Cats and Calicivirus Infection--The Evolving Pattern of Disease
World Small Animal Veterinary Association World Congress Proceedings, 2006
Alan Radford1; Karen P. Coyne; Susan Dawson; Carol J. Porter; Rosalind M. Gaskell2
1Senior Lecturer in Small Animal Studies and 2Professor, University of Liverpool Veterinary Teaching Hospital, Leahurst
Neston, S. Wirral, UK


Feline calicivirus (FCV) is a highly infectious pathogen of cats with a widespread distribution. The virus typically causes moderate, self-limiting acute upper respiratory tract disease. However, some strains induce lameness and recently, more virulent strains have evolved, particularly in the USA. The prevalence of FCV is likely to be broadly proportional to the number of cats in the household (2,3,11,26). Privately owned pet cats kept in small numbers have relatively low prevalence (~10%). In contrast, cats living in colonies or at shelters have a higher chance of being infected (1,12,22). Indeed, in some colonies we have found prevalence values of 50-90% over prolonged periods of time (4,21).

The virus belongs to the Caliciviridae, a family of RNA viruses which includes important pathogens of man (noroviruses and sapoviruses; together the commonest causes of infectious gastroenteritis in people) and animals including the vesiviruses (e.g., FCV, canine calicivirus) and the lagoviruses (rabbit haemorrhagic disease virus and European brown hare syndrome virus) (10).

Having an RNA genome, we should expect FCV to have a high degree of genomic plasticity. This is a reflection of the lack of proofreading and associated low fidelity generally attributable to viral RNA-dependent RNA polymerases (7). This mechanism for error-prone replication should afford FCV great adaptability and allow it to exploit new environmental niches. Specific current problems associated with FCV that are a reflection of this include the difficulty of choosing representative strains for inclusion in vaccines, the presence of persistently infected cats, and the emergence of hypervirulent strains of FCV.


Clinical Signs

Oral and respiratory disease. Due to the large number of different strains of FCV, a range of clinical signs may be seen. The most consistent signs are relatively mild and include oral ulceration and ocular and nasal discharge. Occasionally, inapparent infections or pneumonia may also be seen. Rarely, and usually in young kittens, the more severe respiratory infections can be fatal (15,16).

Lameness. Calicivirus strains can also cause an acute febrile lameness syndrome, associated with acute synovitis and an increase in quantity of synovial fluid (6,19). It has been suggested that lameness and oral / respiratory disease represent two extremes of a clinical continuum, with some individual strains tending to either extreme, and the majority of strains being able to induce both of these clinical signs (25).

Virulent systemic disease. More recently and more worryingly, highly virulent strains of FCV have emerged, that are associated with outbreaks of disease with high mortality termed FCV-associated virulent systemic disease (VSD--previously haemorrhagic-like fever) (13,14,18,20,23). As well as upper respiratory tract disease, affected cats show to varying degrees pyrexia, cutaneous oedema, ulcerative dermatitis, anorexia and jaundice, with up to 50% of cats dying or being euthanased in extremis. Adult cats are frequently affected more severely than kittens, and worryingly, field vaccination does not appear to be protective. Outbreaks start quickly, generally effect less than 100 animals and disappear rapidly.

So far, FCV-associated VSD has mainly been reported in the USA. In the UK, one outbreak in 2003 has been described affecting a group of five cats in two households (5). In addition, the authors are aware of two outbreaks in France (personal communication H Poulet) and it is possible that considerably more outbreaks occur than have been reported.

Lesions are widespread and include subcutaneous oedema, ulceration of the mouth, and variable levels of ulceration of the skin particularly on the pinnae and pawpads and nares (18). Other lesions are more variable and include bronchointerstitial pneumonia and necrosis in the liver, spleen and pancreas.

VSD has been reproduced experimentally, strongly supporting a role for FCV in this disease (18), and suggesting that mutations within the viral genome may be responsible for the highly virulent phenotype. So far, the FCV strains from each reported outbreak of VSD have been genetically distinct from each other. Therefore, if viral mutations are required to cause the hyper-virulent phenotype, then they must evolve independently in each outbreak. To date, no consistent genetic motif has been reported within the available capsid sequences to differentiate FCV isolates associated with VSD from those associated with more typical FCV-associated disease. This makes diagnosis of VSD difficult.

