Feline calicivirus (FCV) is well-known for its role in causing upper respiratory tract infections with or without ulceration of the oral cavity in both kittens and adult cats. The morbidity in animals with this disease is usually high, but the infection is rarely fatal.
Many infected cats can develop a state of chronic infection and become carriers of the virus, continuing to transmit the virus in a virulent form from the oral cavity and respiratory tract. FCV infection often occurs together with infection by feline herpesvirus-1 (FHV-1), but, in contrast to this latter, more than 40 strains of calicivirushave been identified so far: these strains differ greatly with regards to both virulence and antigenicity.
In the last few years (since the first identified cases in 1998), a different strain of highly virulent calicivirushas been isolated, and named virulent systemic feline calicivirus(VS-FCV). This strain causes widespread vasculitis, multiorgan failure and death in over 60% of the subjects affected. The clinical signs of patients with VS-FCV are initially the same as those of the known classical forms caused by the other strains of calicivirus, such as oral ulcers, fever and joint pain. However, as indicated by the term “systemic”, VS-FCV is characterized by progression into a more serious disease, with the development of oedema (particularly of the limbs and muzzle), alopecia, crusting and ulceration of the skin (especially around the nostrils and foot pads) and jaundice because of involvement of the liver and pancreas. The systemic lesions can include broncho-interstitial pneumonia and necrosis of the liver (Fig. 1), spleen and pancreas. In detailed studies the calicivirus antigen has been found in the skin, nasal mucosa, lungs, pancreas and endothelial cells of the skin. Cats infected by this strain of FCV are usually regularly vaccinated adults and have never shown the typical manifestations of feline calicivirus infection.
The disease is more severe in regularly vaccinated adult cats.
So far, VS-FCV has been found almost exclusively in groups of cats living together; some single cases have been reported but all occurred in cats with a history of staying in crowded environments, such as veterinary clinics or breeding facilities. The incubation period of systemic FCV is 1 to 5 days in a nosocomial environment, but can be up to 12 days in a domestic setting. In every documented case the disease has appeared spontaneously in the affected population, probably because of mutation of a calicivirus strain already circulating within the population into a more virulent form. This hypothesis is supported by genomic analysis of the virulent strains, which are unique, in the absence of shared mutations that could explain the change in virulence. Cats living in catteries and breeding facilities are the most infected populations. Serious epizoonotic phenomena have occurred in veterinary shelters because of the introduction of sick animals from catteries. This variant is so pathogenic that the disease tends to be self-limiting within a few weeks and its environmental spread is, therefore, limited. However, in at least two reported cases that we are aware of, veterinary staff caring for an infected cat transmitted the disease to their own domestic cats.
A clinical suspicion of infection by VS-FCV can be raised by:
- a history of recent exposure to possible infectious agents (having stayed in a breeding facility or cattery, admitted to a veterinary clinic, etc.);
- the presence of general systemic clinical signs of infection by calicivirus (infection of the upper respiratory tract, oral ulcers, limping) which precede the distinctive signs of VS-FCV;
- exclusion of other causes of vasculitis.
It has been observed that animals that survive the infection and are clinically healed characteristically rapidly develop severe forms of hyperplastic-ulcerative gingivo-stomatitis (Fig. 2 and Fig. 3) which last over time. In this specific case, the causative role of caliciviruswould seem to be certain, but it is presumed that these subjects also have underlying alterations to the immune system.
Fig. 2 Fig. 3
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