Feline calicivirus infection

edited December, 2017


The Feline Calicivirus infection guidelines were first published in the J Feline Med Surg 2009; 11: 538-546 and updated in J Feline Med Surg 2015; 17:570-582; the present update of the Vaccination chapter has been authorised by Alan Radford.


Watch a video interview with Prof Alan Radford, Liverpool





Click here to download the Feline Calicivirus file





Feline calicivirus (FCV) is a highly contagious pathogen with a widespread distribution in the feline population. It belongs to the Caliciviridae family, genus Vesivirus; caliciviruses include important pathogens of man (such as the Norwalk virus, one of the commonest causes of infectious gastroenteritis in people) and animals, including the European brown hare syndrome virus and rabbit haemorrhagic disease virus (Green at al., 2000).
Calicivirus particles are hexagonal or star-shaped and show cup-shaped depressions in electron microscopic preparations; the name is derived from Greek calyx meaning cup or goblet (Fig. 1).


03 CALICI false color

Fig. 1. False colour electron micrograph of calicivirus particles (virions)

The virus has a small single-stranded RNA genome of positive (messenger) polarity, which allows it to evolve quickly. It is enclosed by multiple copies of the major capsid protein, the most variable, probably immunodominant protein domain (principally targeted by the host's immune response; Tohya et al., 1997; Radford et al., 1999; Geissler et al., 2002). Despite this variability, there is sufficient antigenic overlap between isolates to allow classification of the viruses as a single serotype (Povey, 1974; Povey and Ingersoll, 1975). However, antigenic differences exist between FCV isolates (Table 1), which creates considerable difficulties when trying to maximise vaccine cross protection. Genetically, most FCVs belong to a single diverse genotype (Glenn et al., 1999, Geissler et al., 1997); a second genotype has recently been described in Japan (Ohe et al., 2006).


Fig. 2. At high magnification, the eponymic goblets (calices) are visible on the virion surface. © Marian C. Horzinek

Fig. 2. At high magnification, the eponymic goblets (calices) are visible on the virion surface. © Marian C. Horzinek





Table 1. Results of cross neutralisation tests between calicivirus strains (vertical) and corresponding hyperimmune goat antisera (horizontal). Symbols: + = neutralisation in both directions; ½ - unilateral neutralisation; -= no neutralisation; Kalunda et al., 1975.






There are no known reservoirs or alternative hosts for FCV, and humans are not susceptible to infection. Apart from the existence of a proper canine calicivirus, FCV-like viruses have been isolated from dogs (Hashimoto et al., 1999; Roerink et al., 1999; Martella et al., 2002; di Martino et al., 2009). Their role in the epidemiology in both carnivores is uncertain (Binns et al., 2000; Helps et al., 2005), but probably not important.
The virus is shed predominantly with oral and nasal secretions in acute disease. On recovery, many cats continue shedding, most of them for at least 30 days post-infection, a few for several years (Wardley, 1976). A small proportion of cats may be resistant to infection (Coyne et al., 2006a), probably dependent on host and virus strain factors.


Feline calicivirus infection is widespread in the general cat population. The prevalence is broadly proportional to the number of cats in a household, and is highest when large groups are housed together. It is low in household cats kept in small groups (~10%; Wardley et al., 1974), but in colonies or shelters, figures between 25% and 40% have been reported (Wardley et al., 1974; Coutts et al., 1994; Bannasch and Foley, 2005; Helps et al., 2005). The prevalence within individual colonies is variable, ranging from low (Radford et al., 2001; Coyne et al., 2006a) to high (50-90%) values (Radford et al., 2003; Coyne et al., 2006a).


Infection generally occurs through direct contact with secretions from acutely infected and carrier cats (Wardley, 1977). However, the virus survives in the environment and remains infectious for up to one month on dry surfaces at room temperature, and even longer under colder conditions (Doultree et al., 1999; Duizer et al., 2004; Clay et al., 2006). Indirect transmission can therefore occur, especially within the close confines of a cattery, where secretions may contaminate cages, feeding and cleaning tools or personnel. The virus can also remain infectious in flea faeces for up to 8 days, and kittens may be experimentally infected with FCV by contact with infected fleas or their faeces (Mencke et al., 2009).





Cats can be infected with FCV via the nasal, oral or conjunctival route. The oropharynx is the primary site of replication. Transient viraemia occurs 3 to 4 days after infection, at which time the virus is detected in many other tissues. The virus induces necrosis of epithelial cells: vesicles, typically on the margin of the tongue, develop into ulcers; in the affected regions, the dermis is infiltrated with neutrophils. Healing takes place over a period of two to three weeks (Gaskell et al., 2006).
FCV may less commonly affect other tissues, leading to pneumonia (focal alveolitis, progressing to areas of acute exudative pneumonia and then to proliferative, interstitial pneumonia) and lameness (Fig. 3.) Acute synovitis with thickening of the synovial membrane and increased synovial fluid have been noted (Dawson et al., 1994). The pathogenesis of the limping syndrome is not clear; immune complexes are thought to play a role (Bennett et al., 1989). Virus may also be isolated from affected joints (Dawson et al., 1994).


Fig. 3. Calicivirus infection limping syndrome ©Uwe Truyen

Fig. 3. Calicivirus infection limping syndrome ©Uwe Truyen



The pathogenesis of virulent systemic disease caused by FCV (VS-FCV) differs considerably from the typical picture described above. These strains cause widespread vasculitis, multi-organ involvement and death in up to two thirds of the infected cats (Pedersen et al., 2000; Hurley and Sykes, 2003; Schorr-Evans et al., 2003; Coyne et al., 2006b). The pathogenesis of VS-FCV infection is unknown and may include viral evolution and/or immune-mediated components as well as environmental and management factors (Hurley, 2006). Recently, these virulent strains have been shown to grow more rapidly in cell culture (Ossiboff et al., 2007).
Following recovery from acute disease, most cats do not clear the infection for around 30 days; a minority sheds virus for much longer, possibly for life. In these healthy FCV carriers, virus can be localised in the epithelium of the tonsils. However, tonsillectomy does not eliminate the carrier state, suggesting the virus is also located in other sites. It is believed that evolution of the variable capsid protein allows FCV to escape the host immune response and to persist in carrier cats (Johnson, 1992; Kreutz et al., 1998; Radford et al., 1998; Coyne et al., 2007).







Passive immunity acquired via colostrum


Maternally derived antibodies (MDA) are important for protection during the first weeks of life and may interfere with vaccination. There are only few data on the extent and longevity for FCV MDA in cats. In general, their levels are higher and persist for longer than for feline herpesvirus (FHV-1). In an experimental study, the average half-life of MDA was determined to be 15 days and their persistence as 10-14 weeks (Johnson & Povey, 1983). However, in a field study, 20% of kittens at only six weeks of age had no detectable antibodies against a widely used vaccine strain (Dawson et al., 2001).



