Feline Calicivirus (FCV) is one of the major causes of feline infectious upper respiratory tract disease (cat 'flu). Classical cat 'flu follows a short incubation period of three to five days and consists predominantly of signs of upper respiratory tract disease, typically sneezing, rhinitis, nasal discharge, conjunctivitis, ocular discharge and oral ulceration. These signs may be accompanied by pyrexia (raised temperature) and occasionally other manifestations, such as coughing and pneumonia.
From an early stage, transient lameness was also observed as a clinical feature in some cats infected with FCV and it now seems clear that this is, in fact, a common clinical manifestation of FCV infection. The transient lameness associated with FCV has acquired the name 'limping syndrome'.
Limping syndrome is caused by FCV infection
FCV was confirmed as a cause of lameness during studies performed at the University of California, where kittens infected with two different strains of FCV (isolated from cats with transient lameness) exhibited signs of disease 48 to 72 hours after infection. The first clinical sign to develop was pyrexia, accompanied by depression and inappetence. However, within hours of the onset of pyrexia, the kittens were all reported to develop generalised or localised stiffness, manifesting as shifting lameness in some, and an almost complete reluctance to move in others (Pedersen and others 1983). Although none of the cats developed sneezing or ocular discharges, about one third developed oral ulcers (one of the 'classical' signs of FCV infection). Clinical signs were reported to resolve within 48 to 72 hours with no residual effects. The p r ecise cause of the lameness was not determined, although the authors reported pain on manipulation of joints, and generalised hyperaesthesia (pain or hypersensitivity to touch).
FCV can affect the joints
Further information on the role of FCV infection in limping syndrome came from studies performed at the University of Liverpool. In 1989, Bennett and others reported the results of a study which demonstrated that FCV antigens (proteins) could be identified in the synovial membrane (the membrane surrounding the joint space) in several cats either vaccinated with a commercial live FCV vaccine and, or, infected with an isolate of FCV Although none of these cats had shown any signs of lameness, the calicivirus antigens appeared to be within macrophages (a type of white blood cell) and to be associated with the presence of antibodies.
This suggested that the antigen might have been present in the synovial membrane in the form of 'immune complexes' (a combination of the viral antigen and a specific antibody produced against it). Further studies at Liverpool University demonstrated that in addition to the identification viral proteins, the entire virus could be isolated from joints of cats exposed to FCV showing signs of disease including lameness. Furthermore, microscopic examination of the joint tissues from some of these cats provided evidence of an acute inflammatory process (Dawson and others 1994).
These studies therefore demonstrated that following the natural route of exposure to FCV (ie, oronasal exposure), systemic infection arises which can, at least in some circumstances, involve localisation of the virus to joint tissues where it may cause an inflammatory reaction. However, both experimental studies, and also the observations from naturally occurring cases of FCV-associated lameness generally suggest that some strains of FCV have a greater propensity to cause lameness than others.
FCV vaccination and the limping syndrome
A curious feature of the association between FCV infection and the limping syndrome' is that the lameness is most frequently observed in kittens, and often following their first vaccination (which is typically a combination vaccine for feline calicivirus, herpesvirus and parvovirus). Workers at the University of Liverpool investigated the association between the syndrome and FCV vaccination in detail (Dawson and others 1993). They found that of 123 vaccine reactions reported to them, 80 per cent involved lameness (either alone or in combination with other signs such as pyrexia, oral ulceration or respiratory signs. Furthermore, of the cats developing lameness after vaccination, 96 per cent occurred in cats less than six months of age, and 88 per cent occurred after the first vaccination. All of the cats investigated had received one of five different commercial vaccines, and it emerged that one of these vaccines was responsible for over 60 per cent of the transient lameness cases reported (this vaccine has since been changed by the manufacturer). Signs of lameness were reported to develop typically six to seven days after vaccination in these cats. FCV was isolated from oropharangeal swabs of 71 per cent of cats that developed post-vaccination lameness. Investigation of the strains of virus isolated suggested that in many cases there was infection with `wild' virus (le, natural infection with FCV not associated with vaccination), but in some cases the virus isolated was very closely related, or identical to the vaccine virus. In the same study, these investigators also evaluated 19 cats that developed transient lameness not associated with vaccination. FCV was isolated from 89 per cent of these cats, 63 per cent were less than six months of age, and 79 per cent had accompanying clinical signs (pyrexia, oral ulceration).
In conclusion, these studies have helped to establish the role of FCV in the development of a transient polyarthritis (inflammation affecting more than one joint) in cats. From the studies performed, and the number of enquiries regularly received by the Feline Advisory Bureau, it is clear that the limping syndrome is a common manifestation of FCV infection. It occurs most commonly in young cats and its severity can vary from inapparent arthritis and mild limping, through to severe polyarthritis where the cats are reluctant to move, inappetent and seen to be in pain when touched. Although the limping syndrome' is commonly seen after kittens receive their first vaccination, it is clear that the vaccine virus does not always cause these signs, and natural infection with `wild' virus may be involved in some cases.
Most cats affected with this syndrome will spontaneously recover without the need for any treatment. However, if clinical signs are severe, anti-inflammatory medication may be required and veterinary attention should be sought. Although FCV is obviously a common cause of limping syndrome' in young cats, there are numerous other potential causes of lameness, and if clinical signs are severe, or persist for longer than a few days, veterinary attention should always be sought.
Interestingly, we have recently heard of a few cats that appear to have developed signs of lameness very similar to the 'limping syndrome' after receiving only feline leukaemia vi r us vaccination. If anyone has encountered this with their own cats we would be very interested to hear about it.
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