FCV.svgFeline Calicivirus Antibody Test (IFA)

Feline calici virus (FCV) is a virus of the family Caliciviridae that causes disease in cats. It is one of the two important viral causes of respiratory infection in cats, the other being feline herpes virus. FCV can be isolated from about 50% of cats with upper respiratory infections. Cheetahs are the other species of the family Felidae known to become infected naturally. Different strains of FCV can vary in virulence (the degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host). Being an RNA virus, FCV has a high elasticity of its genome, which makes it more adaptable to environmental pressures. This not only makes the development of vaccines more difficult, but also allows for the development of more virulent strains. In persistently infected cats, the gene for the major structural protein of the viral capsid (the outer protein coat of a mature virus) has been shown to evolve through immune-mediated positive selection, which allows the virus to escape detection by the immune system.

A form of FCV has been found to cause a particularly severe systemic disease in cats, similar to rabbit hemorrhagic disease (which is also caused by calici virus). This virus has been called virulent systemic feline calici virus (VS-FCV) or FCV-associated virulent systemic disease (VSD). The disease is caused by direct viral invasion of epithelium and endothelium and secondary host immune response. Strains of VS-FCV have seemingly risen independently of one another since first being described, meaning that not all cases of VS-FCV have spread from a single case. Most of the outbreaks of VS-FCV have been reported in the United States. It was originally described in 1998 in Northern California. The prevalence of FCV varies depending on the environment. In private households, FCV is present in about 10% of cats (either in active or carrier state), while the prevalence in shelters or catteries is 25-40%.

FCV replicates in the oral and respiratory tissues, and is secreted in saliva, feces, urine, and respiratory secretions. It can be transmitted through the air, orally, and on fomites. Infected cats usually shed the virus for two weeks. Following this period, infected cats never shed the virus again or become latently infected and shed the virus continuously or intermittently. Co-infection with either feline herpes virus or feline immunodeficiency virus causes a more severe disease.

Clinical signs in cats infected with FCV may develop acutely, chronically, or not at all. Latent or subclinical infections often become clinical when the cat is stressed, such as at the time of adoption. Acute signs of FCV include fever, conjunctivitis, nasal discharge, sneezing, and ulceration of the mouth (stomatitis). Pneumonia may develop with secondary bacterial infections. In addition to stomatitis, some cats may develop a polyarthritis, both probably immune-mediated through immune complex deposition. Stomatitis and polyarthritis can develop without any upper respiratory infection signs, but fever and loss of appetite may occur. Less commonly, glomerulonephritis can develop in chronic cases secondary to immune complex deposition. The great variability of clinical signs in individual cases of FCV is relate to the relative virulence of different strains of the virus.

VS-FCV can cause a rapid epidemic, with a mortality rate of up to 67%. Initial clinical signs include discharge from the eyes and nose, ulceration in the mouth, anorexia, and lethargy, and occur in the first one to five days. Later signs include fever, edema of the limbs and face, jaundice, and multiple organ dysfunction syndrome. Diagnosis of FCV is difficult without specific tests, because the signs are similar to other feline respiratory diseases, especially feline viral rhinotracheitis. The presence of stomatitis may indicate FCV. Specific tests include virus culture, immunohistochemical staining, and serum specific antibody titers.

Natural immunity from maternal antibodies lasts in the kitten from three to nine weeks. After that kittens are susceptible to FCV. Previous infection does not guarantee lifelong immunity, since an antigenically dissimilar FCV (such as VS-FCV) can cause infection. However, usually after the age of three years, FCV infections are mild or asymptomatic. FCV vaccination will not always prevent disease, but can reduce the severity. FCV vaccines come in two types, inactivated (ATCvet code: QI06AA07) and attenuated (live, but not virulent; in various combination vaccines).

They have been shown to be effective for at least three years. The only vaccine licensed for prevention of VS-FCV is Calici Vax, manufactured by Fort Dodge Animal Health, a division of Wyeth. It also contains a strain of the traditional FCV virus. Since VS-FCV has arisen from variant strains of FCV, it is not certain that a vaccine for one virulent strain will protect against all virulent strains.

Our test for feline calici virus is an indirect fluorescent antibody (IFA) procedure that is carried out on Teflon matted glass slides with calici virus (Black Strain 1984) infected cells fixed to their surface. This method requires the use of diluted patient serum being placed on the slide and incubated for 30-minutes at which time the slide is washed and a fluorescein conjugated anti-cat globulin is placed on the slide. If any antibodies to FCV are present in the patient serum they will combine with the FCV antigen fixed to the slide surface. The fluorescent antibody conjugate will then be bound to the FCV antibodies and the resulting antibody-conjugate complex viewed with an ultraviolet microscope are seen as bright areas of fluorescence in the infected cells. The total number of infected cells on our slides does not exceed 40% which leaves the negative cells to enhance contrast. After vaccination IFA titers of 1:25 correlate with protective levels of antibody.