Active immune response


Virus neutralising antibodies (VNA) appear by approximately seven days post infection (Kahn et al., 1975). In general, antibody titres are higher than for FHV infection and their levels correlate well with protection against homologous challenge (Povey and Ingersoll, 1975). There is a considerable degree of antigenic variability amongst FCV strains, but it was concluded from studies of in vitro cross-reactivity that FCVs belong to a single serotype (Povey, 1974). Prior infection with one strain can significantly reduce the acute clinical signs upon exposure to a heterologous strain, and in some cases oral shedding may be reduced (Povey and Ingersoll, 1975; Knowles et al., 1991). In general, the level of heterologous protection will depend on the virus strains involved. Cats may be protected also in the absence of detectable VNA (Knowles et al., 1991; Poulet et al., 2005), suggesting a role for other immune mechanisms: indeed, cellular responses have been demonstrated in vaccinated cats (Tham and Studdert, 1987). Also, FCV-specific IgG and IgA antibodies have been demonstrated in the saliva during the course of infection (Knowles et al., 1991), although their significance in protection is unknown.



Clinical signs


FCV infection can cause acute oral and upper respiratory signs but also has been associated with chronic stomatitis, which may be immune-mediated. Recently, a new syndrome, the “virulent systemic feline calicivirus (VS-FCV) disease” has been described.



03 FCV Schnuckel 09.07.03 ©Susann-Yvonne Mihaljevic

Fig. 4. Mild epithelial defects after burst calicivirus aphthae ©Susann-Yvonne Mihaljevic




Acute oral and upper respiratory tract disease


Clinical findings may differ, depending on the virulence of the FCV strain concerned, on the age of the affected cats and on husbandry factors. While in some cases infection is subclinical, in many others, there is a typical syndrome of lingual ulceration (Fig. 4, 5.) and a relatively mild acute respiratory disease. More severe signs can resemble the respiratory disease caused by FHV-1.



04- 03- FCV calici tongue map lesions ©Marian C. Horzinek

Fig. 5. Characteristic tongue map-shaped lesions due to FCV infection ©Marian C. Horzinek



Acute oral and upper respiratory disease signs are mainly seen in kittens. The incubation period is 2 to 10 days (Hurley and Sykes, 2003). Oral ulcerations, sneezing and serous nasal discharge are the main signs (Gaskell et al., 2006). Fever is also observed. Anorexia, sometimes accompanied by hypersalivation due to oral erosions - located mainly on the tongue - are usually much more prominent than the signs of rhinitis (Fig. 6.). They usually resolve after several days. In some severe cases, pneumonia, manifested by dyspnoea, coughing, fever and depression can occur, particularly in young kittens.



03 FCV salivation

Fig. 6. Hypersalivation due to oral ulcers after FCV infection.

Chronic stomatitis

FCV can be isolated from nearly all cats with the chronic lymphoplasmacytic gingivitis/stomatitis complex, and many cats test positive by PCR (Dowers et al., 2010, Belgard et al., 2010). It has been suggested to be an immune-mediated reaction to FCV (and potentially other) oral antigens and is characterised by a severe proliferative/ulcerative faucitis. However, the disease has not been reproduced experimentally (Knowles et al., 1991), and the exact role of FCV remains unclear. Although FIV and Bartonella have also been proposed to be involved, the evidence is limited (Glaus et al., 1997; Dowers et al., 2010; Belgard et al., 2010); the consensus is they are not associated with disease in most cats.



Limping syndrome


An acute transient lameness (Fig. 3.) with fever can be associated with FCV infection (Pedersen et al., 1983; Ter Wee et al., 1997) and vaccination. In natural infection, it occurs a few days or weeks after the acute oral or respiratory signs (Pedersen et al., 1983; Bennett et al., 1989).



Virulent systemic feline calicivirus (VS-FCV) infection


Outbreaks of highly virulent and often lethal FCV infection in domestic cats have been described in the United States and in Europe (Pedersen et al., 2000; Coyne et al., 2006b; Reynolds et al., 2009). A single outbreak has also been described in exotic captive felids in the USA (Harrison et al., 2007). The disease has been named “hemorrhagic-like fever” (Pedersen et al., 2000) and “highly virulent feline calicivirus disease” (Schorr-Evans et al., 2003). The causative virus strains are most commonly referred to as “virulent systemic feline calicivirus” (VS-FCV); however, this term is somewhat misleading as all FCV infections are systemic - but the disease caused by other FCV strains is usually local.


The incubation period in natural cases of VS-FCV infection in cats exposed in hospitals is usually 1-5 days; in the home environment it may extent up to 12 days (Hurley and Sykes, 2003). The disease appears to be more severe in adults than kittens. Vaccination did not protect cats against field infections (Hurley and Sykes, 2003), although experimentally, some protection has been shown (Pedersen et al., 2000; Brunet et al., 2005). It is unknown whether this is due to inherent characteristics of hypervirulent strains or simply that vaccine-“susceptible” strains are unlikely to cause outbreaks since vaccination is so widely practiced (Pedersen et al., 2000; Hurley, 2006).


04- 03- FCV calici virulent systemic disease ©Tim Gruffydd-Jones

Fig. 7. VS-FCV virulent systemic disease ©Tim Gruffydd-Jones


In contrast to the common strains, VS-FCV causes systemic disease characterized by severe systemic inflammatory response syndrome, disseminated intravascular coagulation (DIC), multi-organ failure, and commonly death. Mortality is up to 67% (Foley et al., 2006). The clinical signs of this form of disease are variable. The initial findings are frequently typical of a severe acute upper respiratory tract disease. Characteristic signs are cutaneous oedema and ulcerative lesions on the skin and paws (Hurley and Sykes, 2003). Oedema is located mainly on the head and limbs (Fig. 7.). Crusted lesions, ulcers and alopecia can be seen on the nose, lips, and ears, around the eyes (Fig. 8.) and on the footpads (Fig. 9). Some cats are jaundiced (e.g. due to hepatic necrosis, pancreatitis); some may show severe respiratory distress (e.g. due to pulmonary oedema). Thromboembolism and coagulopathy caused by DIC may be observed including petechiae, ecchymoses, epistaxis or bloody faeces (Hurley and Sykes, 2003; Coyne et al., 2006b).


04- 03- FCV calici virulent systemic disease skin lesions ©Tim Gruffydd-Jones

Fig. 8. Crusted lesions and ulcers due to VS-FCV infection ©Tim Gruffydd-Jones













03 FCV virulent systemic disease, paws ©Uwe Truyen

Fig. 9. Viirulent systemic calicivirus disease, excoriations of paws ©Uwe Truyen






















Other clinical pictures

FCV has also been implicated in other diseases like polyps and cystitis; evidence for these associations is lacking (Klose et al., 2010; Larson et al., 2011).








