FCV is often a problem in cat shelters. Management to limit or even prevent virus transmission is as important as vaccination in control. Shelter design and management should be aimed at avoiding cross infection of cats. Cats should be housed individually unless they are known to originate from the same household. Dogs and cats should be housed separately, and flea control should be implemented to minimise the risk of transmission of FCV and other diseases.If acute respiratory disease occurs in a shelter, identification of the agent involved (with differentiation of FCV from FHV-1, Chlamydia felis, Bordetella bronchiseptica, and Mycoplasma spp.) may be useful in deciding on the appropriate preventative measures. In case of an FCV outbreak, it should be considered that FCV can persist in the environment for about one month and is resistant to many common disinfectants. Effective substances include sodium hypochlorite (5% bleach diluted at 1:32), potassium peroxy-monosulfate, chlorine dioxide and commercial products that have been approved for their virucidal activity.New healthy cats should be vaccinated as soon as possible. Modified live virus vaccines are preferred in shelters because of the earlier onset of protection.
The pathogenesis of virulent systemic disease caused by FCV (VS-FCV) differs considerably from the typical picture described above. These strains cause widespread vasculitis, multi-organ involvement and death in up to two thirds of the infected cats (Pedersen et al., 2000; Hurley & Sykes, 2003; Schorr-Evans et al., 2003; Coyne et al., 2006b). The pathogenesis of VS-FCV infection is unknown and may include viral evolution and/or immune-mediated components as well as environmental and management factors (Hurley, 2006). Recently, these virulent strains have been shown to grow more rapidly in cell culture (Ossiboff et al., 2007). Following recovery from acute disease, most cats do not clear the infection for around 30 days; a minority sheds virus for much longer, possibly for life. In these healthy FCV carriers, virus can be localised in the epithelium of the tonsils. However, tonsillectomy does not eliminate the carrier state, suggesting the virus is also located in other sites. It is believed that evolution of the variable capsid protein allows FCV to escape the host immune response and to persist in carrier cats (Johnson, 1992; Kreutz et al., 1998; Radford et al., 1998; Coyne et al., 2007).
Because of the similarity of FCV to norovirus, a common cause of gastroenteritis in humans, FCV has been used as a surrogate for it in research. For instance, studies have been done on the survival of FCV in foodstuffs, the effectiveness of handwashing on FCV removal, and the use of ozone gas to inactivate FCV found in hotel rooms, cruise ship cabins, and healthcare facilities. It is also used in general Caliciviridae research due to its being one of the few of that group of viruses that grows well in vitro.
Feline calicivirus infection is a common respiratory disease in cats. The virus attacks the respiratory tract — lungs and nasal passages — the mouth, with ulceration of the tongue, the intestines, and the musculoskeletal system. It is highly communicable in unvaccinated cats, and is commonly seen in multicat facilities, shelters, poorly ventilated households, and breeding catteries. While vaccination against the calicivirus is strongly advised, vaccinations have failed to decrease the prevalence of the disease. This infection can occur in cat of any age, but young kittens older than six weeks have been found to be most susceptible. Symptoms and Types The following symptoms typically present themselves suddenly: Loss of appetite (anorexia) Eye discharge Nasal discharge Development of ulcers on tongue, hard palate, tip of nose, lips or around claws Pneumonia Difficult breathing after development of pneumonia Arthritis (inflammation of joints) Lameness Painful walk Fever Bleeding from various sites Cause Cats typically acquire feline calcivirus (FCV) after coming into contact with other infected cats, such as in a shelter, cattery, or boarding facility. But because FCV is resistant to disinfectants, cats may come into contact with the virus in almost any environment. Lack of vaccination or improper vaccination is thought be an important risk factor, as well as a lowered immune response due to pre-existing infections or diseases. Diagnosis You will need to give your veterinarian a thorough history of your cat's health, onset of symptoms, and possible incidents or conditions that might have led to this condition. Your veterinarian will perform a thorough physical exam to evaluate all body systems along with the overall health of your cat. A complete blood profile will also be conducted, including a chemical blood profile, a complete blood count, and a urinalysis. The results of these tests, however, are often non-specific and do not provide consistent findings for an initial diagnosis. The more reliable diagnostic test involves identifying a buildup of FCV antibodies. These antibody tests can be used to detect and measure the levels of feline calcivirus antigen and/or antibodies corresponding to the viral antigen (feline calcivirus). A more advanced test that may be used involves growing the isolated viruses under controlled conditions using a technique called cell culture. Diagnostic imaging can be used to determine any damage to the lungs; chest X-rays may show changes in the lung tissue, including consolidation of lung tissue in cats with pneumonia. 1 2 Next prognosisThe prediction of a disease’s outcome in advance urinalysisAn in-depth examination of the properties of urine; used to determine the presence or absence of illness malnutritionA condition of poor health that results from poor feeding or no feeding at all arthritisA medical condition in which the joints become inflamed and causes a great deal of pain. antigenAny substance or item that the body of an animal would regard as strange or unwanted; a foreign disease or virus in the body (toxin, etc.) antibodyA protein in the body that is designed to fight disease; antibodies are brought on by the presence of certain antigens in the system.
