Feline calicivirus (FCV), a non-enveloped, positive-sense, and single-stranded RNA virus, is one of the two feline viral diseases (including FHV-1) responsible for the disease ‘Cat Flu.’ The two virus can infect separately or together. The incidence of calicivirus is believed to be lower than FHV although the clinical symptoms are often confused. The presence of the virus does not necessarily lead to disease. Caliciviruses are among the most common problematic infectious agents of cats, with extraordinarily high rates of infectivity, morbidity and death. Although vaccination against caliciviruses is practised commonly, these vaccines have incomplete efficacy and can contribute to minor morbidity. Caliciviruses are responsible for diseases ranging from acute nuisances and cattery problems to chronic debilitating problems to peracute fatal emerging problems.
At least six different outbreaks of similar disease characterized by high mortality have since been recognized in the United States, but the lesions have not previously been described in detail.
Caliciviruses appear to have a predilection for the epithelium of the oral cavity and the deep tissues of the lungs. Some caliciviruses are non-pathogenic. Some induce little more than salivation and ulceration of the tongue, hard palate, or nostrils; others produce respiratory disease such as pulmonary oedema and interstitial pneumonia. Clinically, it is often impossible to differentiate FHV from FCV infection. Two strains may produce a transient “limping syndrome” without signs of oral ulceration or pneumonia. These strains produce a transient fever, alternating leg lameness, and pain on palpation of affected joints. Signs occur most often in 8- to 12-wk-old kittens and usually resolve without treatment. The syndrome may occur in kittens vaccinated against FCV because no vaccine protects against both of the strains that produce the “limping syndrome.” Serous rhinitis and conjunctivitis also can occur.
Acutely affected cats often develop fever, conjunctivitis, rhinitis (although both conjunctivitis and rhinitis are more typical of FHV infection than FCV), and vesicular stomatitis, including glossitis, faucitis and palatitis. Vesicles rupture within hours or days; therefore observation of small inflamed, painful erosions is more typical.
About 25% of FCV-infected cats develop chronic infection, whereas as many as 50% appear to shed virus chronically after infection. Some of the variance in clinical severity could be due to genetic differences in the infecting viruses, in addition to the individual cat’s immune system’s response to infection. In all endemically infected populations of cats, the FCV isolates exhibit a large amount of genetic variation, often with some isolates that cluster genetically with the vaccine strain.
A number of clinical forms of FCV can present, including:
- Respiratory tract infection – FCV infection commonly causes an upper respiratory infection in cats. Following infection of nasal and oral mucosa via aerosol, a viremia ensues and the virus begins to be shed from nasal and oral orifices for approximately 2 weeks afterwards and, commonly in catteries and shelters, for months. Concurrently, cats develop lymphopenia and neutropenia.
- Virulent systemic disease (FCV-VSD)
- Even more severe disease may occur in cats that have experienced chronic, high-titre FCV infection. These cats can develop progressive immune complex-mediated glomerulonephritis, with chronic renal disease characterised by high urine protein concentrations and high urine protein:creatinine ratios. Many cases occur exclusively in overcrowded, multicat households with marginal management (August, 2006).
Diagnosis of FCV is based on primarily based on clinical signs, which include ocular and nasal exudates, conjunctivitis, oral ulcers and stomatitis, and varying degrees of upper respiratory distress. In virulent systemic disease (FCV-VSD), facial and limb oedema and ulcerative dermatitis may also be seen, in conjunction with respiratory distress.
Exclusion of FHV (most common differential) and isolation of FCV virus using reverse transcriptase PCR (now commercially available worldwide at relatively low costs).
Kittens born to vaccinated Queens have minimal protection against the virus due to the rapid genetic mutations which occur within caliciviruses. As cats mature to 3 years of age, some innate immunity develops and helps improvement in clinical signs. Vaccination for FCV does not prevent infection consistently, although in many instances, the vaccine mitigates signs of severe disease. Vaccines can also stimulate oral shedding of vaccine-strain virus.
Broad-spectrum antibiotics are the normal medical treatment and supportive therapy such as mucolytic agents, good food supplements. Lysine is not useful as it is with FHV infection. Cats that develop chronic LPS gingivitis or glomerulonephritis require more aggressive therapy with acyclovir or other antiviral medications. The prognosis in these cases is guarded.
Quarantine is useful to isolate infected cats and thus minimise spread of the disease. Breeding from chronically infected cats is not recommended.
Vaccinations using core vaccines have shown the highest efficacy at preventing disease when given at 8 and 12 weeks of age, although vaccination offers, at best, a 75% protection from this genetically-mutable virus (August, 2006).
- ↑ Dean, R (2005) Feline calicivirus – a new clinical syndrome. The Feline Centre, University of Bristol
- ↑ Poulet H, Brunet S, Soulier M, Leroy V, Goutebroze S, Chappuis G (2000) Comparison between acute oral/respiratory and chronic stomatitis/gingivitis isolates of feline calicivirus: pathogenicity, antigenic profile and cross-neutralisation studies. Arch Virol 145:243-261
- ↑ Coyne KP, Gaskell RM, Dawson S, Porter CJ, Radford AD. (2007) Evolutionary mechanisms of persistence and diversification of a calicivirus within endemically infected natural host populations. Journal of Virology 81(4):1961-71
- ↑ August, JR (2006) Consultations in feline internal medicine. Vol 5. Elsevier Saunders, USA
- ↑ Gavier-Widen D: Morphologic and immunohistochemical characterization of the hepatic lesions associated with European brown hare syndrome. Vet Pathol 31:327-334, 1994
- ↑ Geissler K, Schneider K, Platzer G, Truyen B, Kaaden OR, Truyen U (1997) Genetic and antigenic heterogeneity among feline calicivirus isolates from distinct disease manifestations. Virus Res 48:193-206
- ↑ Reubel GH, Hoffmann DE, Pedersen NC (1992) Acute and chronic faucitis of domestic cats. A feline calicivirus-induced disease. Vet Clin North Am Small Anim Pract 22:1347-1360
- ↑ Hoover EA, Kahn DE (1975) Experimentally induced feline calicivirus infection: clinical signs and lesions. J Am Vet Med Assoc 166:463-468, 1975
- ↑ Bennett, D, Gaskell, RM., Mills, A et al (1989) Detection of feline calicivirus antigens in the joints of infected cats. Vet Rec 124:329-332
- ↑ Wardley, RC & Povey, RC (1977) The clinical disease and patterns of excretion associated with three different strains of feline caliciviruses. Res Vet Sci 23:7-14
- ↑ Radford, AD et al (1998) Quasispecies evolution of a hypervariable region of feline calicivirus capsid gene in cell culture and in persistently infected cats. J Gen Virol 79:1-10
- ↑ Reubel GH et al (1994) Effect of chronic feline immunodeficiency virus infection on experimental feline calicivirus-induced disease. Vet Microbiol 39:335-351
- ↑ Orr, CM, Gaskell, CJ & Gaskell, RM (1978) Interaction of a combined feline viral rhinotracheitis-feline calicivirus vaccine and the FVR carrier state. Vet Rec 103:200-202
- ↑ Pedersen, NC & Hawkins, KF. (1995) Mechanisms for persistence of acute and chronic feline calicivirus infections in the face of vaccination. Vet Microbiol 47:141-156
- ↑ Gore TC, Lakshmanan N, Williams JR, Jirjis FF, Chester ST, Duncan KL, Coyne MJ, Lum MA, Sterner FJ. (2006) Three-year duration of immunity in cats following vaccination against feline rhinotracheitis virus, feline calicivirus, and feline panleukopenia virus. Vet Ther 7(3):213-22