- Feline Herpesvirus infection
- Click here to download the Feline Herpesvirus file
- Passive immunity acquired via colostrum
- Active immune response
- Clinical signs
- Methods for detecting FHV
- Disease management
- Supportive treatment (Tab. 2)
- Antiviral therapy
- General recommendations on vaccine type and vaccination protocol
- Primary vaccination course
- Disease control in specific situations
- Multi-cat households
- Breeding catteries
- Vaccination of immunocompromised cats
- FIV positive cats
- FeLV-positive cats
- Chronic disease
- Cats receiving corticosteroids or other immunosuppressive drugs
- Further reading:
Feline Herpesvirus infection
The feline herpesvirus infection guidelines were first published in J Feline Med Surg 2009; 11: 547-555 and updated in J Feline Med Surg 2013; 15: 531-533 and in J Feline Med Surg 2015; 17: 570-582; the present update of the vaccination chapter has been authorized by Etienne Thiry.
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 (Fig. 1). In the feline host, FHV replicates in epithelial cells of both the conjunctiva and the upper respiratory tract, and in neurons. Intranuclear inclusion bodies can be seen by light microscopy (Fig. 2). 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).
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, 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 latency.
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 (Fig. 3) 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 herpesviral 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 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).
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|
|Atypical acute disease||Dermatitis|
|Nasal and facial ulcerated and crust forming lesions.
Severe systemic signs, coughing, death (acute death in kittens, "fading kitten syndrome")
|Chronic disease (immune-mediated disease)||Stromal keratitis |
|Corneal oedema, vascularisation, blindness
Chronic sneezing and nasal discharge
|Possibly FHV-related diseases||Corneal sequestra Eosinophilic keratitis Neurological disease Uveitis|
[Note: Exclusion of concurrent infection with other agents is required to determine the FHV aetiology of chronic rhinitis]
FHV infection typically causes acute upper respiratory and ocular disease (Tab. 1), 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 (Fig. 4) 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 (Fig. 6). Occasionally, primary pneumonia (Fig. 7) and a viraemic state are seen, with severe generalized signs and a fatal outcome (Gaskell et al., 2006).
Less frequently, oral ulceration, dermatitis and skin ulcers (Fig. 8) are observed (Hargis and Ginn, 1999), and also neurological signs (Gaskell et al., 2006). 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
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; Nasisse and Weigler, 1997; Stiles et al., 1997a, b; 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 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.
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 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, 2005).
Supportive treatment (Tab. 2)
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 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 (Tab.3). 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|
|nasal flushing with physiological saline solution and nebulization||to clean nasal discharge and to prevent dehydration of the upper airways||recommended several times daily||4|
|highly palatable food||to ensure sufficient food intake||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||4|
|placement of a feeding tube and enteral nutrition||to ensure sufficient food intake||necessary if the cat has not been eating for three days||4|
|Fluid therapy||to control dehydration and restore electrolyte and acid base imbalance||necessary in cats with severe clinical signs||4|
|Antibiotics||to control secondary bacterial infections||broad-spectrum antibiotics with good penetration in the respiratory tract are recommended for cats with severe disease||4|
|Non-steroidal anti- inflammatory drugs||to decrease fever||recommended if cat is severely depressed||4|
|Drugs with mucolytic effects (e.g., bromhexine)||to improve mucous nasal discharge||may be helpful||4|
Table 3. Symptomatic treatment for acute ocular disease (conjunctivitis and keratitis)
|Drug||Comment||ABCD Recommendation||EBM Level|
|Antibiotics||to control secondary bacterial infections||Topical antibiotics||4|
|Anti-inflammatory drugs||To decrease local inflammation||Usually not needed; to avoid corticosteroids||4|
Table 4a: Antiviral drugs topical
|Drug||Type of drug||Route of administration||Efficacy in vitro||Efficacy in vivo||Controlled in-vivo study ?||Comments||EBM level|
