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Feline herpesvirus infection (2012 edition)
What’s new?
This is an updated edition of the Feline Herpesvirus guidelines.
The essential changes with respect to earlier editions are these:
• FHV is the most important cause of corneal ulceration (Hartley, 2010).
• Molecular diagnosis should avoid the use of fluorescein and topical anaesthetics
because these compounds can affect the sensitivity of some PCR methods (Gould,
2011), unless permitted by the diagnostic laboratory.
• Table 2.2. Symptomatic treatment for acute respiratory disease
• Table 2.4. Antiviral drugs recommended for topical and systemic treatment of acute
FHV ocular disease.
• Vaccination provides good protection against clinical signs, and also against viral
shedding, within one week after administration (Jas et al., 2009)
• Maternally derived immunity can interfere with the response to vaccination until 8
weeks of age at an average (Poulet, 2007)
Multi-cat households
• FHV is common in multi-cat households. Depending on the management of such
households, the recommendations will refer either to shelters or to breeding catteries.
• New cats should be quarantined for the first three weeks and cats should be kept
individually – unless known to originate from the same household.
Virus
Feline herpesvirus (FHV), the agent of feline viral rhinotracheitis, is distributed worldwide.
The virus belongs to the order Herpesvirales, family Herpesviridae, subfamily
Alphaherpesvirinae, genus Varicellovirus. Although only one serotype is described, the
virulence can differ between viral strains (Gaskell et al. 2007); differences can also be
observed by restriction endonuclease analysis (Hamano et al. 2005; Thiry 2006).
The genomic double-stranded DNA of FHV is packaged into an icosahedral capsid
surrounded by a proteinaceous tegument and a phospholipid envelope, which contains at least
ten glycoproteins. In the feline host, FHV replicates in epithelial cells of both the conjunctiva
and the upper respiratory tract, and in neurons. The neuronal infection enables the virus to
establish lifelong latency after primary infection. FHV is related antigenically to canine
herpesvirus and phocid herpesviruses 1 and 2; there is no known cross-species transfer
(Gaskell et al., 2006).
The virus is inactivated within 3 hours at 37°C and is susceptible to most commercial
disinfectants, antiseptics and detergents. At 4°C, it remains infectious for about five months,
at 25°C for about a month, and it is inactivated at 56°C in 4-5 minutes (Pedersen, 1987).
Epidemiology
The domestic cat is the main host of FHV, but it has been isolated also from other felids,
including cheetahs and lions, and antibodies have been detected in pumas. There is no
evidence of human infection.
Latent chronic infection is the typical outcome of an acute infection, and intermittent
reactivation gives rise to viral shedding in oronasal and conjunctival secretions. Except in
catteries, contamination of the environment is not important for virus transmission. Virus
shedding by acutely infected cats as well as by latently infected cats experiencing reactivation
are the two main sources of infection (Gaskell and Povey, 1982).
Transplacental infection has not been seen in the field. Latently infected queens may transmit
FHV to their offspring because parturition and lactation are stressful events leading to viral
reactivation and shedding. Kittens may therefore acquire FHV infection at an early age,
before vaccination. The outcome of the infection depends on MDA: when high levels are
present, kittens are protected against disease, experience a subclinical infection that leads to
virus latency, whereas in the absence of sufficient MDA, clinical manifestations may follow
(Gaskell and Povey, 1992).
In healthy small populations, the prevalence of viral shedding may be less than 1%, whereas
in large populations, especially with clinical signs present, up to 20% of the cats may shed
(Coutts et al., 1994; Binns et al., 2000; Helps et al., 2005). In shelters, the risk is higher: with
4% of shedders entering the shelter, after one week, 50% of the cats may excrete the virus
(Pedersen et al., 2004). The low initial prevalence is likely to reflect the intermittent nature of
viral shedding during latency.
