Journal of Feline Medicine
and Surgery (2001) 3, 9–16
doi:10.1053/jfms.2001.0110, available
online at http://www.idealibrary.com on
Ocular manifestations of feline
herpesvirus
College of Veterinary Medicine,
University of Florida, Department
of Small Animal Clinical Sciences,
PO
Box 100126, Gainesville,
Feline herpesvirus-1 (FHV-1) infection is
ubiquitous in the domestic cat population worldwide. The most common clinical
ocular manifestations of infection with FHV-1 are conjunctivitis and keratitis.
This paper reviews the
pathogenesis of feline herpesvirus-1 and
discusses the various clinical ocular manifestations, diagnostic techniques and
treatment of FHV-1-induced diseases. Ocular manifestations include:
conjunctivitis, keratitis, stromal
keratitis, keratoconjunctivitis sicca,
ophthalmia neonatorium, symblepharon, corneal sequestrum, eosinophilic
keratitis and anterior uveitis. Diagnostic techniques discussed include: virus
isolation, fluorescent antibody testing,
serum neutralising titers, ELISA and polymerase
chain reaction. Various therapies are also discussed. © 2001 European Society
of Feline Medicine
Feline herpesvirus-1
is the most frequent cause of conjunctivitis and keratitis in domestic
cats. The virus is ubiquitous in domestic cat populations. Feline herpesvirus-1
(FHV-1) is also the most studied infectious cause of ocular surface disease in
cats. Diagnosis and treatment of ocular manifestations of feline herpesvirus
can be difficult, frustrating and expensive, and recurrences are common in infected
animals. Cats infected with FHV-1 can present with conjunctival, corneal or a
combination of conjunctival and corneal signs. They may also present with or
without systemic illness and upper respiratory signs. FHV-1-associated ocular
diseases include chronic conjunctivitis, symblepharon, keratoconjunctivitis
sicca, eosinophilic keratitis, stromal keratitis and corneal sequestrum. This
paper will review the pathogenesis of FHV-1 and discuss the various clinical
ocular manifestations, diagnostic techniques, and treatment of FHV-1-induced
diseases.
Ocular anatomy and physiology
The feline cornea is comprised of five layers:
outermost stratified squamous epithelium, epithelial
basement membrane, stroma, Descemet’s membrane and innermost endothelium.
Feline conjunctival and corneal epithelium are embryologically derived from
surface ectoderm, and the corneal stroma is derived from neural crest cells (Cook
1999). The corneal epithelium in the normal cat is five to six cell layers
thick, which measures approximately 25–40 _m, and is comprised of stratified
squamous epithelium, wing cells and basal cells (Samuelson 1999).
An epithelial basement membrane anchors
the corneal epithelium to the underlying stroma. The corneal stroma is comprised of parallel lamellar collagen
bundles, and constitutes the majority of the corneal thickness (Samuelson
1999). Corneal sensory nerves, which are branches of the ophthalmic division
of the trigeminal nerve, are located in the superficial corneal stromal layer.
Descemet’s membrane is an acellular layer of collagen fibrils between the
stroma and the inner corneal endothelium (Samuelson 1999). The
endothelium is a single cell layer that functions to keep the cornea from
imbibing water from the aqueous humor bathing the tissues inside the eye. The
mean central corneal thickness has been measured as 578±64 _m by ultrasonic
pachymetry in the cat (Gilger et al 1993). The presence
of a corneal ulceration (absence of epithelium and varying amounts of stroma)
also causes anterior uveitis due to a proposed axon reflex (Gum et
al 1999). Following epithelial removal, activation of the corneal sensory
nerves normally located in the superficial corneal stroma results in
stimulation of the ciliary body musculature and secondary anterior uveitis and
1098–612X/01/010009+08 $35.00/0 © 2001 European Society of Feline Medicine
pain. It is important to remember that whenever a corneal ulcer is present,
there is also secondary anterior uveitis and pain. Corneal sensitivity has been
measured in cats with unilateral dendritic corneal ulcers, and 41/61 (67%)
corneas were found to be less sensitive than the fellow normal eye (Boydell
1997). The decreased corneal sensitivity was not correlated with the
presence or absence of secondary anterior uveitis and pain in this study, and
there was no speculation about the relationship between hypoaesthaesia and
corneal ulceration. Decreased corneal sensitivity or hypoaesthaesia is reported
to occur in humans with Herpes simplex keratitis (Martin
1988).
