Feline calicivirus
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| Electron micrograph of FCV Electron micrograph of FCV
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Feline calicivirus (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 herpesvirus. FCV can be isolated from about 50 percent of cats with upper respiratory infection.[1] Cheetahs are the other species of the family Felidae known to become infected naturally.[1]
The virus
There are different strains of FCV that vary in virulence. 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 allows for the development of more virulent strains.[2] In persistently infected cats, it has been shown that the gene for the major structural protein of the viral capsid evolves through immune-mediated positive selection and allows the virus to escape detection by the immune system.[3]
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 a calicivirus). This virus has been called virulent systemic feline calicivirus (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. It seems that strains of VS-FCV have risen independently of one another since first being described, meaning that not all cases of VS-FCV have spread from a single case.[4] Most of the outbreaks of VS-FCV have been reported in the United States.[2] It was originally described in 1998 in Northern California.[5]
The prevalence of FCV varies depending on the environment. In private households, FCV is present in about 10 percent of cats (either in active or carrier state), while the prevalence in shelters or catteries is 25 to 40 percent.[2]
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.[6] Following this period, infected cats never shed the virus again or become latently infected and shed the virus continuously or intermittently.[7] Coinfection with either feline herpesvirus or feline immunodeficiency virus causes a more severe disease.
Symptoms
Symptoms in cats infected with FCV may develop acutely, chronically, or not at all. Latent or subclinical infections often become symptomatic when the cat is stressed, such as at the time of adoption. Acute symptoms 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 symptoms, 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 symptoms in individual cases of FCV is related 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 percent.[6] Initial symptoms include discharge from the eyes and nose, ulceration in the mouth, anorexia, and lethargy, and occur in the first one to five days.[8] Later symptoms include fever, edema of the limbs and face, jaundice, and multiple organ dysfunction syndrome.
Diagnosis of FCV is difficult without specific tests because the symptoms are similar to other feline respiratory diseases, especially feline viral rhinotracheitis. The presence of stomatitis may indicate FCV. Specific tests include virus culture, polymerase chain reaction (PCR), and immunohistochemical staining.
Treatment and prevention
There is no specific treatment for FCV. Antibiotics are used for secondary bacterial infections. Nursing care and rehydration are used for dehydrated and anorexic cats. Corticosteroids or azathioprine may be used for polyarthritis. Stomatitis is very difficult to treat. Antibiotics, corticosteroids, and tooth extractions all have been used with varying success. Cats on corticosteroids must be monitored carefully for worsening of any upper respiratory infection.
Natural immunity from maternal antibodies lasts in the kitten from three to nine weeks.[6] 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.[6] FCV vaccination will not always prevent disease but will reduce the severity. FCV vaccines come in two types, attenuated (live, but not virulent) and inactivated. They have been shown to be effective for at least three years.[9] Attenuated FCV vaccine has been shown to possibly cause mild upper respiratory infection. Inactivated vaccine does not, but it causes more local inflammation and possibly predisposes the cat to vaccine-associated sarcoma.[6] The only vaccine licensed for prevention of VS-FCV is CaliciVax, manufactured by Fort Dodge Animal Health, a division of Wyeth. It also contains a strain of the traditional FCV virus.[5] 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.[10]
Quarantine is best for control of FCV in catteries and kennels. However, FCV is very contagious and latently infected cats will continue to shed virus, 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) in order to contain it.[11] 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.[2]
Use in research
Because of the similarity of FCV to Norovirus, a common cause of gastroenteritis in humans, FCV as been used as a surrogate for it in research. For instance, studies have been done on the survival of FCV in foodstuffs,[12] the effectiveness of handwashing on FCV removal,[13] and the use of ozone gas to inactivate FCV found in hotel rooms, cruise ship cabins, and healthcare facilities.[14] 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.[15]
Gallery
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![Electron micrograph reveals the morphologic traits exhibited by the feline calicivirus (FCV), a Caliciviridae family member. From Public Health Image Library (PHIL). [16]](/images/5/51/Caliciviridae09.jpeg)
Electron micrograph reveals the morphologic traits exhibited by the feline calicivirus (FCV), a Caliciviridae family member. From Public Health Image Library (PHIL). [16]
![Electron micrograph reveals the morphologic traits exhibited by the feline calicivirus (FCV), a Caliciviridae family member. From Public Health Image Library (PHIL). [16]](/index.php/File:Caliciviridae09.jpeg)
References
- ↑ 1.0 1.1 Fenner, Frank J.; Gibbs, E. Paul J.; Murphy, Frederick A.; Rott, Rudolph; Studdert, Michael J.; White, David O. (1993). Veterinary Virology (2nd ed.). Academic Press, Inc. ISBN 0-12-253056-X.