Pathogenesis
The virus enters via the nasal, oral or conjunctival routes. It causes a lytic infection of the
nasal epithelium with spread to the conjunctival sac, pharynx, trachea, bronchi and
bronchioles. Lesions are characterised by multifocal necrosis of epithelium, with neutrophile
granulocyte infiltration and inflammation. A transient viraemia associated with blood
mononuclear cells is observed after natural infection in young cats (Westermeyer et al., 2009).
This has been observed exceptionally also in neonates (Gaskell et al., 2007).
Viral excretion starts as soon as 24 hours after infection and lasts for 1 to 3 weeks. Acute
disease resolves within 10 to 14 days. Some animals may develop chronic lesions in the upper
respiratory tract and ocular tissues.
Upon infection, the virus spreads along the sensory nerves and reaches neurons, particularly
in the trigeminal ganglia, which are the main sites of latency. Almost all cats experiencing
primary infection become lifelong latent carriers. There are no direct diagnostic methods to
identify latency, because the virus persists as genomic DNA in the nucleus of the latently
infected neurons, without replication. Virus shedding can be induced experimentally in
approximately 70% of latently infected cats by glucocorticoid treatment. Other reactivating
stressful events include lactation (40 %), and moving the cat into a new environment (18%)
(Gaskell and Povey, 1977; Ellis, 1981; Gaskell and Povey, 1982; Pedersen et al., 2004).
Some adult cats show acute lesions at the time of viral reactivation; disease ensuing
reactivation is referred to as recrudescence.
Conjunctivitis may be associated with corneal ulcers, which may develop into chronic
sequestra. Stromal keratitis is a secondary, immune-mediated reaction due to the presence of
virus in the epithelium or stroma. Damage to the nasal turbinates during acute disease is
thought to be a predisposing factor for chronic rhinitis (Gaskell et al., 2007).
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Immunity
Passive immunity acquired via colostrum
During their first weeks of life, kittens are protected against infectious disease by MDA, but
in FHV infection, antibody levels are generally low. They may persist for 10 weeks (Johnson
and Povey, 1985), but may have vanished already at 6 weeks of age (in about 25% of kittens;
Dawson et al., 2001).
Active immune response
Glycoproteins embedded in the herpesviral membrane are important in the induction of
immunity; after infection, the detection of virus neutralizing antibodies (VNA) correlates with
the recognition of FHV glycoproteins (Burgener and Maes, 1988). Furthermore,
immunisation of rabbits with the FHV membrane protein gD led to the production of high
VNA titres (Spatz et al., 1994).
Natural FHV infection does not result in a comprehensive immunity; in general, the immune
response protects against disease but not against infection, and after re-infection, mild clinical
signs have been observed only 150 days after primary infection (Gaskell and Povey, 1979).
VNA titres after natural infection are often low and rise slowly - indeed, they may still be
absent after 40 days (Gaskell and Povey, 1979). VNA most likely contribute to the protection
against acute infection. Other antibody-mediated mechanisms e.g. antibody mediated cellular
cytotoxicity (ADCC) and antibody-induced complement lysis have been demonstrated
(Wardley, 1976). As in other alphaherpesvirus infections, cell-mediated immunity plays an
important role in protection, since the absence of serum antibody in vaccinated cats does not
mean that cats will develop disease; on the other hand, seroconversion did correlate with
protection against a virulent FHV challenge (Lappin et al., 2002).
Although antibody presence and protection against clinical signs are correlated, there is
currently no test available that predicts the degree of protection in individual cats.
Since FHV is a pathogen of the respiratory tract, mucosal cellular and humoral responses are
important. Studies with intranasal vaccines have shown clinical benefits as early as 2-6 days
after vaccination (Lappin et al., 2006; Weigler et al., 1997, Slater and York, 1976).