Most outbreaks of VSD have been associated with the introduction of cats from large rescue colonies into another population (14). It is possible that the high levels of replication of normal FCV strains in large groups of cats such as rescue shelters may provide the required conditions necessary for the independent emergence of these hypervirulent strains. We have recently shown that virus replication in endemically infected colonies of cats is associated with markedly higher levels of biodiversity than those normally seen within a single strain of FCV (4, 21).

Diagnosing FCV-associated VSD in the cat remains somewhat of a conundrum since there are no unique clinical or laboratory markers for the disease. The authors are frequently asked about individual cats with suspicious signs, some of which are also FCV positive. Such individual cats must be treated carefully, but whether these represent actual sporadic cases of VSD is unknown. The index of suspicion for VSD increases dramatically when two or more cats present with the same clinical signs. However, until a marker of virulence is identified, definitive diagnosis will remain difficult.

Crucial to the control of suspect outbreaks is early recognition / suspicion and prompt rigorous biosecurity. It is very important that owners and staff are all aware of the disease and what it looks like. This includes veterinary surgeons at neighbouring practices who may see other cases from the same outbreak. Specific measures must include contact tracing and quarantining of all suspect cats. Actual and suspect cases are perhaps best managed away from the veterinary hospital. However, where cases must be hospitalised, they must be kept in strict isolation and barrier nursed. All staff should be made aware of the case, and those who don't own cats should preferably be involved in the treatment of the affected animal.

The virus is generally considered to survive for up to two weeks in the environment and therefore can be transmitted by direct contact and fomites, and possibly by aerosol. Affected cats are likely to shed virus from their respiratory and oral secretions, but any discharge from skin may also be highly infectious. FCV has also been isolated from faeces and urine. Areas where the cat has been and any equipment require disinfection using a product that has been shown to be effective against FCV. Quaternary ammonium compounds are generally not thought to be completely effective (8,9,13,17). However, a 1:32 dilution of household bleach with some household detergent does seem to be effective providing contact time is sufficient (24). With these measures, all outbreaks seem to have been successfully managed. Whether the end of each outbreak is entirely attributable to disease control measures or includes a cat behavioural and / or virus evolutionary component, remains to be determined.


FCV has been recognised as an important pathogen of cats for over 40 years now. As an RNA pathogen, it seems to rely on evolution to maintain itself in the population. Where the virus came from we do not know. Today we struggle with newly emerged virulent strains and have a clear need to improve the cross-protection offered by our vaccines. What is certainly true is that FCV is still changing. We must expect the clinical features of this virus to change and accordingly, our attempts to control it will need to be continually updated. Sounds interesting.


1.  Bannasch MJ, Foley JE (2005). Epidemiologic evaluation of multiple respiratory pathogens in cats in animal shelters. J Feline Med Surg, 7: 109-19.

2.  Binns SH, Dawson S, Speakman AJ, Cuevas LE, Hart CA, Gaskell CJ, Morgan KL, Gaskell RM (2000). A study of feline URTD with reference to prevalence and risk factors for infection with FCV and feline herpesvirus. J Feline Med Surg, 2: 123-33.

3.  Coutts AJ, Dawson S, Willoughby K, Gaskell RM (1994). Isolation of feline respiratory viruses from clinically healthy cats at UK cat shows. Vet Rec, 135: 555-556.

4.  Coyne KP, Dawson S, Radford AD, Cripps PJ, Porter CJ, McCracken CM, Gaskell RM (2006). Long term analysis of FCV prevalence and viral shedding patterns in naturally infected colonies of domestic cats. Vet Microbiol, in press.

5.  Coyne KP, Jones BR, Kipar A, Chantrey J, et al (2006). Lethal outbreak of disease associated with FCV infection in cats. Vet Rec, 158: 544-50.

6.  Dawson S, Bennett D, Carter S, Bennett M, et al. (1994). Acute arthritis of cats associated with FCV infection. Res Vet Sci, 56: 133-143.

7.  Domingo E, Menendez L, Holland J (1997). RNA virus fitness. Rev Med Virol, 7: 87-96.

8.  Doultree JC, Druce JD, Birch CJ, Bowden DS, Marshall JA (1999). Inactivation of FCV, a Norwalk virus surrogate. J Hosp Infect, 41: 51-7.

9.  Eleraky NZ, Potgieter LN, Kennedy MA (2002). Virucidal efficacy of four new disinfectants. J Am Anim Hosp Assoc, 38: 231-4.