- ↑ 2.0 2.1 2.2 2.3 Radford A, Coyne K, Dawson S, Porter C, Gaskell R (2007). "Feline calicivirus". Vet Res. 38 (2): 319–35. PMID 17296159.
- ↑ Coyne K, Reed F, Porter C, Dawson S, Gaskell R, Radford A (2006). "Recombination of Feline calicivirus within an endemically infected cat colony". J Gen Virol. 87 (Pt 4): 921–6. PMID 16528041.
- ↑ Ossiboff R, Sheh A, Shotton J, Pesavento P, Parker J (2007). "Feline caliciviruses (FCVs) isolated from cats with virulent systemic disease possess in vitro phenotypes distinct from those of other FCV isolates". J Gen Virol. 88 (Pt 2): 506–17. PMID 17251569.
- ↑ 5.0 5.1 "CaliciVax updated to cover virulent systemic feline calicivirus". DVM. Advanstar Communications: 61. Feb. 2007. Check date values in:
|date=(help) - ↑ 6.0 6.1 6.2 6.3 6.4 Foley, Janet E. (2005). "Calicivirus: Spectrum of Disease". In August, John R. (ed.). Consultations in Feline Internal Medicine Vol. 5. Elsevier Saunders. ISBN 0-7216-0423-4.
- ↑ Coyne K, Dawson S, Radford A, Cripps P, Porter C, McCracken C, Gaskell R (2006). "Long-term analysis of feline calicivirus prevalence and viral shedding patterns in naturally infected colonies of domestic cats". Vet Microbiol. 118 (1–2): 12–25. PMID 16911860.
- ↑ Rosenthal, Marie (Feb. 2007). "VS-FCV may be more prevalent than previously thought". Veterinary Forum. Veterinary Learning Systems. 24 (2): 23. Check date values in:
|date=(help) - ↑ Gore T, Lakshmanan N, Williams J, Jirjis F, Chester S, Duncan K, Coyne M, Lum M, Sterner F (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. PMID 17039444.
- ↑ Hurley, Kate Frances (June 2007). "Facts about Feline Calicivirus". Clinician's Brief. North American Veterinary Conference. 5 (6): 30.
- ↑ "Humane Society has to put down facility's 200 felines afeter mass virus outbreak". DVM. Advanstar Communications: 20S. July 2007.
- ↑ Mattison K, Karthikeyan K, Abebe M, Malik N, Sattar S, Farber J, Bidawid S (2007). "Survival of calicivirus in foods and on surfaces: experiments with feline calicivirus as a surrogate for norovirus". J Food Prot. 70 (2): 500–3. PMID 17340890.
- ↑ Mori K, Hayashi Y, Noguchi Y, Kai A, Ohe K, Sakai S, Hara M, Morozumi S (2006). "[Effects of handwashing on Feline Calicivirus removal as Norovirus surrogate]". Kansenshogaku Zasshi. 80 (5): 496–500. PMID 17073262.
- ↑ Hudson J, Sharma M, Petric M (2007). "Inactivation of Norovirus by ozone gas in conditions relevant to healthcare". J Hosp Infect. PMID 17350729.
- ↑ Stuart A, Brown T (2006). "Entry of feline calicivirus is dependent on clathrin-mediated endocytosis and acidification in endosomes". J Virol. 80 (15): 7500–9. PMID 16840330.
- ↑ "Public Health Image Library (PHIL)".