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 can be 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 (acute synovitis with thickening of the synovial membrane and
increased synovial fluid; 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).
The pathogenesis of virulent systemic disease caused by FCV (VS-FCV) differs considerably
from the typical picture described above. These strains cause widespread vasculitis, multiorgan
involvement and death in up to two thirds of the infected cats (Pedersen et al., 2000;
Hurley & 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).