FHV-1 is a DNA _-herpesvirus that induces damage to
mucosal epithelial cells during replication and is a cause of feline viral
rhinotracheitis (Gaskell & Dawson 1998). The disease is
prevalent in domestic cat populations, and there are no other known reservoirs
(Gaskell & Dawson 1998). Nasal, oral and conjunctival
routes of infection have been demonstrated, and the virus is primarily shed in
secretions from these body systems for 1–3 weeks following infection (Gaskell
& Dawson 1998). Certain animals also shed virus transiently in
faeces and urine (Povey 1990), but there is no documented
‘in utero’ transmission (Gaskell &
Dawson 1998). One to 2 days following exposure of naďve animals
to FHV-1, virus replication and epithelial cell necrosis occur in the nasal
turbinates, nasopharynx and conjunctival mucosa (Gaskell &
Dawson 1998). In the ocular tissues, FHV-1 has been shown to
preferentially infect and cause necrosis of the conjunctival epithelium, as
well as replicate in the corneal epithelium (Nasisse et al
1989a). Concurrent secondary bacterial infection can exacerbate clinical
signs of FHV-1-induced upper respiratory tract disease. Mortality rates as high
as 70% of infected kittens have been reported (Povey 1990), but
the mortality rate is low when all susceptible animals are considered (Gaskell
& Dawson 1998). Maternally derived antibody protection persists
between 2 and 10 weeks, but may not protect cats from subclinical infection (Gaskell
& Dawson 1998). Many FHV-1 infections are considered subclinical or
mild, and often are not presented for veterinary attention. Following
infection, approximately 80% of susceptible animals become FHV-1 carriers, and
45% of those spontaneously reactivate and either asymptomatically shed or
develop clinical disease manifestations (Gaskell &
Povey 1977).With the advent of molecular diagnostic
techniques, the percentage of latently
infected carriers reported has actually increased (Reubel et al 1993, Weigler
et al 1997). FHV-1, an ǻ-herpesvirus,
is able to establish latency in neuronal tissue. FHV-1 has been detected in the
trigeminal ganglion of latently infected cats (Gaskell et al 1985, Nasisse
et al 1992, Ohmura et al 1993), as well as
acutely infected cats by day 4 post-infection (Nasisse et al 1992).
Latency is assumed to be lifelong. However, periods of shedding may or may not
occur depending on the presence of stress events in the cat’s life.
Conjunctivitis
Primary FHV-1 infection and viral replication
with secondary bacterial infection results in conjunctivitis. Following a 2–6
day incubation period in neonatal and adolescent cats, serous ocular and nasal
discharge, sneezing, inappetence and fever are common linical signs (Gaskell & Dawson 1998). By
day 4 postinfection, there is diffuse necrosis of the conjunctival epithelium and
often large numbers of intranuclear inclusions in conjunctival epithelial cells
(Nasisse 1990). The conjunctivitis is usually bilateral, and is
manifested as hyperaemia or redness
with serous discharge that progresses over several days to mucopurulent ocular
discharge (Fig 1). Chemosis, which is swelling or oedema
of the conjunctiva, may occur but to a lesser extent than is observed with
bacterial conjunctivitis. Conjunctival infection always occurs with primary
FHV-1 infection, and here may also be limited
corneal replication of the virus (Nasisse 1990). Most cats recover in 10–20 days with no ocular
sequelae. Severe infection or immunosuppression may result in chronic or
recurrent conjunctivitis (Gaskell & Dawson 1998).
Some adult cats may exhibit recrudescence as conjunctivitis in one or both
eyes. The course of clinical disease varies from weeks to months and can recur
(Nasisse 1990).
Keratitis
FHV-1
is the only documented viral cause of feline keratitis. FHV-1-induced corneal
ulceration is primarily a disease of adult cats, and is likely a reactivation
of latent virus.
Figure 1. The
left eye of an adolescent cat presented with
signs of upper respiratory tract
disease and conjunctivitis
attributed to feline herpesvirus-1
infection. Conjunctival
hyperaemia and mild chemosis are
present.
Figure 2. A unilateral dendritic corneal ulcer in a feline
herpesvirus-1 positive cat stained
with fluorescein.
Figure 3. Stromal keratitis caused by feline
herpesvirus-1
infection (courtesy of Dr Michelle
Willis, Columbus, OH,
USA). The inflammation extends into
the deeper stroma of
the left eye of this cat as
evidenced by the opacity and
vascularisation of the cornea.