Clinical signs
Table 1. FHV disease, lesions and clinical signs
[Note: Exclusion of concurrent infection with other agents is required to determine the FHV
aetiology of chronic rhinitis]
Disease type
Pathology
Main clinical manifestations
Classical acute disease
(cytolytic disease)
Rhinitis, conjunctivitis,
superficial and deep corneal
ulcers, in particular dendritic
ulcers
Sneezing, nasal discharge,
conjunctival hyperaemia and
serous discharge
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Atypical acute disease
Chronic disease
(immune-mediated disease)
Possibly FHV-related
diseases
Skin disease
Nasal and facial ulcerated and
crust forming lesions
Viraemia, pneumonia
Severe systemic signs,
coughing, death (acute death
in kittens, “fading kitten
syndrome”)
Stromal keratitis
Corneal oedema,
vascularisation, blindness
Chronic rhinosinusitis
Chronic sneezing and nasal
discharge
Corneal sequestra
Eosinophilic keratitis
Neurological disease
Uveitis
FHV infection typically causes acute upper respiratory and ocular disease, which is
particularly severe in young kittens. Viral replication causes the erosion and ulceration of
mucosal surfaces, resulting in rhinitis, conjunctivitis, and occasionally corneal ulcerative
disease; dendritic ulcers are considered a pathognomonic manifestation (Maggs, 2005). FHV
is the most important cause of corneal ulceration (Hartley, 2010).
Typical clinical signs start with salivation, sneezing and coughing, followed by pyrexia,
depression and anorexia, serous or sero-sanguineous ocular and/or nasal discharge, and
conjunctival hyperaemia (Gaskell et al., 2006). Secondary bacterial infection is common, in
which case secretions become purulent. Occasionally, primary pneumonia and a viraemic
state are seen, with severe generalized signs and a fatal outcome (Gaskell et al., 2006).
Less frequently, oral ulceration, dermatitis, skin ulcers (Hargis et al., 1999) and neurological
signs (Gaskell et al., 2006) occur. Abortion is a rare secondary effect, which it is not a direct
consequence of viral replication - in contrast to herpesvirus infections in other species.
After reactivation and recrudescence, cats may show acute cytolytic disease as described
above. Others may present with chronic ocular immune-mediated disease in response to the
presence of FHV antigen. Experimental infections resulting in stromal keratitis with corneal
oedema, inflammatory cell infiltrates, vascularisation and eventually blindness suggest this
pathogenetic mechanism (Nasisse et al., 1989; Maggs, 2005).
Corneal sequestra and eosinophilic keratitis have been linked to the presence of FHV in the
cornea and/or blood. However, a definite causal association cannot be made since some
affected cats are FHV-negative (Cullen et al., 2005, Nasisse et al., 1998). Viral DNA has been
detected in the aqueous humour of a larger proportion of cats suffering from uveitis as
compared to healthy cats, suggesting that FHV may play a role in the inflammation (Maggs et
al., 1999).
Chronic rhinosinusitis, a frequent cause of sneezing and nasal discharge, has also been
associated with the infection; however, viral DNA is detected only in some affected cats, and
also in healthy controls (Henderson et al., 2004). No FHV replication is seen, which suggests
that the virus might only initiate the condition, which is then perpetuated by immunemediated mechanisms like inflammatory and remodelling phenomena, leading to permanent
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destruction of nasal turbinates and bone, and complicated by secondary bacterial infection
(Johnson et al., 2005).
FHV infection often occurs in combination with feline calicivirus and/or Chlamydophila felis,
Bordetella bronchiseptica, Mycoplasma spp. Other microorganisms, including
Staphylococcus spp. and Escherichia coli may lead to secondary infection of the respiratory
tract, causing a multi-agent respiratory syndrome (Gaskell et al., 2006).
Diagnosis
Methods for detecting FHV
The preferred method to detect FHV in biological samples is PCR, but virus isolation is still
used in several laboratories. The sensitivity and specificity of the tests, especially of PCR,
differ depending on the laboratory because of a lack of standardisation.
