Virulent systemic feline calicivirus (VS-FCV) is a novel pathogen that has erupted in at least 6 epidemic clusters since 1998. The disease is similar to hemorrhagic fevers in humans. Affected cats have systemic vascular compromise and hemorrhagic fever-like signs-most have generalized face and limb swelling, edema consistent with vascular compromise, high fever (39.4° to 42.4° C), multiorgan dysfunction, and sudden death. Signs are caused in part by viral invasion of epithelium and endothelium, coupled with host cytokine responses. Mortality can be up to 67%.

This study evaluated 7 cats with VS-FCV infection-4 kittens and 3 adults. The authors performed FCV culture, evaluated cytokine levels in skin between affected and unaffected controls, and performed sequencing on most of the genomes of 2 VS-FCV strains. They found, on average, that 3.8 of the 9 cytokines tested were elevated in affected tissue. Although it could not be directly concluded that increased local cytokines caused VS-FCV lesions, the findings did suggest an immune-mediated mechanism following viral invasion of endothelium and epithelium that, in severe, generalized cases, could lead to systemic vascular compromise, microthrombus formation, disseminated intravascular coagulation, and death. Sequencing of the capsid gene as well as the whole genome revealed that these VS-FCVs are emerging from several different lineages intermixed with other field-strain FCVs. Numerous mutations were detected in the capsid genotypes, generally in the same region. The authors speculate that this change could result in a novel receptor or other host-virus interactions, particularly targeting epithelial or endothelial cells, warranting further investigation into possible altered host receptor VS-FCV capsid interactions.

COMMENTARY: Within 6 years, hundreds of cases of a frequently fatal, previously undescribed disease in cats were identified. VS-FCV infection is distinctive in its clinical severity; tropism for epithelial and endothelial cells; multisystemic involvement; induction of systemic vascular compromise; and rate of involvement of visceral organs, including lungs, pancreas, and liver. It also frequently causes signs of fever, edema, multiorgan failure, hemorrhage, shock, and death. The mechanisms for lesion development are not known but seem to be at least partly immune-mediated, as is supported by the reported increased severity of disease in older cats.

Why VS-FCV has emerged is not known; one hypothesis is that it occurs because of emergence of a novel virulent VS-FCV genotype. A second plausible mechanism is that several mutant viruses may cause an immune-mediated pathogenesis. Current vaccines do not protect against this calicivirus variant. Practitioners need to be vigilant in looking for this devastating condition. If you suspect a case, email Dr. Kate Hurley at [email protected] or Dr. Janet Foley at [email protected] You may also call the UC Davis program coordinator, Mike Bannasch, at 530-754-7355. In the East, contact Dr. James Richards, director of the Cornell Feline Health Center ([email protected]).

Virulent systemic feline calicivirus infection: Local cytokine modulation and contribution of viral mutants. Foley J, Hurley K, Pesavento PA, et al. J FELINE MED SURG 8:55-61, 2006.