Reactivation
of latent virus has been associated with systemic immunosuppression (feline
leukaemia virus and/or feline immunodeficiency virus infection), environmental
stress (boarding, surgery, moving to a new environment, addition of a new pet)
or systemic corticosteroid administration. Dendritic corneal ulcers are
almost pathognomonic for FHV-1
infection (Fig 2) (Roberts et al 1972, Nasisse
& Weigler 1997), and result from direct cytopathic effect of the
virus in the basal cell layer of the corneal epithelium (Roberts
et al 1972). Theoretically, local immune response suppression allows FHV-1 to reach the
corneal stroma, and subsequent keratitis is mediated by an immune response to
parts of the viral antigen causing stromal damage that is unrelated to virus
replication (Nasisse et al 1995). Dendrites that
coalesce to a map-like appearance are called geographic ulcers (Nasisse
1990). The ocular clinical signs depend on the depth of corneal infection
and the chronicity. Acutely, mild to moderate conjunctivitis, blepharospasm and
ocular discharge are seen. The keratitis may be unilateral or bilateral, and
respiratory disease is absent. Chronically, stromal oedema and vascularisation
may occur. Stromal ulceration can occur, but it seems unlikely that FHV-1 is able
to induce corneal stromal melting (Nasisse 1990).
Stromal
keratitis
Stromal
keratitis refers to infection and inflammation of the deeper corneal tissue.
Stromal keratitis is a less common manifestation of FHV-1 infection, but is
considered to be a very significant form of disease due to the potential for
vision-threatening stromal opacification and scarring (Fig 3) (Nasisse
1990). The mechanism of stromal disease manifestation is not known, but
chronic recurrent episodes of FHV-1 keratitis result in stromal collagen damage
and opacification (Nasisse 1990). Prolonged absence of corneal
epithelium precedes stromal keratitis, and stromal keratitis is not a
manifestation of primary FHV-1 infection (Nasisse et al
1989a).
Keratoconjunctivitis
sicca
Keratoconjunctivitis
sicca (KCS) occurs in cats with either chronic or recurrent
blepharoconjunctivitis, sometimes caused by FHV-1 infection (Glaze
& Gelatt 1999). It is unknown whether the damage is to secretory
glandular tissue that provides the aqueous portion of the tear film or
Figure 4. Keratoconjunctivitis sicca in a 2-year-old cat with
chronic feline herpesvirus
conjunctivitis. Note the dullness
and dry appearance of the cornea.
Figure 5. A corneal sequestrum in a 6-year-old domestic
shorthair cat that had suffered from
recurrent corneal ulcerations
caused by feline herpesvirus-1. The
axial, darkly pigmented
plaque is in the superficial
one-third of the corneal
stroma.
Figure 6. Eosinophilic keratitis in a 3-year-old domestic
shorthair cat with chronic feline
herpesvirus-1 infection.
Both eyes are similarly affected.
There is a temporal corneal
mass that is pink in colour. The
cornea has been stained with
topical fluorescein dye.
to the
ductules that carry the aqueous tears to the cornea (Glaze & Gelatt
1999). Clinical signs can include conjunctival hyperaemia, dry appearance of
the cornea, corneal epithelial hyperplasia and corneal ulceration (Fig 4).
Diagnosis of feline KCS is based on clinical signs and Schirmer tear test
measurement. Normal Schirmer tear test value for the cat is 17±5.7 mm
wetting/60 s (Veith et al 1970). KCS is defined
as tear production of less than 5 mm wetting/60 s (Glaze & Gelatt
1999). Treatment of feline KCS may include administration of
preservative-free artificial tear ointment or solution as often as possible.
Application of 0.15% Hylashield (I-med Pharma), a viscoelastic substance
containing a hyaluronan derivative manufactured to have an increased contact
time, requires less frequent administration. Oral 0.25% pilocarpine can be
administered with food, but caution must be taken to avoid systemic effects of
parasympathomimetic drug toxicity. Topical cyclosporine A (Optimmune 0.1%,
Schering-Plough) is the treatment of choice for canine KCS, but its efficacy
and safety have not been reported in the cat (Glaze & Gelatt
1999). There is also concern about topical cyclosporine use in a cat with
FHV-1, as it may cause local immunosuppression and recurrence of latent
infection.