Quarantine is best for control of FCV in catteries and kennels. However, FCV is very contagious, and latently infected cats will continue to shed viruses, so complete control is difficult. An outbreak of VS-FCV at a humane society in Missouri in 2007 led to the euthanasia of the entire cat population (almost 200 cats) to contain it. FCV may survive several days to weeks in a dry environment and longer in a cooler, wet environment. Quaternary ammonium compounds are not thought to be completely effective, but a 1:32 dilution of household bleach used with a detergent and sufficient contact time does seem to kill the virus.
FCV infection is ubiquitous and may induce severe disease. ABCD therefore recommends that all healthy cats should be vaccinated against FCV. Although vaccination provides good protection against acute oral and upper respiratory tract disease in most cases, it does not prevent cats from becoming infected and from shedding FCV afterwards (Radford et al., 2006). In addition, there is currently no vaccine available that protects equally well against all FCV field strains.
FeLV-infected cats should be kept indoors and isolated, to avoid exposure to FCV, but also to diminish the likelihood of retrovirus transmission to other cats. Asymptomatic FeLV-infected cats should be vaccinated against FCV. Although there is no evidence that FeLV-infected cats are at increased risk of vaccine-induced disease from residual virulence of modified-life virus vaccines, killed vaccines are preferable. FeLV-infected cats may not mount adequate immune responses to rabies vaccines and perhaps neither to other vaccines. Protection of FeLV-infected cats may therefore not be comparable to that achieved in uninfected cats, and more frequent vaccination should be considered.
One very virulent strain of FCV, referred to as “Virulent Systemic Feline Calicivirus” or VS-FCV, causes severe generalized disease. With this strain of FCV, the initial symptoms involve the eyes, nose and mouth, but the infected cat quickly develops a high fever, severe depression, edema of the legs and/or face, jaundice, and symptoms of multiple organ disease. The VS-FCV strain is highly infectious, and the mortality rate is reportedly up to 67%. Fortunately, this particular strain of disease is very rare, with only a handful of outbreaks reported in the US since 1998.
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 related to the relative virulence of different strains of the virus.
Most antivirals used in veterinary medicine only inhibit replication of DNA viruses or retroviruses, and treatment of FCV infections has not entered clinical practice. Ribavirin is one of the few antiviral agents able to inhibit FCV replication in vitro. However, it appears to be very toxic to cats and side effects have precluded its systemic use (Povey, 1978; EBM grade III).Feline interferon-ω (licensed for the treatment of canine parvovirus and feline leukaemia virus infections in some European countries) has been shown to inhibit FCV replication in vitro (Fulton & Burge, 1985; Mochizuki et al., 1994, Taira et al., 2005; EBM grade IV). Controlled field studies, however, are not available. There is some suggestion that strains may vary in their sensitivity to interferon (Ohe et al 2008).