Feline Calicivirus - Group Study Guide

(Answers below)

1. All of the following are considered routes of transmission of Feline Calicivirus EXCEPT:

    A. Direct contact with an infected cat.
    B. A person who has just handled an infected cat and as not washed their hands.
    C. Urine and feces of an infected cat.

    D. All of the above are routes of transmission of FCV.

2. The MOST characteristic clinical sign associated with Feline Calicivirus infection is:

    A. Diffuse interstitial pneumonia
    B. Nasal discharge

    C. Oral ulcerations

    D. Lameness

3. What is/are the best method(s) used to make a definitive FCV diagnosis?

    A. Serology
    B. Virus isolation or PCR
    C. Diagnosis based on clinical signs
    D. Treat and watch for improvement

4. What is the current treatment for diagnosed FCV cases?

    A. Symptomatic/supportive + broad spectrum antibiotics for secondary bacterial infections
    B. High dose glucocorticoids
    C. Ulcer debridement and antiseptic treatment
    D. No treatment, consider euthanasia

5. A kitten is seen at your clinic for respiratory symptoms and oral ulcers. What should be used to appropriately disinfect the surfaces and instruments it contacted?

    A. Isopropyl Alcohol
    B. Chlorhexidine
    C. Sodium hypochlorite (bleach)
    D. Quaternary Ammonium

6. Which statement regarding vaccination for feline calicivirus is incorrect?

    A. Modified-live vaccines should be boostered in 3-4 weeks for maximum protection.
    B. The first vaccine can be given as early as 4 weeks of age in high risk situations.
    C. Vaccination prevents infection with calicivirus, reduces severity of clinical signs, and decreases viral shedding.
    D. Intra-nasal vaccines have a shorter onset of immunity.

7. A soap and water solution is adequate to disinfect and prevent the spread of VS-FCV.

    A. True
    B. False

8. Vaccinated cats are guaranteed protection against VS-FCV.

    A. True
    B. False

9. Which of the following is true regarding VS-FCV?

    A. Isolation is unnecessary during an outbreak of VS-FCV since the disease is generally non-contagious
    B. Vaccination for traditional FCV will prevent infection with VS-FCV
    C. Patients with VS-FCV typically display a prolonged high fever
    D. Diagnosis is confirmed by ELISA

10. Which of the following is false regarding FCV and/or VS-FCV?

    A. The characteristic lesion of FCV is oral ulceration.
    B. Clinical signs of VS-FCV may include prolonged fever, facial and peripheral edema, alopecia, and ulceration of tongue, lips, and nose.
    C. The traditional FCV vaccine protects against 2-3 cross reactive strains of FCV.
    D. Traditional FCV typically has high mortality and VS-FCV has low mortality.

Answers: D, C, B, A, C, C, B, B, C, D

Pathogenesis and Clinical Signs of Feline Calicivirus

Meghan Neal 

Feline Calicivirus (FCV) is a small, non-enveloped, single-stranded RNA virus. All members of the family Felidae can become infected with FCV. Young kittens and adult cats that go through a stressful event are most susceptible to infection. FCV is highly contagious and transmission occurs through aerosolized droplets from salivary, ocular or nasal secretions of infected cats. Susceptible cats get an infection through direct contact with another infected cat or environmental exposure via fomites, which can be carried to susceptible cats by a handler! It is also thought the FCV can be spread in urine and feces, but these are not major sources of infection.

The incubation period for FCV is 5-10 days. The virus replicates mainly in the oral and respiratory tissues, although some strains vary in their tissue tropism and pathogenicity. The virus may survive for weeks within the contaminated environment. FCV is shed continuously from infected cats and convalescent cats may harbor the virus for months. Many infected cats develop a carrier state and will continue to shed the virus intermittently or constantly. Carrier cats are an important source of infection as they may or may not show clinical signs of infection when they are actively shedding the virus. This carrier state may only last a few months, but in some cats it persists for life. Queens that are carriers can pass the infection to their newborn kittens.

There are many different strains of FCV resulting in a range of clinical signs that may be seen. Some strains induce salvation and ulceration of the tongue, hard palate, or nostrils; other strains induce pulmonary edema and interstitial pneumonia.  Certain strains of FCV are non-pathogenic. The most characteristic lesion of FCV is oral ulcerations. Ulcers begin as vesicles, typically on the margin of tongue, and then subsequently rupture with necrosis of the overlying epithelium. Healing of the ruptured ulcers takes 2-3 weeks. Fever, sneezing, ocular and nasal discharges also occur frequently.

Nasal discharge and vesicles & ulcers on the tongue of a cat infected with FCV.

(Photos Courtesy of Merck Animal Health)

Tongue ulcerative glossitis from a FCV case.

(Photo courtesy of Tufts University)

In-apparent infections or pneumonia may be occasionally seen with FCV infection. Pulmonary lesions are less common and are thought to be a result of initial inflammation of the bronchioles and alveoli. This causes acute pulmonary edema that then progresses to an exudative pneumonia and later a proliferative interstitial pneumonia. These lesions will result in dyspnea and altered lung sounds.

Radiographs of interstitial pneumonia.

(Photo courtesy of the Journal of Feline Medicine & Surgery)

Histopathology & gross pathology of interstitial pneumonia from a FCV case.