Ophthalmia
neonatorium and symblepharon
Normally,
the eyelids of kittens remain closed for the first 10–14 days of life to allow
complete development of ocular tissues. Fetal infection with FHV-1 before the
eyelids are open can result in mucopurulent conjunctivitis causing distension
of the eyelids or, ophthalmia neonatorium. The eyelids are fused with varying
amounts of material between the lids and the cornea. Symblepharon is the
adhesion of the conjunctiva to itself or the cornea and is not uncommon in
young animals with a history compatible with FHV-1 infection. Upper respiratory
tract disease and FHV-1-induced conjunctival epithelial necrosis could
theoretically precede symblepharon (Nasisse 1990), although this
has not been proven. The epithelial necrosis needed to produce symblepharon is
profound, and intuitively it would appear that FHV-1 could produce this
necrosis (Glaze & Gelatt 1999). Generally,
there is no treatment for this condition as removal of adhered tissue induces
more damage and can cause further adhesion. Referral to a specialist is indicated if the owner desires to pursue
treatment.
Corneal
sequestrum
Corneal
sequestrum has also been called corneal mummification or corneal nigrum, and is
a disease that is unique to the cat. It is reportedly more common in
brachycephalic cat breeds (Persian, Himalayan, Burmese) (Glaze
& Gelatt 1999), and can occur following corneal ulceration. The
exact cause and pathogenesis of the disease are not known, but stromal collagen
degeneration and tan to brown pigment deposition are characteristic (Fig 5) (Glaze
& Gelatt 1999). While not a specific cause of corneal sequestrum,
FHV-1 has been associated with corneal sequestrum in the cat (Glaze
& Gelatt 1999). Chronic corneal FHV-1 infection causing stromal
damage may result in sequestrum formation (Nasisse 1990).
Polymerase chain reaction (PCR) tests performed on corneal sequestra have been
positive for FHV-1 in 18% (5/28) (Stiles et al 1997a) to 55.5% (86/156) (Nasisse
et al 1998) of cases depending on the sensitivity of the test.
However, in the brachycephalic breeds of cats, FHV-1 detection in corneal
sequestrum samples was less prevalent than expected (Nasisse et al 1998).
Multiple treatment options exist, including observation, keratectomy,
conjunctival pedicle flap and corneoconjunctival transposition.
Eosinophilic
keratitis
Eosinophilic
keratitis or proliferative keratoconjunctivitis is an infiltrative, progressive
form of corneal disease that occurs in cats. On presentation, a pink to white,
irregular, vascularised mass in the peripheral (lateral or nasal) limbal area
that may invade cornea and conjunctiva affects one or both eyes (Fig 6) (Glaze
& Gelatt 1999). Cytologic examination of a tissue scraping reveals
eosinophils, plasma cells and lymphocytes, and is considered diagnostic (Glaze
& Gelatt 1999). FHV-1 has been isolated from eosinophilic keratitis
specimens isolated by indirect immunofluorescence assay in 33.3% (9/27) of
samples (Morgan et al 1996) from one
laboratory, and in 76.3% (45/59) of cases by PCR from another laboratory (Nasisse
et al 1998). The role of FHV-1 in eosinophilic keratitis has yet
to be elucidated. As treatment of eosinophilic keratitis requires topical or
systemic corticosteroid administration, active or latent FHV-1 infection can be
worsened.
Anterior
uveitis
A
recent report found FHV-1 DNA in the aqueous humor of 12/86 cats (14%) with
clinical signs of anterior uveitis that tested negative for other known causes
of uveitis in cats (toxoplasmosis, feline immunodeficiency virus, feline
leukaemia virus-induced lymphosarcoma
and feline infectious peritonitis) (Maggs et al 1999). It
is not known if the presence of intra-ocular FHV-1 was a cause or the result of
uveitis, but the results suggest that FHV-1 can induce anterior uveitis in some
cats (Maggs et al 1999). Further research is needed to determine the prevalence of FHV-1 as a
causative factor for so-called idiopathic uveitis of cats.