Because of the asymptomatic carrier phase, and the fact that viruses in live vaccines may occasionally be shed post-vaccination (Ruch-Gallie et al., 2011), caution should be taken when interpreting any FCV positive result because of the poor correlation between the presence of virus and clinical signs (Sykes et al., 1998). The diagnosis of VS-FCV relies on clinical signs, high contagiousness and high mortality rate and isolation of the same strain from blood of several diseased cats, assessed by sequencing of hypervariable regions of the capsid gene.



Detection of nucleic acid


Conventional, nested and real-time reverse-transcriptase PCR (RT-PCR) assays have been developed to detect FCV RNA in conjunctival and oral swabs, blood, cutaneous scrapings or lung tissue, depending on the clinical form and the outcome of the disease. Diagnostic sensitivity of RT-PCR may depend on both the primers used and the detected strain, because of the high variability of the viral genome; therefore, molecular assays should be optimised using a large panel of strains to minimize false negative results. Multiplex PCR have also been developed in order to detect at the same time both FHV-1 and FCV (Sykes et al., 2001), but such assays may be less sensitive. As well as having the potential to diagnose FCV infection, RT-PCR provides the means of identifying uniquely the virus strain and has proven useful in molecular epidemiology and outbreak investigations. However, consistent genetic markers associated with virulence, specifically hypervirulent strains are as yet unavailable (Abd-Eldaim et al., 2005; Foley et al., 2006; Ossiboff et al., 2007).



Virus isolation


Virus isolation (VI) is a useful method for detecting FCV infection; it indicates the presence of replicating virus and has the advantage of being less sensitive to the effect of strain variation than RT-PCR. FCV replicates in cell lines of feline origin; its rapid growth in tissue culture may compromise identification of concurrent herpesvirus (Pedersen, 1987). Virus can be isolated from nasal, conjunctival or oro-pharyngeal swabs (Gaskell and Dawson, 1998), but VI may fail due to small numbers of virions in the sample, virus inactivation during transit, or to the presence of antibodies in extracellular fluids that prevent virus replication in vitro. The chance of successful VI can be maximised if swabs from both conjunctiva and oropharynx are collected (Marsilio et al., 2005).





FCV antibodies can be detected by virus neutralization or ELISA (Lappin et al., 2002). The seroprevalence is generally high in cat populations due to natural infection and vaccination. Consequently, the presence of specific antibodies is not useful to diagnose infection (Gaskell and Dawson, 1998; EBM grade I). Levels of VNA can be used to predict whether a cat is protected or not, but must be interpreted properly, as false negative results may be obtained if VNA do not cross-react with the laboratory strains used in the test. In addition, titres may appear higher when homologous rather than heterologous virus-antibody pairs are used. When the strain used is not defined, it makes interpretation of the results difficult (Scott and Geissinger 1997, 1999; Dawson et al., 2001; Gore et al., 2006).



Disease management


Treatment of acute upper respiratory tract disease


Cats severely affected by FCV infection need intensive nursing care and supportive therapy. The resolution of dehydration and restoration of electrolyte and acid-base disturbances preferably by intravenous fluid administration is required in cats with severe clinical signs. Food intake is extremely important. Many cats with FCV infection do not eat mainly because of pyrexia and/or ulcers in the oral cavity, sometimes also because of their loss of smell due to nasal congestion. Non-steroidal anti-inflammatory drugs can be used to decrease fever and oral pain. Food may be blended to cause less pain when eating, should be highly palatable, and may be warmed up to increase the smell. If the cat is not eating for more than three days, placement of a feeding tube and enteral nutrition is indicated. At the clinician’s discretion, antibiotics should be given to cats with severe disease and suspected secondary bacterial infection. Broad-spectrum antibiotics should be chosen. It is crucial to use antibiotics with good penetration in the respiratory tract and/or oral cavity. If there is nasal discharge, this should be cleaned away several times a day with physiological saline solution, and ointment should be applied locally. If there is a mucous nasal discharge, drugs with mucolytic effects (e.g. bromhexine) may be helpful, and nebulisation with saline can be used to combat dehydration of the airways.



Antiviral therapy of acute upper respiratory disease


Most antivirals used in veterinary medicine only inhibit replication of DNA viruses or retroviruses, and treatment of FCV infections has not entered clinical practice. Ribavirin is one of the few antiviral agents able to inhibit FCV replication in vitro. However, it appears to be very toxic to cats and side effects have precluded its systemic use (Povey, 1978; EBM grade III). Feline interferon-ω (licensed for the treatment of canine parvovirus and feline leukaemia virus infections in some European countries) has been shown to inhibit FCV replication in vitro (Fulton and Burge, 1985; Mochizuki et al., 1994; Taira et al., 2005; EBM grade IV). Controlled field studies, however, are not available. There is some suggestion that strains may vary in their sensitivity to interferon (Ohe et al., 2008).



Treatment of VS-FCV infection


In outbreaks of VS-FCV, severely affected cats have been treated with intensive care supportive treatment (e.g. fluid therapy, antibiotics) plus steroids and interferon, and clinical improvement was reported anecdotally. However, controlled clinical studies have not been published; so specific treatment for the disease is not currently known (Hurley, 2006; EBM grade III).



Treatment of chronic stomatitis


A full description of the treatment of chronic stomatitis is beyond the scope of these guidelines. However, several modalities have been used to treat chronic ulceroproliferative stomatitis, although controlled studies are lacking. Recommended options depend on the disease severity and stage and include antibiotics plus rigorous dental cleaning, corticosteroids and/or other immunosuppressant or immunomodulatory drugs (gold salts, clorambucil, thalidomide and cyclosporine; White et al., 1992; Addie et al., 2003; Vercelli et al., 2006; EBM grade IV) and full teeth extractions (Hennet, 1994; EBM grade III).


Anecdotal and clinical case reports have suggested the use of both feline interferon-ω and human interferons to treat cats with chronic stomatitis associated with FCV shedding, by intra-lesional or combined systemic plus intralesional application (Southerden and Gorrel, 2007). Again, controlled studies on using that treatment are currently not available. Topical oral interferon has been shown to lead to statistical improvement, in clinical scores, but this improvement was not different from cats receiving steroid alone (Hennet et al., 2011; EBM grade IV).



General recommendations on vaccine type and vaccination protocol


FCV infection is ubiquitous and may induce severe disease. ABCD therefore recommends that all healthy cats should be vaccinated against FCV. Although vaccination provides good protection against acute oral and upper respiratory tract disease in most cases, it does not prevent cats from becoming infected and from shedding FCV afterwards (Radford et al., 2006). In addition, there is currently no vaccine available that protects equally well against all FCV field strains.


Currently, FCV is combined with FHV-1 in divalent vaccines (only in some countries) or, more commonly, with other antigens. Both modified live and inactivated parenteral vaccines are available. Modified live intranasal vaccines are no longer available in Europe, but still current in the USA.