The PCR variants currently used to detect FHV DNA in conjunctival, corneal or
oropharyngeal swabs, corneal scrapings, aqueous humour, corneal sequestra, blood or biopsy
specimens include conventional PCR, nested PCR and real-time PCR (Hara et al., 1996;
Helps et al., 2003; Marsilio et al, 2004; Maggs et al., 1999a; Nasisse et al., 1997; Stiles et al.,
1997a, 1997b; Sykes et al 2001, Vögtlin et al., 2002; Weigler et al., 1997). Most PCR primers
are based on the highly conserved thymidine kinase gene.
Molecular diagnostic methods are more sensitive than virus isolation or indirect
immunofluorescence (Burgesser et al., 1999; Reubel et al., 1993; Stiles et al., 1997; Weigler
et al., 1997; EBM grade I).
Because of the minute amounts of viral nucleic acid detectable by PCR, positive test results
should be interpreted with caution – they may not prove any association with the disease. The
sensitivity of PCR depends on the test format (Maggs and Clarke, 2005); the system should
include a control to measure feline DNA, to estimate the quantitaty of material on the swab,
and to check for inhibitory substances. Due to its high sensitivity, PCR may also detect viral
DNA in scrapings of the cornea and/or tonsils suggesting non-productive infection (Maggs et
al., 1999b; Reubel et al., 1993; Stiles et al., 1997a). Consequently, its diagnostic value for
clinical infection may be poor, depending on the test sensitivity, the samples analysed
(biopsies and corneal scrapings yield positive results more frequently than conjunctival
samples) and the population tested (e.g. shelter cats are more likely to test positive than
household cats).
Additionally, PCR tests can detect FHV DNA in modified-live virus vaccines (Maggs and
Clarke, 2005); it is unknown if vaccinal strains are detected in recently vaccinated animals
and for how long after vaccination.
A positive PCR result may indicate low level shedding or viral latency and does not mean that
the virus is responsible for the observed clinical signs, although it indicates the possibility of
recurring signs in the future. However, when quantitative real-time PCR is used (Vögtlin et
al., 2002; EBM grade II), the amount of virus measured may provide additional information
on the etiological importance of the agent: when high viral loads are present in the nasal
secretion or tears, this suggests active replication and involvement of the virus in the clinical
signs. If low copy numbers are detected in corneal scrapings, this would indicate a latent
infection.
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When considering molecular diagnosis in clinical practice, the use of fluorescein and topical
anaesthetics should be avoided, because these compounds may affect PCR sensitivity (Gould,
2011). It is advisable to contact the diagnostic laboratory in advance for details of sample
collection and shipping, which is mostly done with regular mail at ambient temperature
(Maggs 2005). Using the same sample, PCR allows the simultaneous detection of other feline
pathogens frequently implicated in respiratory and ocular diseases, especially Chlamydophila
felis and, less reliably, feline calicivirus (Helps et al., 2003; Marsilio et al., 2004).
Virus isolation (VI) is an alternative method of diagnosing FHV infection. It is less sensitive
than PCR but does indicate that viable virus, not just DNA, is present.
In cats undergoing primary FHV infection, the virus can be detected by isolation from
conjunctival, nasal or pharyngeal swabs or scrapings, or from post-mortem lung samples. In
chronic infections, VI may be difficult.
Asymptomatic FHV carriers can be detected by VI, but both the positive and negative
predictive value of VI is low (Gaskell and Povey, 1977; Maggs et al., 1999b). Samples must
be collected before application of fluorescein or Rose Bengal stain, which inhibit viral
replication in cell culture (Brooks et al., 1994; Storey et al., 2002). Also, clinical specimens
must be sent quickly to the laboratory, and refrigerated during shipping. For these logistic
reasons and despite its good sensitivity in acute disease, VI is not routinely used for FHV
infection diagnosis.
FHV-specific antigen can be detected by immunofluorescence assay (IFA) on conjunctival or
corneal smears or biopsy specimens. As for VI, the use of fluorescein should be avoided
before sampling, which may give false-positive results and make test interpretation difficult.