It is
important to perform thorough physical and ophthalmic examinations on all cats
suspected of having FHV-1 infection. Acute FHV-1 infection is usually diagnosed
based on ocular and respiratory clinical signs, but sometimes laboratory
testing is necessary for diagnosis. Conjunctival cytology samples may be
examined in acute, primary FHV-1 infections particularly for the presence of
intranuclear inclusion bodies; however, the inclusions are not identifiable
with Wright-Giemsa stain and therefore may be overlooked (Nasisse
& Weigler 1997). In chronic cases, conjunctival cytology may be
supportive but is rarely diagnostic because the predominant cell type observed
is the neutrophil (Nasisse & Weigler 1997). Characteristic
clinical signs help lead to a diagnosis of FHV-1 keratitis. Staining with rose
Bengal will help identify early dendritic lesions prior to the disruption of
the corneal epithelium. Rose Bengal is a vital dye that stains dead and
degenerating cells, and maybe normal cells at high stain concentrations (Strubbe
& Gelatt 1999).
Application of topical sodium fluorescein stain will identify corneal
epithelial disruption and resultant corneal ulceration. If fluorescent antibody
testing is to be considered, the sample
must be obtained prior to fluorescein staining for ulceration (da
Silva Curiel et al 1991). Laboratory confirmation is often
difficult with chronic keratitis and, in these cases, if clinical suspicion and
response to therapy are not convincing
for
FHV-1, PCR sample submission should be considered. Virus isolation (VI) is
considered the ‘gold standard’ for diagnosis of herpesvirus infections (Nasisse
& Weigler 1997). Virus isolation detects cytopathic effects of FHV-1
replication in feline cell lines (Nasisse & Weigler 1997).
Samples that cannot be run immediately should be stored in the refrigerator
(4°C) to prevent loss of virus titre with freezing and thawing (Nasisse
& Weigler 1997). The
test is sensitive in acute infections, but less sensitive for chronic
infections (Nasisse & Weigler 1997), unless during
a reactivation episode. Serology (ELISA) or serum neutralising (SN) titres are
diagnostic tests performed by many laboratories. The tests are not considered
to be clinically useful because of the high
prevalence of vaccination against feline viral rhinotracheitis (FHV-1)
with resultant systemic antibody titres (Gaskell &
Dawson 1998). In testing chronic infected cats, paired serum
sample titres are not likely to be of benefit because the titres tend to
plateau with chronic infections (Nasisse & Weigler 1997).
Fluorescent antibody (FA) testing can be performed on corneal or conjunctival
smears. Both direct and indirect assays are available, but most laboratories
run an indirect testing method because antibody conjugation is not required (Nasisse
& Weigler 1997). Fluorescent antibody testing for FHV-1 lacks
sensitivity because of the required subjective judgement of laboratory personnel. Also, particularly in
chronic infections, virus may already be bound to host antibody (Nasisse
& Weigler 1997), and result in a false negative test. A recent
report found that FA testing was more often positive with acute respiratory
tract disease than in normal cats or cats with chronic ocular disease (Maggs
et al 1999). If samples are to be collected for FA testing, it
is recommended to do so prior to staining the eye with topical sodium
fluorescein, as the dye may create false positive results during FA testing (da
Silva Curiel et al 1991). PCR tests allow amplification and
identification of extremely small amounts of material of interest. The test is
highly sensitive and specific, and has revolutionised diagnostic testing for
many infectious organisms including FHV- 1. False positive results can occur
with PCR. Nested PCR, which utilises a second
primer pair internal to the initial primer, is particularly susceptible
to contamination (Stiles et al 1997b). PCR has been
shown to be useful in diagnosing cats with FHV-1 conjunctivitis, which has been a difficult subset of cats to
diagnose (Nasisse et al 1998). Currently in
the USA, FHV-1 PCR testing is available through Antech Diagnostics (Irvine, CA)
and the Colorado State University Veterinary Diagnostic Laboratory (Ft.
Collins, CO). A positive PCR demonstrates that the animal was infected at some
time point but does not prove that an active viral infection is occurring at
the time of sample collection (Lutz et al 1999). FHV-1 DNA has
been detected in numerous ocular tissues using PCR technology. The exact
relationship between the DNA and presence or absence of ocular disease is still
open to debate. Similarly, the role of ocular disease in the reactivation
scheme is poorly understood. Recent reports have compared the usefulness of
various available diagnostic tests for FHV-1. One report compared VI, FA, SN
and ELISA in normal cats, cats with upper respiratory tract signs, and cats
with chronic ocular signs (Maggs et al 1999). A high
seroprevalence was found with ELISA in all populations. FA and VI commonly
detected FHV-1 in normal cats, as well as in cats with clinical signs of FHV-1
infection, and the authors concluded that if both tests were run in conjunction
and found to be negative, FHV-1 could be excluded as a cause of disease (Maggs
et al 1999). Nested PCR testing has identified FHV-1 infection
in 54% of conjunctivitis cases, 12% of normal conjunctival samples, 18% of
corneal sequestra and 46% of normal corneas (Stiles et al 1997a). Nasisse
et al (1998) reported positive single PCR test results of FHV-1
detection in 76.3% of eosinophilic keratitis samples, 55.1% of corneal
sequestra and 5.9% of normal corneal tissue. Nested PCR tests were reported to
be more sensitive than VI or FA testing in cats with conjunctivitis or with
upper respiratory tract disease and conjunctivitis (Stiles et al 1997b).