FCV vaccines provide protection mainly by inducing humoral immunity (VN antibodies). As the virus can mutate quickly, field strains could evolve resistance to any vaccine-induced immune response, particularly if a vaccine is used for a prolonged period of time in the population (Lauritzen et al., 1997). Although there are some studies that lend support to this hypothesis (Addie et al., 2008), the evidence for FCV escaping vaccine-induced immunity at a population level is not convincing (Porter et al., 2008). Such studies are conducted to obtain more information about the strains circulating in Europe, and vaccine companies are seeking to identify newer strains that provide wider cross protection (Poulet et al., 2005). The most commonly used vaccine strains are F9, which is the oldest, isolated in the 1950s, FCV 255, and two new strains G1 and 431 (Poulet et al., 2000; Poulet et al., 2005).


Recently, one manufacturer has introduced a hypervirulent strain into its vaccine in the USA (Huang et al., 2010), and a Japanese research group has developed a triple strain vaccine (Masubuchi et al., 2010); however, at the time of writing (2015) these are not available in Europe. Some vaccine companies do not state the strain of virus used in their vaccine.


In the absence of compelling published data, it is difficult to make a general recommendation about which vaccine strain or strains to use. However, if disease is occurring in fully vaccinated cats that are housed in groups, then changing to a different vaccine antigen may offer advantages.


The impact of vaccination on the shedding of field viruses is controversial, with some studies showing a moderate reduction (Poulet et al., 2005; Jas et al., 2009) whilst others show that vaccination might actually extend the period of virus shedding after infection (Dawson et al., 1991; Pedersen and Hawkins, 1995). Live parenteral and intranasal FCV vaccine strains can be shed, although it seems rare (Pedersen and Hawkins, 1995; Radford et al., 1997, 2000, 2001; Coyne et al., 2007; Ruch-Gallie et al., 2011).


Live vaccines retain some pathogenic potential and may induce disease if administered incorrectly, e.g. when accidentally aerosolised or spilled on the skin and ingested (Dawson et al., 1993; Pedersen and Hawkins, 1995; Radford et al., 1997 and 2000). However, this appears to be a rare event.


Cats that have recovered from caliciviral disease are probably not protected for life against further episodes of disease, particularly those caused by different strains. Therefore, vaccination of recovered, healthy cats is generally recommended, even in situations where FCV is endemic.


The value of serological tests in predicting protection is limited, because antibodies to the calicivirus strain used in a laboratory test may not necessarily protect against the strains that the cat will subsequently be exposed to in the field.



Primary vaccination course

Kittens: ABCD recommends that all kittens should be vaccinated against FCV. Because MDA can interfere with the response to vaccination, the primary course of vaccination is usually started at around nine weeks of age, although some vaccines are licensed for use at an earlier age. Kittens should receive a second vaccination two to four weeks later, but not earlier than at twelve weeks of age. This protocol has been developed to ensure optimal protection. However, due to a longer persistence of MDA some kittens may fail to respond to this protocol (Dawson et al., 2001; EBM grade I). Therefore, in high-risk situations, particularly where FCV has been shown to cause disease in vaccinated kittens, a third vaccination at 16 weeks should be considered. 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. We recommend using the same brand for the entire primary vaccination course.


Older cats of uncertain FCV vaccination status should also receive two injections with an interval of two to four weeks, and a boost one year later, using vaccines containing the same virus strains. This applies even if the vaccine contains modified live virus.




The issue of recommended intervals between boosters is still controversial. However, based on positive study results published by several independent groups, ABCD recommends that boosters should be given at triennial intervals to protect individual cats against FCV field infections (EBM grade II) for cats in low-risk situations, mainly indoor-only cats with little or no contact to others. However, owners should be made aware that as time since the last vaccination increases, the degree of clinical protection decreases.


However, cats in crowded high-risk situations (e.g. boarding catteries) should be revaccinated at yearly intervals. For other cats, an informed decision should be made on the basis of a risk-benefit analysis. The ABCD recommends a single injection if the interval since the last vaccination is not more than three years. If the interval exceeds three years, two vaccinations would ensure optimal protection. Boosters using FCV vaccines from different manufacturers are acceptable. The ABCD appreciates that single-component FCV vaccines are currently unavailable. Annual boosters that protect against other antigens may in practice entail more frequent boosters than triennially.



Disease control in specific situations




FCV is often a problem in cat shelters. Management to limit or even prevent virus transmission is as important as vaccination in control. Shelter design and management should be aimed at avoiding cross infection of cats. Cats should be housed individually unless they are known to originate from the same household. Dogs and cats should be housed separately, and flea control should be implemented to minimise the risk of transmission of FCV and other diseases. If acute respiratory disease occurs in a shelter, identification of the agent involved (with differentiation of FCV from FHV-1, Chlamydia felis, Bordetella bronchiseptica, and Mycoplasma spp.) may be useful in deciding on the appropriate preventative measures. In case of an FCV outbreak, it should be considered that FCV can persist in the environment for about one month and is resistant to many common disinfectants. Effective substances include sodium hypochlorite (5% bleach diluted at 1:32), potassium peroxy-monosulfate, chlorine dioxide and commercial products that have been approved for their virucidal activity. New healthy cats should be vaccinated as soon as possible. Modified live virus vaccines are preferred in shelters because of the earlier onset of protection.



Breeding catteries


FCV can be a major problem for cat breeders. Infection most often appears as upper respiratory disease in young kittens, typically at around 4-8 weeks as MDA wanes. Disease in such young kittens can be severe and frequently involves all the kittens in the litter; some kittens may die. Vaccination of the queen will not prevent virus shedding, but may be beneficial in ensuring that the kittens benefit from higher levels of MDA through the colostrum and milk, providing protection for the first month or so of life.


Revaccinations should take place prior to mating. Vaccination during pregnancy is not recommended. Modified live virus vaccines are not licensed for use in pregnant cats and if considered at all, an inactivated vaccine must be used. Queens should kitten in isolation, and in order to avoid the risk of exposure to potential carrier cats, the litter should not mix with other cats until it has been fully vaccinated. Early vaccination should be considered for litters from queens that had infected litters previously or for which there is concern of infection. The earliest age for which FCV vaccines are licensed is six weeks, but vaccination may be considered even earlier in kittens deemed to be at risk. When levels of MDA may be too low to protect, vaccination should be repeated every two weeks until the primary vaccination course is concluded at twelve weeks.


When all other control strategies have failed, early weaning into isolation from around four weeks of age is an alternative approach to protect kittens against infection from their mothers.