IFA is less sensitive than VI or PCR, especially in chronic infections (Nasisse et al., 1993;
Burgesser et al., 1999). No correlation between VI and IFA has been observed, but a
combination of both methods may diagnose the presence of FHV better than either test alone
(Nasisse et al., 1993; Maggs et al., 1999b). Because of its low sensitivity and the interference
with fluorescein, often used in ophthalmology practice, IFA is not the most suitable
diagnostic test in chronic ocular disease (Nasisse et al., 1993).
Serology
Antibodies to FHV can be detected by neutralization test or ELISA in serum, aqueous humour
and cerebrospinal fluid (Dawson et al., 1998; Maggs et al., 1999b). Due to natural infection
and vaccination, seroprevalence is high, and the demonstration of specific antibodies
consequently does not correlate with disease and active infection (Maggs et al., 1999b; EBM
grade I).
Moreover, antibody detection does not allow differentiation between infected and vaccinated
animals, neutralizing antibodies are undetectable until 20 to 30 days after a primary infection,
and titres may be low, both in animals with acute and chronic disease. Consequently serology
is of limited value in the diagnosis of feline herpesvirus infection (Nasisse and Weigler, 1997;
Maggs et al., 1999b; Maggs, 2005).
Disease management
Supportive treatment
The restoration of fluids, electrolytes and the acid-base balance (e.g. replacement of losses of
potassium and bicarbonate due to salivation and reduced food intake), preferably by
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intravenous administration, is required in cats with severe clinical signs. Food intake is
extremely important. Many sick cats do not eat because of their loss of smell due to nasal
congestion, or because of ulcers in the oral cavity. Food may be blended to cause less pain
when eating, should be highly palatable, and may be warmed up to increase the smell.
Appetite stimulants (e.g. cyproheptadine) may be used. If the cat has not eaten for three days,
placement of a nasal or oesophageal feeding tube is indicated.
To prevent bacterial infection, antibiotics should be given in all acute cases of feline upper
respiratory tract disease, preferably broad-spectrum products with good penetration in the
respiratory tract.
Severely affected cats need intensive nursing care and appropriate supportive therapy. Nasal
discharge should be cleaned away several times a day using physiologic saline solution, and
local ointment applied. Drugs with mucolytic effects (e.g. bromhexine) may be helpful. Eye
drops or ointment can be administered several times a day. Nebulisation of saline can be used
to take care of dehydration of the airways.
Vitamins are used, but their value is unproven.
Table 2. Symptomatic treatment for acute respiratory disease
Drug
Comment
ABCD recommendation
EBM
level
Topical treatment
nasal flushing with
physiological saline solution
and nebulization
highly palatable food
to clean nasal discharge and
to prevent dehydration of the
upper airways
to ensure sufficient food
intake
placement of a feeding tube
and enteral nutrition
to ensure sufficient food
intake
recommended several times daily
4
necessary, if cats do not eat because of pyrexia
and/or ulcers in the oral cavity, or because of
their loss of smell due to nasal congestion:
food can be blended and warmed up to
increase smell
necessary if the cat has not been eating for
three days
4
necessary in cats with severe clinical signs
4
broad-spectrum antibiotics with good
penetration in the respiratory tract are
recommended for cats with severe disease
recommended if cat is severely depressed
4
may be helpful
4
4
Systemic treatment
Fluid therapy
to control dehydration and
restore electrolyte and acid
base imbalance
to control secondary bacterial
infections
Antibiotics
Non-steroidal antiinflammatory drugs
Drugs with mucolytic effects
(e.g., bromhexine)
to decrease fever
to improve mucous nasal
discharge
4
Table 3. Symptomatic treatment for acute ocular disease (conjunctivitis and keratitis)
Drug
Comment
ABCD recommendation
EBM
level
Antibiotics
Anti-inflammatory drugs
to control secondary bacterial
infections
To decrease local inflammation
Topical antibiotics
4
Usually not needed; to avoid corticosteroids
4
Antiviral therapy
Table 4. Antiviral drugs recommended for topical and systemic treatment of acute FHV
ocular disease. The drugs are listed in decreasing order of preference.
