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Feline calicivirus infection - The European Advisory Board on Cat ...

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field study, 20% of kittens at <strong>on</strong>ly six weeks of age had no detectable antibodies against awidely used vaccine strain (Daws<strong>on</strong> et al. 2001).Active immune resp<strong>on</strong>seVirus neutralising antibodies (VNA) appear by approximately seven days post <str<strong>on</strong>g>infecti<strong>on</strong></str<strong>on</strong>g>(Kahn et al., 1975). In general, antibody titres are higher than for FHV <str<strong>on</strong>g>infecti<strong>on</strong></str<strong>on</strong>g> and theirlevels correlate well with protecti<strong>on</strong> against homologous challenge (Povey & Ingersoll, 1975).<str<strong>on</strong>g>The</str<strong>on</strong>g>re is a c<strong>on</strong>siderable degree of antigenic variability am<strong>on</strong>gst FCV strains, but it wasc<strong>on</strong>cluded from studies of in vitro cross-reactivity that FCVs bel<strong>on</strong>g to a single serotype(Povey, 1974). Prior <str<strong>on</strong>g>infecti<strong>on</strong></str<strong>on</strong>g> with <strong>on</strong>e strain can significantly reduce the acute clinical signsup<strong>on</strong> exposure to a heterologous strain, and in some cases oral shedding may be reduced(Povey & Ingersoll, 1975; Knowles et al., 1991). In general, the level of heterologousprotecti<strong>on</strong> will depend <strong>on</strong> the virus strains involved.<strong>Cat</strong>s may be protected also in the absence of detectable VNA (Knowles et al., 1991; Poulet etal., 2005), suggesting a role for other immune mechanisms: indeed, cellular resp<strong>on</strong>ses havebeen dem<strong>on</strong>strated in vaccinated cats (Tham & Studdert, 1987). Also, FCV-specific IgG andIgA antibodies have been dem<strong>on</strong>strated in the saliva during the course of <str<strong>on</strong>g>infecti<strong>on</strong></str<strong>on</strong>g> (Knowleset al., 1991), although their significance in protecti<strong>on</strong> is unknown.Clinical signsFCV <str<strong>on</strong>g>infecti<strong>on</strong></str<strong>on</strong>g> can cause acute oral and upper respiratory signs but also has been associatedwith chr<strong>on</strong>ic stomatitis, which may be immune-mediated. Recently, a new syndrome, the“virulent systemic feline <str<strong>on</strong>g>calicivirus</str<strong>on</strong>g> (VS-FCV) disease” has been described.Acute oral and upper respiratory tract diseaseClinical findings may differ, depending <strong>on</strong> the virulence of the FCV strain c<strong>on</strong>cerned, <strong>on</strong> theage of the affected cats and <strong>on</strong> husbandry factors. While in some cases <str<strong>on</strong>g>infecti<strong>on</strong></str<strong>on</strong>g> issubclinical, in many others, there is a typical syndrome of lingual ulcerati<strong>on</strong> and a relativelymild acute respiratory disease. More severe signs can resemble the respiratory disease causedby FHV-1.Acute oral and upper respiratory disease signs are mainly seen in kittens. <str<strong>on</strong>g>The</str<strong>on</strong>g> incubati<strong>on</strong>period is 2 to 10 days (Hurley and Sykes, 2003). Oral ulcerati<strong>on</strong>s, sneezing and serous nasaldischarge are the main signs (Gaskell et al., 2006). Fever is also observed. Anorexia,sometimes accompanied by hypersalivati<strong>on</strong> due to oral erosi<strong>on</strong>s - located mainly <strong>on</strong> thet<strong>on</strong>gue - are usually much more prominent than the signs of rhinitis. <str<strong>on</strong>g>The</str<strong>on</strong>g>y usually resolveafter several days. In some severe cases, pneum<strong>on</strong>ia, manifested by dyspnoea, coughing, feverand depressi<strong>on</strong> can occur, particularly in young kittens.Chr<strong>on</strong>ic stomatitisFCV can be isolated from nearly all cats with the chr<strong>on</strong>ic lymphoplasmacyticgingivitis/stomatitis complex, and many cats test positive by PCR (Dowers 2010, Belgard2010). It has been suggested to be an immune-mediated reacti<strong>on</strong> to FCV (and potentiallyother) 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

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