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«ABCD GUIDELINES ON: 2. FELINE HERPESVIRUS-1 2.1 Biology of the virus 2.1.1 Virus properties 2.1.2 Epidemiology 2.2 Pathogenesis 2.3 Immunity 2.3.1 ...»

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ABCD GUIDELINES ON:

2. FELINE HERPESVIRUS-1

2.1 Biology of the virus

2.1.1 Virus properties

2.1.2 Epidemiology

2.2 Pathogenesis

2.3 Immunity

2.3.1 Passive immunity acquired via colostrum

2.3.2 Active immune response against FHV-1

2.4 Clinical signs

2.5 Diagnosis of feline herpesvirus infection

2.5.1 Methods detecting FHV-1

2.5.2 Detection of infection by serology

2.6 Feline herpesvirus disease management

2.6.1 Supportive Treatment

2.6.2 Antiviral therapy

2.7 General recommendations on vaccine type and vaccination protocol

2.7.1 Primary vaccination course

2.7.2 Booster vaccinations

2.8 Feline herpesvirus disease control in specific situations

2.8.1 Shelters

2.8.2 Breeding catteries

2.8.3 Vaccination of immunocompromised cats

2.9 References

–  –  –

The European Advisory Board on Cat Diseases is an independent panel of 17 veterinarians from ten European countries, with an expertise in immunology, vaccinology and/or feline medicine.

The ABCD was set up to compile guidelines for the prevention and management of major feline infectious disease in Europe based on current scientific knowledge and available vaccines.

Animal healthcare company Merial helped set up the European ABCD and financially supports its activities. This work would not have been possible without the financial support of Merial.

© July 2006 by the European Advisory Board on Cat Diseases. All rights reserved.

–  –  –

2.1.1 Virus properties Feline herpesvirus 1 (FHV-1) is the agent of feline viral rhinotracheitis and is distributed worldwide. The virus belongs to the family Herpesviridae, subfamily Alphaherpesvirinae, genus Varicellovirus. Although only one serotype is described, the virulence can differ between viral strains (Gaskell et al. 2007). Some differences can also be observed by restriction endonuclease analysis of viral DNA (Hamano et al. 2005; Thiry 2006).

FHV-1 is a typical herpesvirus: the genomic double-stranded DNA is packaged into an icosahedral capsid surrounded by a proteinaceous tegument and a phospholipid envelope. At least ten different glycoproteins are present on the envelope. FHV-1 grows in both epithelial cells of the conjunctiva and the upper respiratory tract, and in neurones. The neuronal infection enables the virus to establish lifelong latency after primary infection. FHV-1 is related antigenically to canine herpesvirus and phocid herpesviruses 1 and 2, although 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 commercially available disinfectants, antiseptics and detergents. At low temperatures, the virus has shown to remain infective for five months (154 days at 4°C), although its survival is shorter at higher temperatures (33 days at 25°C, 4-5 minutes at 56°C) (Pedersen, 1987).

2.1.2 Epidemiology The domestic cat is the main host of FHV-1 but the virus 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 for FHV-1 acute infection and intermittent reactivation gives rise to viral shedding in oronasal and conjunctival secretions. Apart from in catteries, contamination of the environment is not a primary source for transmission. Virus shedding from acutely infected cats and from latently infected cats experiencing reactivation are the two main sources of infection (Gaskell and Povey, 1982).

Transplacental infection has not been demonstrated in the field. Latently infected queens may transmit FHV-1 to their offspring because parturition and lactation are typical stress-inducing factors leading to viral reactivation and shedding. Kittens may therefore acquire FHV-1 infection at a very early age before vaccination. The outcome depends on the level of maternally derived antibodies (MDA). When high levels are present, kittens are protected against disease and develop subclinical infection leading to latency whereas in the absence of sufficient MDA, clinical disease may follow (Gaskell and Povey, 1992).