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Topical treatment
Drug
Type of drug
Route of
administration
Efficacy
in vitro
Efficacy
in vivo
Trifluridine
Nucleoside
analogue
Topical
Use every hour
for 1st day and
every 4 hours
thereafter
(Maggs, 2001)
Excellent
n.d.
Controlled
study in
vivo?
no
Cidofovir
Nucleoside
analogue
0.5% solution
applied topically
yes
yes
yes
Idoxuridine
Nucleoside
analogue
Topical
use initially ever
2-4 hours
(Maggs, 2001)
excellent
n.d.
no
Ganciclovir
Nucleoside
analogue
Topical
excellent
n.d.
n.d.
Aciclovir
Nucleoside
analogue
Topical and oral
Poor
(high
doses may
be needed
to
overcome
viral
resistance)
some
yes
Comments
EBM
level
Topical treatment of
choice in ocular FHV
manifestations. Some cats
averse to topical
application. Toxic if given
systemically. (Maggs,
2001)
Topical treatment for
ocular FHV; potent drug
with only two daily
applications (Fontenelle et
al., 2008; Maggs, 2010)
Topical treatment for
ocular FHV. Difficult to
source, pharmacists can
formulate a 0.1%
ophthalmic solution.
Toxic if given
systemically.
Topical treatment for
ocular FHV. Good in
vitro activity (van der
Meulen et al, 2006;
Maggs et al, 2004)
Least in vitro effect of all
herpes antivirals (van der
Meulen et al, 2006,
Williams et al., 2004),
moderate in vivo effect
(Williams et al., 2005).
Synergy in combination
with human IFN−α
(Weiss, 1989). Toxic
systematically. (Maggs,
2001; Maggs, 2010)
3
Tested in conventional
and SPF cats
experimental challenge,
against primary infection
(Malik et al., 2009;
Thomasy et al., 2011)
Safe and licensed for use
in cats.
3
3
3
3
3
Systemic treatments
Famciclovir
Nucleoside
analogue
(prodrug)
Oral, 90 mg/kg tid for
21 days
Feline IFN-ω
Interferon
Systemic
1 MU/kg SC sid or eod
Yes (for
penciclovir,
as famciclovir
is a prodrug
of
penciclovir)
yes
yes
yes
n.d.
yes
Oral
50,000 – 100,000 Units
daily
Human IFNα
Interferon
A combined topical and
oral pre-treatment before
experimental FHV
infection was not
beneficial (Haid et al.,
2007)
Topical; dilute 10MU
vial in 19ml 0.9% NaCl
and use as eye drops: 2
drops in each eye 5 times
a day for 10 days (Jongh,
2004).
SC high dose
yes
yes
yes
PO low dose
yes
yes
yes
5-35 Units daily
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Used along with L-lysine
in chronic infections.
Less bioactive than feline
interferon.
5-35 Units daily reduces
clinical signs but not
FHV shedding. Used
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3
L-lysine
Amino-acid
500 mg bid, not added to
food
yes
yes
yes
along with l-lysine in
chronic infections.
No published evidence of
side effects, conflicting
efficacy reports ; can
reduce spontaneous ocular
viral shedding rates in
latently infected cats
experiencing reactivation;
to be administered as
separate bolus, not added
to foods (Maggs, et al,
2000, 2001, 2003, 2007;
Stiles et al. 2002; Rees et
al., 2008; Drazenovich et
al., 2009; Maggs, 2010;
Gould, 2011)
n.d. = not determined; eod = every other day; sid = once daily; bid = twice daily; tid = three
times daily.
The drugs listed may not be readily available or licensed for cats.
Other drugs have been proposed for the treatment of FHV ocular infections, including
bromovinyldeoyuridine, HPMA, ribavirin, valacyclovir, vidarabine, foscarnet and lactoferrin.
However, the efficacy of these drugs has not been proven.