Vaccination of immunocompromised cats


Vaccines cannot generate optimum protection in animals with compromised immune function, such as deficient nutrition, genetic and acquired, viral immunodeficiencies, systemic disease, concurrent administration of immunosuppressive drugs and environmental stress. Efforts should be made to protect immunocompromised cats from exposure to infectious agents and to correct these conditions prior to vaccination; if this cannot be assured, vaccination should be performed nevertheless and repeated after the animal has fully recovered. Based on safety considerations, ABCD recommends inactivated vaccines in these circumstances. Modified live FCV vaccines should not be used in immunocompromised individuals, as the failure to control replication of the vaccine virus could lead to clinical signs.



FIV positive cats


Vaccination of FIV-infected cats is controversial. FIV-infected cats are capable of mounting immune responses to administered antigens except during the terminal phase of infection, but also primary immune responses may be delayed or diminished (Dawson et al., 1991; Reubel et al., 1994; Foley et al., 2003; EBM grade III). FCV vaccination was less effective in cats shortly after experimental infection with FIV, as compared to uninfected cats, and vaccination might enhance long-term shedding of FCV (Dawson et al., 1991).


Immune stimulation of FIV-infected lymphocytes in vitro promotes FIV replication. In vivo, vaccination of chronically infected cats with a synthetic peptide was associated with a decrease in the CD4+/CD8+ ratio (Lehmann et al., 1992; Reubel et al., 1994). Therefore, a potential trade-off to protection from FCV-related disease is the progression of FIV infection as a result of increased virus production. Thus, only FIV cats with a high risk of exposure to infectious agents that are clinically healthy or in a stable medical condition should be vaccinated, and only killed vaccines used.



FeLV-positive cats


FeLV-infected cats should be kept indoors and isolated, to avoid exposure to FCV, but also to diminish the likelihood of retrovirus transmission to other cats. Asymptomatic FeLV-infected cats should be vaccinated against FCV. Although there is no evidence that FeLV-infected cats are at increased risk of vaccine-induced disease from residual virulence of modified-live virus vaccines, killed vaccines are preferable. FeLV-infected cats may not mount adequate immune responses to rabies vaccines and perhaps neither to other vaccines. Protection of FeLV-infected cats may therefore not be comparable to that achieved in uninfected cats, and more frequent vaccination should be considered.



Chronic disease


Exceptions from the general rule to vaccinate only healthy animals apply for cats with chronic illness, where vaccination may sometimes be necessary. Manufacturers evaluate vaccine safety and efficacy in healthy animals and accordingly, vaccines are labelled for use in healthy animals only. Nonetheless, cats with stable chronic conditions such as renal disease, diabetes mellitus or hyperthyroidism should receive vaccines at the same frequency as healthy cats. In contrast, cats with acute illness, debilitation, or high fever should not be vaccinated.


In cats with chronic stomatitis and FCV infection, administration of a modified live FCV vaccine is best avoided (EBM grade IV).



Cats receiving corticosteroids or other immunosuppressive drugs


In cats under corticosteroid treatment, vaccination should be considered carefully. Depending on dosage and duration, corticosteroids may cause functional suppression of cell-mediated immune responses in particular. In dogs, corticosteroids do not hamper effective immunization if given for short periods of time at low to moderate doses (Nara et al., 1979), but the effect of corticosteroids on vaccine efficacy in cats is not known. Hence the use of corticosteroids and/or other immunosuppressants at the time of vaccination should be avoided.





Abd-Eldaim M, Potgieter L, Kennedy M (2005): Genetic analysis of feline caliciviruses associated with a hemorrhagic-like disease. J Vet Diagn Invest 17, 420-429.


Addie D, Poulet H, Golder MC, McDonald M, Brunet S, Thibault JC, Hosie MJ (2008): Ability of antibodies to two new caliciviral vaccine strains to neutralise feline calicivirus isolates from the UK. Vet Rec 163(12), 355-357.


Addie DD, Radford A, Yam PS, Taylor DJ (2003): Cessation of feline calicivirus shedding coinciding with resolution of chronic gingivostomatitis in a cat. J Small Anim Pract 44(4), 172-176.


Bannasch MJ, Foley JE (2005): Epidemiologic evaluation of multiple respiratory pathogens in cats in animal shelters. J Feline Med Surg 7, 109-119.


Belgard S, Truyen U, Thibault JC, Sauter-Louis C, Hartmann K (2010): Prevalence of feline calicivirus, feline immunodeficiency virus, feline leukemia virus, feline herpesvirus and Bartonella henselae in cats with chronic gingivostomatitis. Berl Munch Tierarztl Wochenschr 123(9-10), 369-376.


Bennett D, Gaskell RM, Mills A, Knowles J, Carter S, McArdle F (1989): Detection of feline calicivirus antigens in the joints of infected cats. Vet Rec 124(13), 329-332.


Binns SH, Dawson S, Speakman AJ, Cuevas LE, Hart CA, Gaskell CJ, Morgan KL, Gaskell RM (2000): A study of feline upper respiratory tract disease with reference to prevalence and risk factors for infection with feline calicivirus and feline herpesvirus. J Feline Med Surg 2, 123-133.


Brunet S, Jas D, David F, Bublot M, Poulet H (2005): Feline calicivirus: vaccinations against virulent strains. In Comparative and emerging virus infections of dogs and cats. Conference of the European Society of Veterinary Virology 2005, Liverpool.


Clay S, Maherchandani S, Malik YS, Goyal SM (2006): Survival on uncommon fomites of feline calicivirus, a surrogate of noroviruses. Am J Infect Control 34, 41-43.


Coutts AJ, Dawson S, Willoughby K, Gaskell RM (1994): Isolation of feline respiratory viruses from clinically healthy cats at UK cat shows. Vet Rec 135, 555-556.


Coyne KP, Dawson S, Radford AD, Cripps PJ, Porter CJ, McCracken CM, Gaskell RM (2006a): Long term analysis of feline calicivirus prevalence and viral shedding patterns in naturally infected colonies of domestic cats. Vet Microbiol 118(1-2), 12-25.


Coyne KP, Gaskell RM, Dawson S, Porter CJ, Radford AD (2007): Evolutionary mechanisms of persistence and diversification of a calicivirus within endemically infected natural host populations. J Virol 81(4), 1961-1971.


Coyne KP, Jones BRD, Kipar A, Chantrey J, Porter CJ, Barber PJ, Dawson S, Gaskell RM, Radford AD (2006b): Lethal outbreak of a disease associated with feline calicivirus infection in cats. Vet Rec 158, 544-550.


Dawson S, Bennett D, Carter SD, Bennett M, Meanger J, Turner PC, Carter MJ, Milton I, Gaskell RM (1994): Acute arthritis of cats associated with feline calicivirus infection. Res Vet Sci 56, 133-143.


Dawson S, McArdle F, Bennett M, Carter M, Milton IP, Turner P, Meanger J, Gaskell RM (1993): Typing of feline calicivirus isolates from different clinical groups by virus neutralisation tests. Vet Rec 133(1), 13-17.


