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.
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 and a relatively
mild acute respiratory disease. More severe signs can resemble the respiratory disease caused
by FHV-1.
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. They usually resolve
after several days. In some severe cases, pneumonia, manifested by dyspnoea, coughing, fever
and depression can occur, particularly in young kittens.
FCV can be isolated from nearly all cats with the chronic lymphoplasmacytic gingivitis/stomatitis complex. 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, as does the role of coinfections with FIV and Bartonella (Glaus et al., 1997).
An acute transient lameness with fever can be associated with FCV infection (Ter Wee et al., 1997; Pedersen et al., 1983) 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).
Outbreaks of highly virulent and often lethal FCV infection have recently been described in
the United States and in Europe (Pedersen et al., 2000; Coyne et al., 2006b). 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
(Hurley, 2006; Pedersen et al., 2000).
In contrast to the common strains, VS-FCV causes systemic disease characterized by severe
systemic inflammatory response syndrome, disseminated intravascular coagulation, multiorgan
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. Crusted lesions, ulcers and alopecia can be seen on the
nose, lips, and ears, around the eyes and on the footpads. 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).