General recommendations on vaccine type and vaccination
protocol
This infection is common and may induce severe, even life-threatening disease. ABCD
therefore recommends that all cats should be vaccinated against FHV. Vaccines provide
protection through both an antibody response and cellular immunity. Vaccination provides
protection against clinical signs and reduces viral shedding within one week after
administration (Jas et al., 2009), but – like in other respiratory tract infections - it does not
provide full protection; about 90% reduction in clinical scores has been achieved following
experimental challenge soon after vaccination (Gaskell et al., 2007). Even less protection is
expected under particular circumstances like extreme challenge doses or immunosuppression.
Field strain variation does not play a role in protection provided by vaccination.
Vaccination protects against disease, but not necessarily against infection. However, it can
reduce field virus excretion (Gaskell et al., 2007).
Most current FHV vaccines are combined with FCV, either as bivalent products (only in some
countries) or with additional antigens. Both modified live and inactivated parenteral vaccines
are available. Subunit FHV vaccines and modified intranasal vaccines have been or still are
available elsewhere, but no longer in Europe.
For routine vaccination, there is no reason to prefer any FHV vaccine above another, since all
are based on a single serotype. Modified live vaccines retain some pathogenic potential and
may rarely induce disease, e.g. when accidentally aerosolised or spilt on the skin and taken up
during grooming.
The value of serological tests in predicting protection is controversial. Methodological issues
can complicate comparison of titres (particularly when obtained from different laboratories),
and they are no good predictors of protection. Also, cats without any evidence of
seroconversion have been found protected (Lappin et al., 2002; Mouzin 2004). Vaccinated
cats usually develop an anamnestic response upon field infection.
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2
Primary vaccination course
Maternal antibodies interfere with the response to vaccination until 8 weeks of age on average
(Poulet, 2007); the primary course of vaccination is therefore usually started at around nine
weeks of age, although some products are licensed for earlier use. Kittens should receive a
second vaccination two to four weeks later, with the second given around twelve weeks of
age. This protocol has been developed to ensure optimal protection. For longer intervals, no
information is available.
In contrast to vaccines against other infectious agents, where a single vaccination is
acceptable for adult cats of unknown or uncertain vaccination status, in the case of FHV two
vaccinations at an interval of two to four weeks are recommended, irrespective of the vaccine
type.
Booster vaccinations
ABCD recommends that boosters should be given at annual intervals to protect individual
cats against field infections. In low-risk situations (e.g. indoor-only cats without contact to
other cats), three-yearly intervals are recommended. An informed decision should be taken on
the basis of a risk-benefit analysis, but annual boosters are particularly important in high risk
situations e.g. for boarding and breeding catteries.
Experimental studies and serological surveys in the field have clearly shown that immunity
against FHV lasts longer than one year (Lappin et al., 2002, Mouzin et al., 2004; EBM grade
II). However, there is a significant proportion of cats for which this is not true. While most
cats in the field either have antibody against FCV and FPV, or show an anamnestic response
after the booster, only around 30% have titres against FHV, and around 20% fail to react to
booster vaccinations (Lappin et al., 2002, Mouzin et al., 2004). In experimental vaccine
efficacy studies, protection clearly decreases with time.
If booster vaccinations have lapsed, a single injection is adequate if the interval since the last
vaccination is less than three years; if it is more than three years, two injections three weeks
apart should be applied.
Boosters using FHV vaccines produced by another manufacturer are acceptable.
Cats that have recovered from disease caused by FHV may not enjoy lifelong protection
against further episodes. In most clinical cases, the causative agent will not have been
identified and the cat may contract infection with other respiratory pathogens. To be on the
safe side, vaccination of recovered cats is generally recommended.
Disease control in specific situations
Multi-cat households
FHV infection is common in multi-cat households. Depending on the management, ABCD
recommendations will refer either to shelters or to breeding catteries.
