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Feline herpesvirus infection


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., 2004; 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.,

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 one month, and it is inactivated at 56°C in
4-5 minutes (Pedersen, 1987).


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

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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, 1982).

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


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

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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.,

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).


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 herpesvirus envelope 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

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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 et al., 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 (Slater and York, 1976; Weigler et
al., 1997b; Lappin et al., 2006).

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 Rhinitis, conjunctivitis, Sneezing, nasal

(cytolytic disease) superficial and deep corneal discharge, conjunctival
ulcers, in particular dendritic hyperaemia and serous
ulcers discharge

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Atypical acute disease Dermatitis Nasal and facial ulcerated
and crust forming lesions

Viraemia, pneumonia Severe systemic signs,

coughing, death (acute
death in kittens, “fading
kitten syndrome”)

Chronic disease Stromal keratitis Corneal oedema,

(immune-mediated vascularisation,
disease) blindness

Chronic rhinosinusitis Chronic sneezing and

nasal discharge

Possibly FHV- Corneal sequestra

related diseases Eosinophilic keratitis
Neurological disease

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).

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Less frequently, oral ulceration, dermatitis, skin ulcers (Hargis and Ginn, 1999)
and neurological signs (Gaskell et al., 2006) occur. Abortion is a rare secondary
effect, which 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 (Nasisse et al., 1998; Cullen et
al., 2005). 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., 1999b).

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 immune-mediated mechanisms like
inflammatory and remodelling phenomena, leading to permanent 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 Chlamydia
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).


Methods for detecting FHV

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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

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; Nasisse and Weigler, 1997; Stiles et al., 1997a, 1997b;
Weigler et al., 1997a; Maggs et al., 1999a; Sykes et al., 2001; Vögtlin et al., 2002;
Helps et al., 2003; Marsilio et al., 2004). Most PCR primers are based on the
highly conserved thymidine kinase gene.

Molecular diagnostic methods are more sensitive than virus isolation or indirect
immunofluorescence (Reubel et al., 1993; Stiles et al., 1997b; Weigler et al.,
1997a; Burgesser et al., 1999; 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 quantity 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 (Reubel et al.,
1993; Stiles et al., 1997a; Maggs et al., 1999b). 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

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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

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 Chlamydia 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

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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).


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,

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 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

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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
Topical treatment
nasal flushing with to clean nasal discharge recommended several times daily 4
physiological saline and to prevent dehydration
solution and nebulization of the upper airways
highly palatable food to ensure sufficient necessary, if cats do not eat because of 4
food intake 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

placement of a feeding to ensure sufficient necessary if the cat has not been 4
tube and enteral nutrition food intake eating for three days

Systemic treatment
Fluid therapy to control dehydration necessary in cats with severe clinical signs 4
and restore electrolyte
and acid base imbalance
Antibiotics to control secondary broad-spectrum antibiotics with good 4
bacterial infections penetration in the respiratory tract are
recommended for cats with severe
Non-steroidal anti- to decrease fever recommended if cat is severely depressed 4
inflammatory drugs

Drugs with mucolytic effects to improve mucous may be helpful 4

(e.g., bromhexine) nasal discharge

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Table 3. Symptomatic treatment for acute ocular disease (conjunctivitis and
Drug Comment ABCD recommendation EBM
Antibiotics to control secondary Topical antibiotics 4
bacterial infections
Anti-inflammatory drugs To decrease local Usually not needed; to avoid corticosteroids 4

Antiviral therapy

Table 4. Antiviral drugs recommended for topical and systemic treatment of acute
ocular disease. The drugs are listed in decreasing order of preference.

Topical treatment
Drug Type of drug Route of Efficacy Efficacy Controlled Comments EBM
administration in vitro in vivo study in level
Trifluridine Nucleoside Topical Excellent n.d. no Topical treatment of 3
analogue Use every hour choice in ocular FHV
for 1st day and manifestations. Some
every 4 hours cats averse to topical
thereafter application. Toxic if
(Maggs, 2 001) given systemically
Cidofovir Nucleoside 0.5% solution yes yes yes Topical treatment for 3
analogue applied topically ocular FHV; potent
drug with only two
daily applications
(Fontenelle et al.,
2008; Maggs, 2010)

Idoxuridine Nucleoside Topical excellent n.d. no Topical treatment for 3

analogue use initially every ocular FHV. Difficult
2-4 hours to source,
(Maggs, 2001) pharmacists can
formulate a 0.1%
ophthalmic solution.
Toxic if given

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Ganciclovir Nucleoside Topical excellent n.d. n.d. Topical treatment 3
analogue for ocular FHV.
Good in vitro
activity (Maggs
and Clarke, 2004;
van der Meulen et
al., 2006)

Aciclovir Nucleoside Topical and oral Poor some yes Least in vitro effect of 3
analogue (high all herpes antivirals
doses (van der Meulen et
may be al., 2006; Williams et
needed al., 2004), moderate
to in vivo effect
overcom (Williams et al.,
e viral 2005). Synergy in
resistance combination with
) human IFN−α
(Weiss, 1989). Toxic
2001; Maggs, 2010)

Systemic treatments
Famciclovir Nucleosid Oral, 90 mg/kg tid for Yes (for yes yes Tested in conventional 3
e 21 days penciclovir, and SPF cats
analogue as experimental
(prodrug) famciclovir is challenge, against
a prodrug primary infection (Malik
of et al., 2009; Thomasy
penciclovir) et al., 2011)
Feline IFN-ω Interferon Systemic yes n.d. yes Safe and licensed for 4
1 MU/kg SC sid or eod use in cats.

Oral A combined topical

50,000 – 100,000 and oral pre-treatment
u nits daily before experimental
FHV infection was not
beneficial (Haid et al.,
Topical; dilute 10MU
vial in 19ml 0.9% NaCl
and use as eye drops:
2 drops in each eye 5 Used along with L-
times a day for 10 days lysine in chronic
(Jongh, infections

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Human IFN- Interferon SC high dose yes yes yes Less bioactive than 3
α feline interferon.

PO low dose yes yes yes

5-35 units daily
reduces clinical signs
5-35 units daily
but not FHV shedding.
Used along with l-
lysine in chronic

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.

The amino acid l-lysine has been proposed for systemic treatment, to be
administered as a bolus, separate from food. No side effects have been published,
but reports on efficacy are conflicting (Maggs, 2001, 2010; Stiles et al., 2002;
Maggs et al., 2003, 2007; Rees and Lubinski, 2008; Drazenovich et al., 2009;
Gould, 2011). Cave et al. (2014) investigated the effects of physiologic
concentrations of l-lysine on the in vitro replication of FHV at L-arginine levels
sufficient to maintain cell growth. FHV was not inhibited at any l-lysine
concentration studied. The in vivo efficacy of the measure on primary and recurrent
FHV infection is unknown.

Other drugs have been proposed for the treatment of FHV ocular infections,
including bromovinyldeoxyuridine, HPMA, ribavirin, valacyclovir, vidarabine,
foscarnet and lactoferrin. However, the efficacy of these drugs has not
been proven.

General recommendations on vaccine type and vaccination


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

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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). In addition it can reduce field virus
excretion (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.

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
might retain some pathogenic potential and may rarely induce disease, e.g.
when accidentally aerosolised or spilt on the skin and taken up during

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 et al., 2004). Vaccinated cats
usually develop an anamnestic response upon field infection.

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.

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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

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 might not be 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. Furthermore, 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.

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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.


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 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 against disease for the
first weeks of life.

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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 neither 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.

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

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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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For further reading:

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Missouri; 271-278.

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