In healthy small populations, the prevalence of viral shedding may be less than 1% whereas in large populations, especially with clinical disease present, prevalence may be up to 10 20% (Coutts et al., 1994; Binns et al., 2000; Helps et al., 2005). In shelters, risk of contagion is higher: with only 4% of shedding cats entering the shelter, 50% of cats present may excrete the virus one week later (Pedersen et al., 2004). This low prevalence is likely to reflect the intermittent nature of viral shedding during latency.

ABCD guidelines on Feline Herpes Virus-1 3/17

2.2 Pathogenesis The virus enters via the nasal, oral or conjunctival routes. It causes a lytic infection of the nasal epithelium with spread to the conjunctival sac, pharynx, trachea, bronchi and bronchioles. Lesions are characterised by multifocal necrosis of epithelium, with neutrophilic infiltration and inflammation. A transient viraemia associated with blood mononuclear cells can be observed rarely after natural infection. This may be observed exceptionally in neonates or hypothermic individuals as viral replication is usually restricted to lower temperature tissues (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.

During 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 virus replication. Reactivation of virus shedding can be induced experimentally by glucocorticoid treatment in approximately 70% of cats. Other stressors that may cause reactivation include lactation (40 %), and the cat moving into a new environment (18%) (Gaskell and Povey, 1977; Ellis, 1981; Gaskell and Povey, 1982; Pedersen et al., 2004).

Some adult cats may show acute lesions at the time of viral reactivation. Disease at 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 the stroma. In some cases damage to the nasal turbinates in acute disease is thought to predispose some cats to developing chronic rhinitis (Gaskell et al., 2007)

2.3 Immunity

2.3.1 Passive immunity acquired via colostrum Kittens are protected against disease by maternally derived antibodies (MDA) during the first weeks of their lives but in general levels of MDA for FHV infection are low. It has been demonstrated that MDA may persist for 2-10 weeks (Johnson & Povey, 1985) although in a more recent study levels of MDA were shown to be low, with approximately 25% of kittens appearing negative for MDA as early as 6 weeks of age (Dawson et al., 2001).

2.3.2 Active immune response against FHV-1 Glycoproteins embedded in the membrane of the herpesviruses are important in the induction of immunity; following infection the detection of virus neutralizing antibodies (VNA) correlates with the recognition of FHV glycoproteins (Burgener and Maes, 1988).

Furthermore, immunisation of rabbits with FHV-gD led to the production of high titres of VNAs, indicating a role of these proteins in the induction of VNA (Spatz et al., 1994).

Solid immunity is not induced after natural infection; in general the immune response protects against disease but not against infection and mild clinical signs have been observed following reinfection, only 150 days after primary infection (Gaskell and Povey, 1979). The titres of VNA induced by natural infection are often low and rise slowly. Indeed, VNA may still be absent 40 days post infection (Gaskell and Povey, 1979). VNA most likely contribute to the ABCD guidelines on Feline Herpes Virus-1 4/17 protection against acute infection. Other antibody-mediated mechanisms e.g. antibody mediated cellular cytotoxicity (ADCC) and antibody-induced complement lysis have been demonstrated (Wardley, 1976). However, (as with other alpha-herpesviruses) cell-mediated cellular immunity plays an important role in protection, since the absence of detectable serum antibody levels in vaccinated cats does not necessarily indicate that cats are susceptible to disease (Lappin et al., 2002). On the other hand, seroconversion did correlate with protection against virulent FHV challenge (Lappin et al., 2002). It is important to take into consideration that presence of antibodies against any infectious agent may provide an indirect indication of cellular immune responses, since T-lymphocytes are required for maintenance of Blymphocyte function.

Although a general correlation between presence of antibodies to FHV-1 and protection against clinical signs has been demonstrated for FHV-1 infection, there is currently no reliable 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. Several studies with intranasal vaccines have shown clinical benefits as early as 2days after vaccination (Lappin et al., 2006; Weigler et al., 1997, Slater & York, 1976).