10. Green K, Ando T, Balayan M, Berke T, Clarke I, et al (2000). Taxonomy of the caliciviruses. J Infect Dis, 181 Suppl 2: S322-30.

11. Harbour DA, Howard PE, Gaskell RM (1991). Isolation of FCV and feline herpesvirus from domestic cats 1980 to 1989. Vet Rec, 128: 77-80.

12. Helps CR, Lait P, Damhuis A, Bjornehammar U, Bolta D, Brovida C, Chabanne L, Egberink H, Ferrand G, Fontbonne A, Pennisi MG, Gruffydd-Jones T, Gunn-Moore D, Hartmann K, Lutz H, Malandain E, Mostl K, Stengel C, Harbour DA, Graat EA (2005). Factors associated with upper respiratory tract disease caused by feline herpesvirus, FCV, Chlamydophila felis and Bordetella bronchiseptica in cats: experience from 218 European catteries. Vet Rec, 156: 669-73.

13. Hurley KE, Pesavento PA, Pedersen NC, Poland AM, Wilson E, Foley JE (2004). An outbreak of virulent systemic FCV disease. J Am Vet Med Assoc, 224: 241-9.

14. Hurley KF, Sykes JE (2003). Update on FCV: new trends. Veterinary Clinics of North America: Small Animal Practice, 33: 759-772.

15. Kahn DE, Gillespie JH (1971). Feline viruses: Pathogenesis of picornavirus infection in the cat. Am J Vet Res, 32: 521-531.

16. Love DN, Baker KD (1972). Sudden death in kittens associated with a feline picornavirus. Aus Vet J, 48: 643.

17. Marks PJ, Vipond I, Carlisle D, Deakin D, Fey RE, Caul EO (2000). Evidence for airborne transmission of Norwalk-like virus in a hotel restaurant. Epidem Infect, 124: 481-7.

18. Pedersen NC, Elliott JB, Glasgow A, Poland A, Keel K (2000). An isolated epizootic of hemorrhagic-like fever in cats caused by a novel and highly virulent strain of FCV. Vet Microbiol, 73: 281-300.

19. Pedersen NC, Laliberte L, Ekman S (1983). A transient febrile "limping" syndrome of kittens caused by two different strains of FCV. Feline Practice, 13: 26-35.

20. Pesavento PA, MacLachlan NJ, Dillard-Telm L, Grant CK, Hurley KF (2004). Pathologic, immunohistochemical, and electron microscopic findings in naturally occurring virulent systemic FCV infection in cats. Vet Pathol, 41: 257-63.

21. Radford AD, Dawson S, Ryvar R, Coyne K, Johnson DR, Cox MB, Acke EF, Addie DD, Gaskell RM (2003). High genetic diversity of the immunodominant region of the feline calicivirus capsid gene in endemically infected cat colonies. Virus Genes, 27: 145-55.

22. Radford AD, Sommerville LM, Dawson S, Kerins AM, Ryvar R, Gaskell RM (2001). Molecular analysis of isolates of feline calicivirus from a population of cats in a rescue shelter. Vet Rec, 149: 477-481.

23. Schorr-Evans EM, Poland A, Pedersen NC (2003). An epizootic of highly virulent feline calicivirus disease in a hospital setting in New England. J Fel Med Surg, 5: 217-226.

24. Scott FW (1980). Virucidal disinfectants and feline viruses. Am J Vet Res, 41: 410-414.

25. TerWee T, Lauritzen A, Sabara M, Dreier KJ, Kokjohn K (1997). Comparison of the primary signs induced by experimental exposure to either a pneumotrophic or a 'limping' strain of feline calicivirus. Vet Microbiol, 56: 33-45.

26. Wardley RC, Gaskell RM, Povey RC (1974). Feline respiratory viruses--their prevalence in clinically healthy cats. JSAP, 15: 579-586.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Karen P. Coyne
University of Liverpool
Veterinary Teaching Hospital
Neston S Wirral, United Kingdom

Susan Dawson
University of Liverpool
Veterinary Teaching Hospital
Neston S Wirral, United Kingdom

Rosalind M. Gaskell
University of Liverpool
Veterinary Teaching Hospital
Neston S Wirral, United Kingdom

Carol J. Porter
University of Liverpool
Veterinary Teaching Hospital
Neston S Wirral, United Kingdom

Alan Radford
University of Liverpool
Veterinary Teaching Hospital
Neston S Wirral, United Kingdom

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