Shelters
FHV infections can pose a problem in cat shelters. Management to prevent and limit the
spread of infection is as important as vaccination. In shelters where incoming cats are mixed
with resident ones, high infection rates are frequent. To control this situation, newcomers
should be quarantined for the first three weeks, and kept individually – unless known to be
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from the same household. Shelter design and management measures should be aimed at
avoiding cross infections. New cats should be vaccinated as soon as possible when they are
healthy and no contraindications to vaccination have been found. If there is a particularly high
risk, e.g. past or recent FHV infections, modified live vaccines are used, as these provide
earlier protection. In an acute respiratory disease outbreak, identification of the agent involved
- with differentiation between FHV and FCV - can be useful in deciding on the appropriate
preventive measures.
Breeding catteries
FHV infections can be a major problem in breeding catteries, where they most often appear in
young kittens before weaning - typically around 4 to 8 weeks of age, when maternally derived
immunity wanes. The source of infection is often the queen, who is the virus carrier and
whose latent infection has been reactivated in the course of kittening and lactation.
Infection in such young kittens is often severe, involving the entire litter. Mortality can be
important, and some kittens that have recovered from the acute disease are left with
complications, notably chronic rhinitis. Vaccination of the queen is no option since it will not
prevent her from becoming a carrier. However, if the queen has a good antibody titre, the
kittens will benefit from high levels of MDA transferred through the colostrum, which
provide protection for the first weeks of life.
Booster vaccinations of the queen may therefore be indicated, which should ideally take place
prior to mating. Exceptionally, vaccination during pregnancy may be considered (if this
measure had been overlooked), but vaccines are not licensed for use in pregnant cats, and in
this situation, an inactivated product is preferable.
Queens should kitten in isolation, and litters should not mix nor have contacts with other cats
until they have been fully vaccinated. Early vaccination should be considered for litters from
queens that had infected litters previously. The earliest age for which FHV vaccines are
licensed is 6 weeks, but kittens may become susceptible to infection earlier than this as MDA
wanes. Vaccination from around 4 weeks of age may be considered, to be repeated every 2
weeks until the primary vaccination course is given as usual.
Early weaning into isolation from around 4 weeks of age is an alternative approach to
protecting kittens from maternal infection. There are no reliable tests that will identify carrier
queens and predict which may infect their kittens.
Vaccination of immunocompromised cats
Vaccines will not establish immunity in animals with a compromised immune function.
Systemic disease, genetic and virus-induced immunodeficiency, poor nutrition, concurrent
administration of immunosuppressive drugs and severe, prolonged stress all are
compromising factors. Such patients should be protected from exposure to infectious agents
in the first place, but vaccination using an inactivated product should be considered.
FIV positive cats
FIV-positive healthy cats should be protected against FHV, by confining them indoors. If this
is not possible, vaccination should be considered. Concerns have been raised that vaccination
may contribute to the progression of FIV disease, but the benefit of protecting a potentially
immunocompromised cat outweighs this small risk. Also, other infections may contribute to
FIV progression.
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In FIV-positive cats with a history of clinical problems but in a stable medical condition,
vaccination should be considered to ensure that FHV protection is maintained. In cats
suffering from FIV-related disease, vaccination is generally discouraged, as in any
systemically ill cat.
FeLV-positive cats
The same considerations apply to FeLV-positive cats. Vaccination is contra-indicated if there
are clinical signs related to the FeLV infection. If the cat appears healthy, vaccination should
be considered to maintain protection, if prevention of exposure to FHV cannot be ensured.
Chronic disease
Booster vaccination should be continued in cats with stable chronic conditions, such as
hyperthyroidism and renal disease. Such cats are often elderly and the consequences of
infection can be particularly severe.
Cats receiving corticosteroids or other immunosuppressive drugs
Depending on the dosage and duration of treatment, corticosteroids may cause suppression of
immune responses. The effect of corticosteroids on vaccine efficacy in cats is not known,
nevertheless concurrent use of corticosteroids at the time of vaccination should be avoided.
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