encephalitis. Safety
ing, exaggerat- must always be the overriding priority. Manipulation and
of the cat may provoke biting at a time when the
ed emotional restraint
salivary glands are already infected. The ABCD stipuresponses (irrilates that the differential diagnosis should be based
tability,
rage,
on the cat’s history (see box on page 590),
and observation of the animal inside the
fearfulness, photocarrier, with a view to reducing the
phobia,
attacking
risks of exposure to veterinary
inanimate objects).
personnel.
The tendency to bite
indiscriminately may be due to loss of
inhibitory control by cortical neurons over the
subcortical bite reflex; these cats turn and
snap at anything that touches them around
the mouth, without warning or showing any
emotion. Pruritus at the bite site has been
observed.22
If a limb was bitten, then neurological signs
start from the spinal cord, with an ascending
lower motor neuron paralysis occurring
before the brain signs. The encephalitis rapidly spreads throughout the CNS producing
ataxia, disorientation, paralysis, seizures and
status epilepticus, ultimately followed by
coma and death from respiratory arrest.
The furious form is more often seen in cats,
which show behavioural abnormalities, as
described above.23 The paralytic phase (paraparesis, incoordination, generalised paralysis,
coma and death) usually begins a few days
after the first clinical signs.
Isolated case reports of rabies survival have
been published for cats, dogs and humans, but
death usually occurs after a clinical course of
1–10 days.18,24 Cats often die within 3–4 days25
(25% of fatalities occur within 4 days), while
progression in dogs is more rapid (2 days).26
Atypical forms with a chronic course have
been described in cats after experimental infection.8
Vaccine-induced rabies in cats was observed
in the past when modified-live virus vaccines
were used. Neurological signs occurred several weeks after vaccination and were characterised mostly by progressive upper motor
neuron limb paralysis and cranial nerve
deficits.
Diagnosis
A definitive rabies diagnosis is obtained
by post-mortem laboratory investigation.
However, serological tests are used for postvaccinal control, especially in the context of
international movements.
JFMS CLINICAL PRACTICE
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R E V I E W / ABCD guidelines on feline rabies
Assessing the likelihood of rabies
Is the cat from or near to an endemic
area, or travelling from there?
rabbit tissue culture inoculation test.
The mouse inoculation test can be used
only if rabbit tissue culture is not available;
✜ PCR is presently not recommended for
routine diagnosis but may be useful for
epidemiological studies or for confirmatory
diagnosis only in reference laboratories.
The list of reference experts and laboratories
can be found on the OIE website (www.oie.int).
NO
YES or unknown
Does the cat have outdoor access?
NO
YES or unknown
Has the cat been vaccinated against
rabies?
YES
NO or unknown
Is the cat less than 1 month of age?
YES
RABIES
UNLIKELY
NO or unknown
NO
Is the cat sick?
YES or unknown
Has the onset been sudden (<1 day)?
YES
NO or unknown
Have the clinical signs progressed
(worsened) in the past 3–5 days?
NO
YES or unknown
Does the cat show at least one of
the following clinical signs?
✜ Behavioural changes
✜ Cranial nerve deficits
✜ Seizures
✜ Muscular twitching or tremors
✜ Aimless pacing
✜ Tendency to bite
✜ Lower motor neuron paralysis
✜ Severe ataxia
✜ Depressed sensorium
NO
YES
Adapted from Tepsumethanon et al46
OIE recommendations
The following are recommendations from
experts at the OIE First International
Conference ‘Rabies in Europe’ (Kiev, 15–18
June 2005):
✜ Routine laboratory diagnosis should be
undertaken using only the techniques specified
by the OIE (Terrestrial Manual) and the
WHO (Laboratory Techniques in Rabies);
✜ The fluorescent antibody test is the
primary method recommended;
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JFMS CLINICAL PRACTICE
✜ Confirmation should be based on the
RABIES
POSSIBLE
Virus and antigen detection
To confirm rabies in people and animals, only
direct virus or antigen detection methods are
used. Brain tissue (especially thalamus, pons
and medulla) is preferred for post-mortem
diagnosis, but other organs (eg, salivary
glands) are also used. Samples should be
shipped according to the national and international regulations, and care should be taken
to avoid contamination. The specimens
should be shipped refrigerated for virus isolation or at room temperature in 50% glycerol/
phosphate-buffered saline.
✜ Fluorescent antibody test The fluorescent
antibody test (FAT) is recommended by the
WHO and OIE for fresh or glycerol samples.27
On fresh samples, FAT provides a reliable
diagnosis in 95–99% of all lyssavirus cases; on
formalin-fixed tissue the test is less sensitive.
It can also be used to detect virus in cell
culture and in brain tissue of mice that had
been inoculated with homogenates of
suspected material.