Dawson S, Smyth NR, Bennett M, Gaskell RM, McCracken CM, Brown A, Gaskell CJ (1991): Effect of primary-stage feline immunodeficiency virus infection on subsequent feline calicivirus vaccination and challenge in cats. AIDS 5, 747-750.


Dawson S, Willoughby K, Gaskell RM, Woog G, Chalmers WCK (2001): A field trial to assess the effect of vaccination against feline herpesvirus, feline calicivirus and feline panleukopenia virus in 6-week-old kittens. J Feline Med Surg 3, 17-22.


Di Martino B, Di Rocco C, Ceci C, Marsilio F (2009): Characterization of a strain of feline calicivirus isolated from a dog faecal sample. Vet Microbiol 139(1-2), 52-57.


Doultree JC, Druce JD, Birch CJ, Bowden DS, Marshall JA (1999): Inactivation of feline calicivirus, a Norwalk virus surrogate. J Hosp Infect 41, 51-57.


Dowers KL, Hawley JR, Brewer MM, Morris AK, Radecki SV, Lappin MR (2010): Association of Bartonella species, feline calicivirus, and feline herpesvirus 1 infection with gingivostomatitis in cats. J Feline Med Surg 12(4), 314-321.


Duizer E, Bijkerk P, Rockx B, De Groot A, Twisk F, Koopmans M (2004): Inactivation of caliciviruses. Appl Environ Microbiol 70, 4538-4543.


Foley J, Hurley K, Pesavento PA, Poland A, Pedersen NC (2006): Virulent systemic feline calicivirus infection: local cytokine modulation and contribution of viral mutants. J Feline Med Surg 8, 55-61.


Foley JE, Leutenegger CM, Dumler JS, Pedersen NC, Madigan JE (2003): Evidence for modulated immune response to Anaplasma phagocytophila sensu lato in cats with FIV induced immunosuppression. Comp Immunol Micribiol Infect 26, 103-113.


Fulton RW, Burge LJ (1985): Susceptibility of feline herpesvirus 1 and a feline calicivirus to feline interferon and recombinant human leukocyte interferons. Antimicrob Agents Chemother 28(5), 698-699.


Gaskell R, Dawson S (1998): Feline respiratory disease. In: Infectious diseases of the dog and cat, Greene CE (Ed), WB Saunders Company, Philadelphia (USA), 97-106.


Gaskell RM, Dawson S, Radford AD (2006): Feline respiratory disease. In: Infectious diseases of the dog and cat, Greene CE (Ed), Saunders Elsevier, 145-154.


Geissler K, Schneider K, Platzer G, Truyen B, Kaaden OR, Truyen U (1997): Genetic and antigenic heterogeneity among feline calicivirus isolates from distinct disease manifestations. Virus Res 48(2), 193-206.


Geissler K, Schneider K, Truyen U (2002): Mapping neutralizing and non-neutralizing epitopes on the capsid protein of feline calicivirus. J Vet Med B Infect Dis Vet Public Health 49(1), 55-60.


Glaus T, Hofmann-Lehmann R, Greene C, Glaus B, Wolfensberger C, Lutz H (1997): Seroprevalence of bartonella henselae Infection and correlation with disease status in cats in Switzerland. J Clin Microb 35 (11), 2883-2885.


Glenn M, Radford AD, Turner PC, Carter M, Lowery D, DeSilver DA, Meanger J, Baulch-Brown C, Bennett M, Gaskell RM (1999): Nucleotide sequence of UK and Australian isolates of feline calicivirus (FCV) and phylogenetic analysis of FCVs. Vet Microbiol 67(3), 175-193.


Gore TC, Lakshmanan N, Williams JR, Jirjis FF, Chester ST, Duncan KL, Coyne MJ, Lum MA, Sterner FJ (2006): Three-year duration of immunity in cats following vaccination against feline rhinotracheitis virus, feline calicivirus, and feline panleukopenia virus. Vet Ther 7(3), 213-222.


Green KY, Ando T, Balayan MS, Berke T, Clarke IN, Estes MK, Matson DO, Nakata S, Neill JD, Studdert MJ, Thiel HJ (2000): Taxonomy of the caliciviruses. J Infect Dis 181 Suppl 2, S 322-330.


Harrison TM, Sikarskie J, Kruger J, Wise A, Mullaney TP, Kiupel M, Maes RK (2007): Systemic calicivirus epidemic in captive exotic felids. J Zoo Wildl Med 38(2), 292-299.


Hashimoto M, Roerink F, Tohya Y, Mochizuki M (1999): Genetic analysis of the RNA polymerase gene of caliciviruses from dogs and cats. J Vet Med Sci 61, 603-608.


Helps CR, Lait P, Damhuis A, Bjornehammar U, Bolta D, Brovida C, Chabanne L, Egberink H, Ferrand G, Fontbonne A, Pennisi MG, Gruffydd-Jones T, Gunn-Moore D, Hartmann K, Lutz H, Malandain E, Mostl K, Stengel C, Harbour DA, Graat EA (2005): Factors associated with upper respiratory tract disease caused by feline herpesvirus, feline calicivirus, Chlamydophila felis and Bordetella bronchiseptica in cats: experience from 218 European catteries. Vet Rec 156, 669-673.


Hennet P (1994): Results of periodontal and extraction treatment in cats with gingivostomatitis. In Proceedings of the World Veterinary Dental Congress, 49.


Hennet PR, Camy GA, McGahie DM, Albouy MV (2011): Comparative efficacy of a recombinant feline interferon omega in refractory cases of calicivirus-positive cats with caudal stomatitis: a randomised, multi-centre, controlled, double-blind study in 39 cats. J Feline Med Surg 13(8), 577-587.


Huang C, Hess J, Gill M, Hustead D (2010): A dual-strain feline calicivirus vaccine stimulates broader cross-neutralization antibodies than a single-strain vaccine and lessens clinical signs in vaccinated cats when challenged with a homologous feline calicivirus strain associated with virulent systemic disease. J Feline Med Surg 12(2), 129-137.


Hurley KF (2006): Virulent Calicivirus infection in cats. In Proceedings American College of Veterinary Internal Medicine Congress 2006.


Hurley KF, Sykes ES (2003): Update on feline calicivirus: new trends. Vet Clin North Am Small Anim Prac 33(4), 759-772.


Jas D, Aeberlé C, Lacombe V, Guiot AL, Poulet H (2009): Onset of immunity in kittens after vaccination with a non-adjuvanted vaccine against feline panleucopenia, feline calicivirus and feline herpesvirus. Vet J 182(1), 86-93.


Johnson RP (1992): Antigenic change in feline calicivirus during persistent infection. Can J Vet Res 56, 326-330.


Johnson RP, Povey RC (1983): Transfer and decline of maternal antibody to feline calicivirus. Can Vet J 24, 6.