every hour for 1st day and every 4 hours thereafter (Maggs, 2001)
|Excellent||n.d.||no||Topical treatment of choice in ocular FHV manifestations. Some cats averse to topical application. Toxic if given systemically (Maggs, 2001)||3|
|Cidofovir||Nucleoside analogue||0.5% solution applied topically||yes||yes||yes||Topical treatment for ocular FHV; potent drug with only two daily applications (Fontenelle et al., 2008; Maggs, 2010)||3|
use initially ever 2-4 hours (Maggs, 2001)
|excellent||n.d.||no||Topical treatment for ocular FHV. Difficult to source, pharmacists can formulate a 0.1% ophthalmic solution. Toxic if given systemically.||3|
|Ganciclovir||Nucleoside analogue||Topical||excellent||n.d.||n.d.||Topical treatment for ocular FHV. Good in vitro activity (Maggs and Clarke, 2004; van der Meulen et al., 2006)||3|
|Aciclovir||Nucleoside analogue||Topical and oral||Poor|
(high doses may be needed to overcome viral resistance)
|some||yes||Least in vitro effect of all herpes antivirals (Williams et al., 2004; van der Meulen et al, 2006), moderate in vivo effect (Williams et al., 2005). Synergy in combination with human IFN-α (Weiss, 1989). Toxic systemically (Maggs, 2001; Maggs, 2010)||3|
Table 4b. Antiviral drugs systemic
|Drug||Type||Route of administration||Efficacy in vitro||Efficacy in vivo||Controlled in-vivo study?||Comments||EBM level|
|Famciclovir||Nucleoside analogue (prodrug)||Oral, 90 mg/kg tid for 21 days||yes (for penciclovir, as famciclovir is a prodrug of penciclovir)||yes||yes||Tested in conventional and SPF cats experimental challenge, against primary infection (Malik et al., 2009; Thomasy et al., 2011)||3|
|Feline IFN-ω||Interferon||Systemic: 1 MU/kg SC sid or eod|
Oral: 50k – 100k Units daily
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).
|yes||n.d.||yes||Safe and licensed for use in cats. A combined topical and oral pre-treatment before experimental FHV infection was not beneficial (Haid et al., 2007) Used along with L-lysine in chronic infections.||4|
|Human IFN-α||Interferon||SC high dose|
PO low dose
5-35 Units daily
|Less bioactive than feline interferon. 5-35 Units daily reduces clinical signs but not FHV shedding. Used along with l-lysine in chronic infections.||3|
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 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. 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 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 et al., 2004). Vaccinated cats usually develop an anamnestic response upon field infection.
Primary vaccination course
Kittens: 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 9 weeks of age, although some products are licensed for earlier use. Kittens should receive a second vaccination 2 to 4 weeks later, with the second given around 12 weeks of age. This protocol has been developed to ensure optimal protection. For longer intervals, no information is available. After the kitten primary vaccination course all cats receive an additional vaccine dose at 10 to 16 months of age; this will ensure adequate vaccine induced immunity for cats that may not have adequately responded to the primary course.
Adult cats: 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 2 to 4 weeks are recommended, irrespective of the vaccine type, and a boost one year later.
ABCD recommends that further revaccinations 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 may suffice. An informed decision should be taken on the basis of a risk-benefit analysis, but annual revaccinations 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 may not be true. While most cats in the field either have antibody against FCV and FPV, or show an anamnestic response after the revaccination, only around 30% have titres against FHV, and around 20% fail to react to revaccinations (Lappin et al., 2002; Mouzin et al., 2004). In experimental vaccine efficacy studies, protection clearly decreases with time.
If revaccinations have lapsed, a single injection is adequate if the interval since the last vaccination is not more than three years; if it is more than three years, two injections three weeks apart should be applied.
Boosters using FHV vaccines produced by different manufacturers 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 still generally recommended.
Disease control in specific situations
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.
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.
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 discouraged, as in any systemically ill cat.
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.
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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