Feline Calicivirus (FCV) is an important and common cause of Upper Respiratory Infection (URD) and oral disease in cats. This virus occurs worldwide with various strains that vary greatly in virulence (the ability to produce disease). Clinical disease may vary from subclinical (not clinically apparent) to combinations of oral, respiratory disease, and lameness. There are more than 40 strains of FCV, one of which may have high mortality rates and is referred to as the virulent systemic (VS), or the hemorrhagic form of FCV. Thankfully, the hemorrhagic form of FCV is rare with only six reported outbreaks since 1998 in the United States. When encountered, the hemorrhagic form of FCV causes sloughing of the skin, subcutaneous edema, and high mortality rates of up to 60%. Domestic as well as exotic species of felines are affected by this virus.

Transmission is mainly by direct cat-to-cat contact, but indirect transmission is possible by a contaminated environment or objects. Calicivirus may also be carried by a contaminated handler to a susceptible cat. The virus is shed in nasal, ocular, and oral secretions. It is thought that fecal and urinary shedding of virus may occur, but it is not a major source of infection. The virus may survive up to one week in a contaminated environment. Aerosol transmission is not a major factor in disease dissemination but may transmit the virus a couple of meters. Infected cats usually shed virus for 2 to 3 weeks, however carrier cats may shed virus for months to years - even lifelong shedding may occur. It is estimated that from 20 to 30% of cats in the general population may be shedding FCV at any point in time.

Cats in groups appear to be more commonly affected, including cats being boarded, in shelters, and in catteries, probably a secondary reaction to stress. All age groups are susceptible to calicivirus but young kittens seem to be more severely affected except for the VS-FCV strain which affects adults more severely. Reinfection commonly occurs.

The VS-FCV exclusively occurs in populations of group-housed cats, especially shelter and rescue catteries. This mutation is believed to occur spontaneously from caliciviruses already circulating in that particular group of cats.

The incubation period (time from infection untill clinical signs of disease are seen) is 2-6 days for calicivirus or 1 to 5 days with the hemorrhagic form of the virus.

Calicivirus appears to have a predilection for the epithelium of the oral cavity and deep tissues of the lung (lower respiratory tract). Clinical signs include salivation, ulceration of the tongue, hard palate, or nostril, gingivitis, fever, inappetance, and depression. Serous nasal discharge and conjunctivitis may occur but are more commonly seen with Feline Viral Rhinotracheitis Virus (FVRV). In severe cases, difficulty breathing caused by pneumonia and pulmonary edema is seen. FCV is also associated with chronic
stomatitis (infection of the mouth) but the precise role of the virus in this syndrome is not totally clear. Two strains of Calicivirus may produce a transient “limping syndrome”. When lameness occurs it is usually not accompanied by the typical clinical signs of ulceration or pneumonia characteristically associated with FCV. These strains produce a transient fever with alternating leg lameness. Pain will be exhibited on palpation of affected joints. Lameness typically occurs in 8 to 12 week-old kittens and usually resolves without treatment.

Treatment is largely supportive. Antibiotics are used against secondary bacterial invaders and subsequent pneumonia. Antihistamines may help with congestion while ophthalmic ointments are used when conjunctivitis is present. Oxygen and nebulization may be necessary in severe cases of pneumonia. Fluid therapy should be used to correct dehydration. Force-feeding may be necessary, especially with severe oral ulceration. Recovery is typically uneventful, except with the VS-FCV, where high mortality rates occur. Death in these cases is caused by systemic vasculitis with disseminated intravascular coagulation ending in multiple organ and system failure.

A presumptive diagnosis is based on the presence of typical clinical signs. Diagnosis may be confirmed by virus isolation from oral, throat, nasal, or conjunctival swabs.

FCV is easily inactivated in the environment through the use of a dilute hypochlorite solution (1 part clorox to 40 parts water), and most disinfectants and detergent mixtures are typically effective against the virus. Infected cats should be treated only under strict isolation procedures.

Several strains of FCV are used in commercial vaccines. Not every strain will be neutralized by every vaccine. It is also thought that the FCV strains may be continually changing. Current evidence suggests that multivalent FCV vaccines may increase the proportion of strains that may be inactivated by vaccination. Modified-live, inactivated and intranasal vaccines are available. Injectable vaccines are reasonably effective against disease but do not prevent the carrier state. Clinical signs of upper respiratory disease, especially sneezing, are commonly seen following intranasal vaccination. There is currently one killed, adjuvanted vaccine available for the VS-FCV with several others under development. The risk of VS-FCV infection is low at this time, therefore vaccination of household pets with this variant is not currently recommended.

The Feline Advisory Panel considers FCV a core vaccine. In kittens, an initial series of vaccinations should begin at 6 weeks of age and be repeated every 3 weeks until the patient reaches 16 weeks of age. All cats should be vaccinated one year later and then revaccinated every 1 to 3 years according to the manufacturer’s recommendations and the potential for exposure to the virus. Cats placed in known high-risk situations such as boarding, grooming, cat shows, catteries, outdoor life, and shelters should be vaccinated shortly before those risks are likely to be encountered. In high risk shelters intranasal injection may be preferable for the rapid onset of protection (2 to 6 days).

Dr. Janet Foley at the school of veterinary medicine at the University of California at Davis is currently conducting an ongoing investigation of VS-FCV and may be contacted for recommendations regarding sample submissions in order to obtain definitive diagnosis. She may be contacted at 530/754-7355 or at (jefoley@ucdavis.edu).


References:


Ettinger, Stephen, DVM and Edward C. Feldman DVM. Textbook of Veterinary Internal Medicine. 6th Edition 2005, Elsevier, Inc. pp.667 – 669.

Kahn, Cynthia, Editor. The Merck Veterinary Manual. Merck Co. 9th Edition. 2005. Pp.1238 – 1240.

Wolf, Alice. “Adverse Vaccine Events and Update on Feline Calicivirus”. NAVC/WVC Proceedings 2008. Merial Vaccine Symposium. Pp. 5-7.

The 2006 American Association of Feline Practitioners Feline Vaccine Advisory Panel Report. Journal of the American Veterinary Medical Association, Vol 229, No. 9, November 1, 2006.