Kahn DE, Hoover EA, Bittle JL (1975): Induction of immunity to feline caliciviral disease. Infect Immunol 11, 1003.


Kalunda M, Lee KM, Holmes DF, Gillespie JH (1975): Serologic classification of feline caliciviruses by plaque-reduction neutralization and immunodiffusion. Am J Vet Res 36(4 Pt.1), 353-356.


Klose TC, MacPhail CM, Schultheiss PC, Rosychuk RA, Hawley JR, Lappin MR (2010): Prevalence of select infectious agents in inflammatory aural and nasopharyngeal polyps from client-owned cats. J Feline Med Surg 12(10), 769-774.


Knowles JO, McArdle F, Dawson S, Carter SD, Gaskell CJ, Gaskell RM (1991): Studies on the role of feline calicivirus in chronic stomatitis in cats. Vet Microbiol 27, 205-219.


Kreutz LC, Johnson RP, Seal BS (1998): Phenotypic and genotypic variation of feline calicivirus during persistent infection of cats. Vet Microbiol 59, 229-236.


Lappin MR, Andrews J, Simpson D, Jensen WA (2002): Use of serologic tests to predict resistance to feline herpesvirus 1, feline calicivirus, and feline parvovirus infection in cats. J Am Vet Med Assoc 220 (1), 38-42.


Larson J, Kruger JM, Wise AG, Kaneene JB, Miller R, Fitzgerald SD, Kiupel M, Maes RK (2011): Nested case-control study of feline calicivirus viruria, oral carriage, and serum neutralizing antibodies in cats with idiopathic cystitis. J Vet Intern Med 25(2), 199-205.


Lauritzen A, Jarrett O, Sabara M (1997): Serological analysis of feline calicivirus isolates from the United States and United Kingdom. Vet Microbiol 56, 55-63.


Lehmann R, von Beust B, Niederer E, Condrau MA, Fierz W, Aubert A, Ackley CD, Cooper MD, Tompkins MB, Lutz H (1992): Immunization-induced decrease of the CDA+:CD8+ ratio in cats experimentally infected with feline immunodeficiency virus. Vet Immunol Immunopathol 35, 199-214.


Marsilio F, Martino BD, Decaro N, Buonavoglia C (2005): A novel nested PCR for the diagnosis of calicivirus infections in the cat. Vet Microbiol 105, 1-7.


Martella V, Pratelli A, Gentile M, Buonavoglia D, Decaro N, Fiorente P, Buonavoglia C (2002): Analysis of the capsid protein gene of a feline-like calicivirus isolated from a dog. Vet Microbiol 85, 315-322.


Masubuchi K, Wakatsuki A, Iwamoto K, Takahashi T, Kokubu T, Shimizu M (2010): Immunological and genetic characterization of feline caliciviruses used in the development of a new trivalent inactivated vaccine in Japan. J Vet Med Sci 72(9), 1189-1194.


Mencke N, Vobis M, Mehlhorn H, D Haese J, Rehagen M, Mangold-Gehring S, Truyen U (2009): Transmission of feline calicivirus via the cat flea (Ctenocephalides felis). Parasitol Res 105(1), 185-189.


Mochizuki M, Nakatani H, Yoshida M (1994): Inhibitory effects of recombinant feline interferon on the replication of feline enteropathogenic viruses in vitro. Vet Microbiol 39(1-2), 145-152.


Nara PL, Krakowka S, Powers TE (1979): Effects of prednisolone on the development of immune response to canine distemper virus in beagle pups. Am J Vet Res 40(12), 1742-1747.


Ohe K, Sakai S, Sunaga F, Murakami M, Kiuchi A, Fukuyama M, Furuhata K, Hara M, Soma T, Ishikawa Y, Taneno A (2006): Detection of Feline calicivirus (FCV) from Vaccinated Cats and Phylogenetic Analysis of its Capsid Genes. Vet Res Commun 30(3), 293-305.


Ohe K, Takahashi T, Hara D, Hara M (2008): Sensitivity of FCV to recombinant feline interferon (rFeIFN). Vet Res Commun 32(2), 167-174.


Ossiboff RJ, Sheh A, Shotton J, Pesavento PA, Parker JS (2007): Feline caliciviruses (FCVs) isolated from cats with virulent systemic disease possess in vitro phenotypes distinct from those of other FCV isolates. J Gen Virol 88, 506-527.


Pedersen NC (1987): Feline calicivirus. In: Virus infections of carnivores. Appel MJ (Ed), Elsevier Science Publishers BV, New York, 339-346.


Pedersen NC, Elliott JB, Glasgow A, Poland A, Keel K (2000): An isolated epizootic of hemorrhagic-like fever in cats caused by a novel and highly virulent strain of feline calicivirus. Vet Microbiol 73, 281-300.


Pedersen NC, Hawkins KF (1995): Mechanisms for persistence of acute and chronic feline calicivirus infections in the face of vaccination. Vet Microbiol 47(1-2), 141-156.


Pedersen NC, Laliberte L, Ekman S (1983): A transient febrile "limping" syndrome of kittens caused by two different strains of feline calicivirus. Feline Practice 13, 26-35.


Porter CJ, Radford AD, Gaskell RM, Ryvar R, Coyne KP, Pinchbeck GL, Dawson S (2008): Comparison of the ability of feline calicivirus (FCV) vaccines to neutralise a panel of current UK FCV isolates. J Feline Med Surg 10(1), 32-40.


Poulet H, Brunet S, Leroy V, Chappuis G (2005): Immunisation with a combination of two complementary feline calicivirus strains induces a broad cross-protection against heterologous challenges. Vet Microbiol 106(1-2), 17-31.


Poulet H, Brunet S, Soulier M, Leroy V, Goutebroze S, Chappuis G (2000): Comparison between acute oral/respiratory and chronic stomatitis/gingivitis isolates of feline calicivirus: pathogenicity, antigenic profile and cross-neutralisation studies. Arch Virol 145(2), 243-261.


Povey RC (1974): Serological relationships among feline caliciviruses. Infect Immun 10, 1307-1314.


Povey RC (1978): Effect of orally administered ribavirin on experimental feline calicivirus infection in cats. Am J Vet Res 39(8), 1337-1341.


Povey C, Ingersoll J (1975): Cross-protection among feline calicviruses. Infect Immun 11, 877-885.


Radford AD, Bennett M, McArdle F, Dawson S, Turner PC, Glenn MA, Gaskell RM (1997): The use of sequence analysis of a feline calicivirus (FCV) hypervariable region in the epidemiological investigation of FCV related disease and vaccine failures. Vaccine 15, 1451-1458.


Radford AD, Dawson S, Coyne KP, Porter CJ, Gaskell RM (2006): The challenge for the next generation of feline calicivirus vaccines. Vet Microbiol 117(1), 14-18.