Primary
FHV-1 infections are typically confined to the conjunctiva and are generally
self-limiting. Supportive care of the upper respiratory signs, including
management of anorexia and dehydration, is important. Non-specific treatment of
FHV-1-induced conjunctivitis is directed towards prevention of secondary
bacterial conjunctival infection. The most common bacterial isolates are Chlamydia
and Mycoplasma. Topical oxytetracycline or chloramphenicol is used
four times daily for its effectiveness against Chlamydia and Mycoplasma.
Antiviral medications are usually reserved for FHV-1 keratitis. Response to
treatment is variable at best. Epithelial keratitis has a much better prognosis
than chronic stromal keratitis, in which the response to antiviral drugs is
often poor (Glaze & Gelatt 1999). The mechanism
of action of topical antiviral medications is static not cidal; therefore,
frequent administration is recommended. This is often difficult for cat owners
to accomplish as many of the medications are topically irritating to cats. The
in vitro efficacy of topical antivirals against FHV-1 is
trifluridine>idoxuridine>
vidarabine>bromovinyldeoxyuridine>acyclovir (Nasisse et al
1989b). Trifluridine or trifluorothymidine (Viroptic, GlaxoWellcome) is
typically administered four to nine times daily for 2 days, and then the
frequency is gradually reduced over the next 14–21 days. It may cause mild
transient irritation of the conjunctiva and cornea. Cats that are irritated by
trifluridine administration may benefit from use of a different topical
antiviral medication. Resistance to
trifluridine may also occur and substitution with idoxuridine or vidarabine
(adenine arabinoside) is recommended in those cases. Systemic administration of
antiviral drugs has been investigated in the cat. Acyclovir is an effective
drug for human herpesvirus, but cannot reach effective plasma concentration in
cats, and is therefore not recommended (Nasisse 1989b, Weiss
1989). Valacyclovir is another purine nucleoside that is considered more bioavailable
and is converted to acyclovir after oral dosing but was found to be extremely
toxic to cats and is not recommended (Nasisse et al 1997b).Oral
supplementation with the amino acid L-lysine has been shown to decrease the
viral shedding rate in FHV-1 positive cats (Maggs &
Nasisse 1997). L-lysine may be a competitive inhibitor of arginine
as well as an arginase inducer, and FHV-1 growth in vitro has been shown to be
markedly inhibited with L-lysine supplementation (Collins et al 1995).
Current recommendation is to administer 250 mg of L-lysine orally once daily.
Low dose oral interferon _-2a (Roferon-A, Roche Pharmaceuticals) was shown to
have a dose-dependent beneficial effect on severity of clinical signs with
acute FHV-1 infection in experimental cats, especially if administered before
infection occurred (Nasisse et al 1996). However,
pre-exposure administration is unlikely to happen in clinical practice. Due to
the local immune suppression and retardation of corneal epithelialisation that
occur with topical corticosteroid use, corticosteroid administration should not
be considered with most forms of FHV-1 infections (Nasisse 1990).
Corticosteroid use may also encourage reactivation of latent infection and
hasten ocular disease sequelae. Rarely, topical steroids are used with chronic
stromal keratitis in an attempt to decrease the FHV-1 antigenic immune response
and conceivably decrease corneal scar size (Nasisse 1990).
This must be done very selectively and with great caution.
Infection
with FHV-1 is common in domestic cats despite vaccination. There are many acute
and chronic ocular manifestations of FHV-1 infection. Conjunctivitis and
keratitis are the two ocular disease forms most commonly encountered in feline
practice. Conjunctivitis is usually selflimiting, although chronic infections
can occur and are challenging to diagnose and treat. Keratitis can be vision
threatening, and aggressive management to limit sequelae is indicated. Virus
isolation, fluorescent antibody testing, serum neutralising titers, ELISA and
PCR each has a place in the diagnosis of FHV-1 infection.
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