✜ Immunochemical tests Other suitable
methods include immunochemical tests using
the avidin–biotin peroxidase system, ELISA,
and direct blot enzyme immunoassay.
The rapid rabies enzyme immunodiagnosis
is an alternative to FAT but detects only the
‘classical’ rabies virus; agreement with the
FAT is between 96 and 99%.28
✜ Inoculation to laboratory animals and
cell cultures Inoculation techniques and
cell cultures are used to confirm inconclusive
results obtained with FAT on organs or
negative results when human exposure has
been reported. Newborn or 3–4-week-old
mice are inoculated intracerebrally, and FAT
is used to detect the virus 5–11 days later.
Animal inoculation tests should be replaced
by cell culture tests, which are as sensitive,
less time consuming and ethically acceptable.
Rabies virus replicates in mouse
neuroblastoma cell lines, and the presence
of antigen is revealed by FAT, with results
available within 2–4 days.
✜ Histology and immunohistochemistry
Histological and immunohistochemical
methods to detect Negri bodies are of low
sensitivity, especially in autolysed tissues, and
are not recommended for routine diagnosis.
Author's personal copy
R E V I E W / ABCD guidelines on feline rabies
✜ Other direct methods Monoclonal
✜ ELISA ELISA kits for the detection of
antibodies, nucleic acid probes or PCR
and sequencing can be used by reference
laboratories to identify rabies virus, especially
some variants. These techniques can
distinguish vaccine and field strains and may
identify the geographic origin of the strain.
antibodies in sera from vaccinated cats and
dogs are commercially available. Test results
can be obtained within 4 h. The sensitivity and
specificity of these tests need to be assessed
before they can be officially accepted.29–31
Disease management
Antibody detection
✜ Seroneutralisation tests Techniques such
as fluorescent antibody virus neutralisation
(FAVN) or rapid fluorescent focus inhibition
(RFFIT) are widely used. The former test
is based on the neutralisation of a given
concentration of rabies virus (CVS strain) in
vitro before inoculating BHK-21 C13 cells.
The antibody concentration is determined by
titration; however, it is not expressed as a titre
value (reciprocal of serum dilution) but in
International Units per millilitre (IU/ml), by
comparison with an OIE standard serum of
dog origin (OIE Reference Laboratory for
Rabies, Nancy, France). A value of 0.5 IU/ml
has been defined as the minimum to correlate
with immune protection. The two techniques,
RFFIT and FAVN, give equivalent results.
Va c c i n a t i o n
General considerations
Post-exposure treatment
Post-exposure vaccination of cats depends on
the national public health regulations. It is
forbidden in many countries and usually not
authorised in cases of clinical suspicion.
Supportive or specific treatment is ineffective
in rabid cats, and treatment is not considered,
likewise for public health reasons.7
Preventive vaccination
Because of the public health risk, rabies vaccines are core vaccines in countries where
rabies is endemic (see box below), and they
must be administered in accordance with local
or state regulations. In countries without rabies,
vaccination is optional; it is recommended if a
cat should move into a rabies-endemic area.
Core/optional
vaccine
traditional vaccines: they are innocuous,
Because of the public health risk,
induce adequate humoral immune responsFeline rabies is controlled mostly by inactivatrabies vaccines are core vaccines in
es and do not require rabies virus to be
ed vaccines.30 Several products containing
countries where rabies is endemic, and they
must be administered in accordance with local
handled.37 They also induce less inflamthe rabies virus are on the market, which
or state regulations. In countries without rabies,
mation at the site of injection.41
induce protection after a single injection.33 In
vaccination is optional; it is recommended if
Fortunately, current vaccines crosscats and dogs, rabies neutralising antibodies
the cat should move into a rabies-endemic
protect against other lyssaviruses. All cat
generally peak between 4–6 weeks after the
area.
and dog sera containing >5 IU/ml neutralise
first immunisation. The available vaccines are
EBL-1 and EBL-2, regardless of vaccine/virus
very efficient: cats and dogs with neutralisation
strain; of sera with values between 0.5–5 IU/ml,
values higher than 0.5 IU/ml – regardless of the
87% neutralise EBL-1 and 53% EBL-2 (AR Fooks,
time elapsed since vaccination – have a high probapersonal communication). However, depending on the
bility of surviving a rabies virus infection. Cats respond
genetic distance between novel isolates from bats in Eurasia
better than dogs; >97% of cats have been shown to develop antiand ‘classical’ rabies virus, protection may not be sufficient.42
body concentrations *0.5 IU/ml after the first vaccination, many
33
even >5 IU/ml. Only a tiny proportion of cats that succumbed to
rabies had a vaccination history of one injection or more.7 Since Primary course
In contrast to all other inactivated vaccines, a single rabies vaccina1993, when the new EU regulations on pet movement were put in
place, no single case of vaccine failure has been documented.33 tion induces long-lasting immunity. Kittens should be vaccinated at
12–16 weeks of age to avoid
Rabies vaccines are generalinterference from MDA, and
ly considered to be safe,
revaccinated 1 year later
even in neonatal kittens.