–  –  –

ABCD guidelines on Feline Herpes Virus-1 5/17 Typical clinical signs are pyrexia, depression and anorexia, serous or serosanguineous ocular and/or nasal discharge, conjunctival hyperaemia, sneezing and, less frequently, salivation and coughing (Gaskell et al., 2006). Secondary bacterial infection is common in which case secretions tend to become purulent. In certain susceptible kittens, the disease may be more severe and FHV-1 infection has been associated with primary pneumonia and a viraemic state that can produce severe generalized signs and eventually death (Gaskell et al., 2006).

Less frequent clinical signs associated with FHV-1 are oral ulceration or dermatitis and skin ulcers (Hargis et al, 1999) and neurological signs (Gaskell et al., 2006). Abortion may occur as a rare secondary clinical sign, although, in contrast to other herpesviruses, it is not a direct consequence of viral replication.

After reactivation and recrudescent disease, some cats may show acute cytolytic disease as described above. Others may show chronic ocular immune-mediated disease in response to the presence of FHV-1 virus. Strong experimental evidence suggests that stromal keratitis, associated with corneal oedema, inflammatory cell infiltrates and vascularisation and eventually blindness, is an example of this disease mechanism (Nasisse et al., 1989; Maggs, 2005).

Corneal sequestra and eosinophilic keratitis in cats have been linked to the presence of FHV-1 in the cornea and/or blood in some of the affected cats. However, a definite causal association cannot be made since some affected cats are negative to FHV-1 (Cullen et al., 2005, Nasisse et al., 1998). FHV-1 DNA has been also detected in aqueous humor of a larger proportion of cats suffering from uveitis compared to healthy cats, suggesting that FHV-1 may cause uveal inflammation (Maggs et al., 1999).

Chronic rhinosinusitis, a frequent cause of chronic sneezing and nasal discharge in cats, has been associated with FHV-1 infection. Viral DNA can be detected in some affected cats, but is also found in controls without clinical signs (Henderson et al., 2004). Recent investigations show that the virus is not actively replicating in such cats, suggesting that chronic rhinosinusitis might be initiated by FHV-1 infection, but perpetuated by immune-mediated mechanisms producing inflammatory and remodelling phenomena, leading to permanent destruction of nasal turbinates and bone complicated by secondary bacterial infection (Johnson et al., 2005).

Very often, FHV-1 infection occurs combined with feline calicivirus and/or Chlamydophila felis, Bordetella bronchiseptica, Mycoplasma spp. and other micro-organisms, including Staphylococcus spp., Escherichia coli, may lead to secondary infection of the respiratory tract, causing a multi-agent respiratory syndrome (Gaskell et al., 2006).

2.5 Diagnosis of feline herpesvirus infection

2.5.1 Methods detecting FHV-1 PCR is now the preferred method to detect FHV-1 in biological samples. Viral isolation lost interest but is a valid method still used in several laboratories. The sensitivity and the specificity of the tests, and especially PCR, are good but may differ depending on the laboratory because there is no harmonisation. These tests, and immunofluorescence are described in this chapter.

2.5.1.1 Detection of nucleic acid PCR is currently used to detect FHV-1 DNA in conjunctival, corneal or oropharyngeal swabs, corneal scrapings, aqueous humor, corneal sequestra, blood or biopsies. Conventional PCR, ABCD guidelines on Feline Herpes Virus-1 6/17 nested-PCR and real-time PCR are used routinely to detect FHV-1 DNA in diagnostic laboratories (Hara et al., 1996; Helps et al., 2003; Marsilio et al, 2004; Maggs et al., 1999a;

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

Molecular diagnostic methods appear to be more sensitive than virus isolation or indirect immunofluorescence (Burgesser et al., 1999; Reubel et al., 1993; Stiles et al., 1997; Weigler et al., 1997).



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