Radford AD, Dawson S, Ryvar R, Coyne K, Johnson DR, Cox MB, Acke EF, Addie DD, Gaskell RM (2003): High genetic diversity of the immunodominant region of the feline calicivirus capsid gene in endemically infected cat colonies. Virus Genes 27, 145-155.


Radford AD, Dawson S, Wharmby C, Ryvar R, Gaskell RM (2000): Comparison of serological and sequence-based methods for typing feline calicivirus isolates from vaccine failures. Vet Rec 146, 117-123.


Radford AD, Sommerville L, Ryvar R, Cox MB, Johnson DR, Dawson S, Gaskell RM (2001): Endemic infection of a cat colony with a feline calicivirus closely related to an isolate used in live attenuated vaccines. Vaccine 19, 4358-4362.


Radford AD, Turner PC, Bennett M, McArdle F, Dawson S, Glenn MA, Williams RA, Gaskell RM (1998): Quasispecies evolution of a hypervariable region of the feline calicivirus capsid gene in cell culture and in persistently infected cats. J Gen Virol 79, 1-10.


Radford AD, Willoughby K, Dawson S, McCracken C, Gaskell RM (1999): The capsid gene of feline calicivirus contains linear B-cell epitopes in both variable and conserved regions. J Virol 73, 8496-8502.


Reubel GH, Dean GA, George JW, Barlough JE, Pedersen NC (1994): Effects of incidental infections and immune activation on disease progression in expermimentally feline immunodeficiency virus-infected cats. J Acq Immun Defic Syndrome 7, 1003-1015.


Reynolds BS, Poulet H, Pingret JL, Jas D, Brunet S, Lemeter C, Etievant M, Boucraut-Baralon C (2009): A nosocomial outbreak of feline calicivirus associated virulent systemic disease in France. J Feline Med Surg 11(8), 633-644.


Roerink F, Hashimoto M, Tohya Y, Mochizuki M (1999): Genetic analysis of a canine calicivirus: evidence for a new clade of animal caliciviruses. Vet Microbiol 69, 69-72.


Ruch-Gallie RA, Veir JK, Hawley JR, Lappin MR (2011): Results of molecular diagnostic assays targeting feline herpesvirus-1 and feline calicivirus in adult cats administered modified live vaccines. J Feline Med Surg 13(8), 541-545.


Schorr-Evans EM, Poland A, Johnson WE, Pedersen NC (2003): An epizootic of highly virulent feline calicivirus disease in a hospital setting in New England. J Feline Med Surg 5(4), 217-226.


Scott FW, Geissinger CM (1997): Duration of immunity in cats vaccinated with an inactivated feline panleukopenia, herpesvirus and calicivirus vaccine. Feline Practice 25, 12-19.


Scott FW, Geissinger CM (1999): Long-term immunity in cats vaccinated with an inactivated trivalent vaccine. Am J Vet Res 60, 652-658.


Southerden P, Gorrel C (2007): Treatment of a case of refractory feline chronic gingivostomatitis with feline recombinant interferon omega. J Small Anim Pract 48(2), 104-106.


Sykes JE, Allen JL, Studdert VP, Browning GF (2001): Detection of feline calicivirus, feline herpesvirus 1 and Chlamydophila psittaci mucosal swabs by multiplex RT-PCR/PCR. Vet Microbiol 81(2), 95-108.


Sykes JE, Studdert VP, Browning GF (1998): Detection and strain differentiation of feline calicivirus in conjunctival swabs by RT-PCR of the hypervariable region of the capsid protein gene. Arch Virol 147(7), 1321-1334.


Taira O, Suzuki M, Takeuchi Y, Aramaki Y, Sakurai I, Watanabe T, Motokawa K, Arai S, Sato H, Maehara N (2005): Expression of feline interferon-alpha subtypes in Esherichia coli, and their antiviral activity and animal species specificity. J Vet Med Sci 67, 543-545.


TerWee T, Lauritzen A, Sabara M, Dreier KJ, Kokjohn K (1997): Comparison of the primary signs induced by experimental exposure to either a pneumotrophic or a 'limping' strain of feline calicivirus. Vet Microbiol 56, 33-45.


Tham KM, Studdert MJ (1987): Antibody and cell-mediated immune responses to feline calicivirus following inactivated vaccine and challenge. J VetMed B 34, 640-654.


Tohya Y, Yokoyama N, Maeda K, Kawaguchi Y, Mikami T (1997): Mapping of antigenic sites involved in neutralization on the capsid protein of feline calicivirus. J Gen Virol 78, 303-305.


Vercelli A, Raviri G, Cornegliani N (2006): The use of oral cyclosporin to treat feline dermatosis: a retrospective analysis of 23 cases. Vet Dermatol 17, 201-206.


Wardley RC (1976): Feline calicivirus carrier state. A study of host/virus relationship. Arch Virol 52, 243-249.


Wardley RC (1977): The clinical disease and patterns of excretion associated with three different strains of feline caliciviruses. Res Vet Sci 23, 7-14.


Wardley RC, Gaskell RM, Povey RC (1974): Feline respiratory viruses - their prevalence in clinically healthy cats. J Small Anim Pract 15, 579-586.


White SD, Rosychuk RA, Janik TA, Denerolle P, Schultheiss P (1992): Plasmacell stomatitis-pharyngytis in cats: 40 cases (1973-1991). J Am Vet Med Assoc 200(9), 1377-1380.



Further reading


Helps CR, Lait P, Tasker S, Harbour D (2002): Melting curve analysis of feline calicivirus isolates detected by real-time reverse transcription PCR. J Virol Methods 106 (2), 241-244.


McCann KB, Lee A, Wan J, Roginski H, Coventry MJ (2003): The effect of bovine lactoferrin and lactoferricin B on the ability of feline calicivirus (a norovirus surrogate) and poliovirus to infect cell cultures. J Appl Microbiol 95(5), 1026-1033.


Pesavento PA, MacLachlan NJ, Dillard-Telm L, Grant CK, Hurley KF (2004): Pathologic, immunohistochemical, and electron microscopic findings in naturally occurring virulent systemic feline calicivirus infection in cats. Vet Pathol 41, 257-263.


Scansen BA, Wise AG, Kruger JM, Venta PJ, Maes RK (2004): Evaluation of a p30 genebased real-time reverse transcriptase polymerase chain reaction assay for detection of feline caliciviruses. J Vet Intern Med 18(1), 135-138.


Sosnotsev SV, Belliot G, Chang KO, Onwudiwe O, Green KY (2005): Feline calicivirus VP2 is essential for the production of infectious virions. J Virol 79, 4012-4024.


Wilhelm S, Truyen U (2006): Real-time reverse transcription polymerase chain reaction assay to detect a broad range of feline calicivirus isolates. J Virol Methods 133(1), 105-108.


Back to Top