Cats respond better than dogs; >97% of
(depending on the data sheet
Inactivated vaccines may
cats developed antibody concentrations
recommendations for the
carry a risk of incomplete
respective brand of vaccine).
virus inactivation, but this is
*0.5 IU/ml after the first vaccination,
National or regional legislation
very small.34 They have also
regarding vaccination type and
been associated with the
many even >5 IU/ml.
intervals should be adhered to.
development of injection site
sarcomas in cats.35
These considerations led to continued efforts to develop safer Booster vaccination
rabies vaccines. New products include recombinant subunit pro- Although some vaccines protect against virulent rabies virus
teins, recombinant viral vectors and DNA-based vaccines.36–40 challenge for 3 years and upwards, national or local legislation
Recombinant live vector vaccines have some advantages over may call for annual boosters.43
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R E V I E W / ABCD guidelines on feline rabies
KEY POINTS
✜ Rabies occurs worldwide, with geographical exceptions. Large regions of Europe are now free of terrestrial rabies
as a result of wildlife vaccination programmes.
✜ The cat is considered as being a high-risk species for rabies transmission to humans in some European countries.
✜ Virus is shed in the saliva some days before the onset of clinical signs.
✜ The average incubation period in cats is 2 months, but may vary from 2 weeks to several months, or even years.
✜ Due to the presence of colostral antibodies, it is recommended that vaccination of kittens is not started earlier than
12 weeks of age.
✜ There is a low risk of cats becoming infected with rabies virus or other lyssaviruses from bats.
✜ Two disease manifestations have been identified in cats: the furious and the dumb form. Nearly all rabid cats (90%)
show the furious form.
✜ Death usually occurs after a clinical course of 1–10 days. Cats often die within 3–4 days.
✜ Feline rabies is controlled mostly by adjuvanted inactivated vaccines, which induce protection after a single
injection.
✜ Cats respond better than dogs, with more than 97% developing antibody concentrations *0.5 IU/ml
after the first vaccination.
✜ Kittens should be vaccinated at 12–16 weeks of age and revaccinated 1 year later.
✜ Some vaccines protect against virulent rabies virus challenge for 3 years and upwards,
but national or local legislation may call for annual boosters.
Disease control in specific
situations
Shelters
In rabies-endemic areas, stray cats should
always be approached with caution. Handling
and nursing of rescued animals should be considered hazardous, even if they appear healthy.
Breeding catteries
Breeding catteries are not at risk, because
pedigree cats are usually kept strictly indoors;
their vaccination may be required under local
or state regulation.
Immunocompromised cats
✜ Feline leukaemia virus (FeLV) or feline
immunodeficiency virus (FIV) positive
cats In rabies-endemic areas, FIVseropositive cats should be kept indoors.
Though this is an effective preventive
measure, national or regional legislation
must be adhered to. For outdoor cats with a
risk of exposure to rabies virus, vaccination
is strongly advised. Feline leukaemia viruspositive cats may not be able to mount
adequate immune responses to some rabies
vaccines.44 If FeLV-infected cats are allowed
to roam in rabies-endemic areas (this is not
recommended), more frequent vaccinations
(eg, every 6 months) are justified.
✜ Cats with concurrent disease Cats with
any acute illness should not be vaccinated.
Those with chronic conditions, such
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JFMS CLINICAL PRACTICE
as renal disease, diabetes mellitus or
hyperthyroidism, should be vaccinated
regularly if they are at risk of exposure.
✜ Cats receiving corticosteroids or other
immunosuppressive drugs In cats
receiving corticosteroids or other
immunosuppressive drugs, the need for
vaccination should be considered carefully.
Depending on dosage and duration of
treatment, corticosteroids may cause
functional suppression of (particularly cellmediated) immune responses, but studies
for rabies vaccines are lacking. In dogs,
corticosteroids do not appear to result in
ineffective immunisations if given for short
periods at moderate doses.45 In general,
concurrent use of corticosteroids and
vaccines should be avoided.
Acknowledgements
The European Advisory Board on Cat Diseases
(ABCD) is indebted to Dr Karin de Lange for
her judicious assistance in organising this
special issue, her efforts at coordination,
and her friendly deadline-keeping. The tireless
editorial assistance of Christina EspertSanchez is gratefully acknowledged. The
groundwork for this series of guidelines would
not have been possible without financial
support from Merial. The ABCD particularly
appreciates the support of Dr Jean-Christophe
Thibault, who respected the team’s insistence
on scientific independence.
Author's personal copy
R E V I E W / ABCD guidelines on feline rabies
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