(Photos courtesy of Tufts University)

Some FCV strains can also cause an acute febrile lameness syndrome. Such strains produce a transient fever, alternating leg lameness, and pain on palpation of the joints. Lesions seen in the joints of cats with FCV-associated lameness include synovitis with thickening of the synovial membrane and an increase in quantity of synovial fluid within the joint. Unfortunately, vaccination does not protect against the strains that cause this lameness syndrome.

FCV has also been found in cats with lymphocytic-plasmacytic gingivitis and stomatitis. An acute febrile response, inappetence, and depression are common signs. Serous rhinitis and conjunctivitis also can occur.

Lymphocytic-plasmacytic stomatitis in a cat.

(Photo courtesy of Apex Dog and Cat Dentistry)

References:

“Feline calicivirus”

Alan D. Radford, Karen P. Coyne, Susan Dawson, Carol J. Porter and Rosalind M. Gaskell

Vet. Res. 38 (2) 319-335 (2007)

DOI: http://dx.doi.org/10.1051/vetres:2006056

“Feline Calicivirus Infection”

VCA Animal Hospitals

http://www.vcahospitals.com/main/pet-health-information/article/animal-health/feline-calicivirus-infection/4132

“Feline Respiratory Disease Complex”

The Merck Veterinary Manual

http://www.merckmanuals.com/vet/respiratory_system/respiratory_diseases_of_small_animals/feline_respiratory_disease_complex.html?qt=feline%20calicivirus&alt=sh

Subbiah, E. VM 8124 Veterinary Virology Course Notes, Feline Viruses. Spring 2013; Lecture 27. 

Case Descriptions of Virulent Systemic Feline Calicivirus

Meliasa Robinson

When should you suspect something more than the traditional FCV??

Feline Calicivirus is an important pathogen with regards to feline upper respiratory disease. When a relatively young cat is presented for upper respiratory systems (especially a kitten) the top two differentials are usually Feline Herpesvirus (FHV) and Feline Calivirus (FCV). You may consider also want to include Chlamydophila or Bordetella but they are not as common as the viruses. Both viruses involve some component of nasal discharge and sneezing, typical upper respiratory signs. FHV tends to have more of an ocular component including corneal ulcers, while FCV has more of an oral component with oral ulcers and may also present with concurrent limping. FCV may involve conjunctivitis but does not typically cause corneal ulcers like FHV. Based on signs you can usually differentiate the two pretty easily but if you are unsure running a PCR on nasal swabs or having virus isolation to differentiate the two are viable options. Keep in mind that PCR will be positive if the cat was vaccinated for FHV. FCV is usually treated symptomatically but many cats clear the virus on their own.

In a brief description FCV doesn’t sound that bad, it is highly contagious but not very fatal. So in an otherwise healthy kitten who gets good supportive are can be a good turnout. This is not the case with Virulent Systemic Feline Calicivirus (VSFCV). VSFCV is a severely virulent and contagious strain that results in significantly higher mortality rates than the traditional FCV, not to mention it does not discriminate between vaccinated and non-vaccinated pets (N.C. Pedersena, 2000). VSFCV is associated with more systemic signs such as involvement in the lungs and vascular system. It is important to differentiate early between VSFCV and traditional FCV as treatment needs to more aggressive and systemic in one versus the other. An epizootic of highly fatal FCV infection was described in the paper “An isolated epizootic of hemorrhagic-like fever in cats caused by a novel and highly virulent strain of feline calicivirus”. To better illustrate how severe VSFCV can be the index case and two of the severe resulting cases from the index will be described in detail. For a detailed account of the entire outbreak please see the paper.

In this epizootic there were a total of 7 cases. The index cat was a 4 month old shelter kitten brought in for severe upper respiratory signs on Sept 12th and spent a total of 40 days at the hospital for treatment. One of the veterinary assistant’s cats Ria, 6 year old female was brought in for a dental Oct 8th and returned four days later with signs of swelling and lethargy that eventually turned into crusting. Two other cats in Ria’s household, her sons Ari and Ian, which were not directly exposed to the hospital came up with signs similar to mom. Ari’s signs were first noted on Oct 19th; they were more severe and will be detailed further. Ian’s was brought in for signs on Oct 21st but eventually made a recovery. A client’s cat came into the hospital for castration on Oct 12 and like Ria returned 4 days later with signs of depression and lethargy that later turned into ulcerative lesions. A house mate of this cat came in Oct 16 for conjunctivitis and 2 weeks later had alopecia and crusty lesions similar to those of the other cats. Both cases made an uneventful recovery. The last case was the cat of a veterinary technician at the same hospital. That cat was brought in Nov 6th with signs but was ultimately euthanized Nov 9th due to a progressive decline. All the cases can be traced back to some contact or spread from the index case; also all cases were FELV and FIV negative. Only two cases had virus isolation of FCV which were determined to be the same strains.



The Index Case:

Female kitten from shelter, 4 months old with severe upper respiratory infection. The infection develops to crusty lesions on the face and oral vesicles. The kitten was treated for a total of 40 days before being well enough to be adopted. After adoption the kitten died 1 week later from intussuception.



Ria:

Ria, 6 year old female spayed domestic feline, strictly indoors vaccinated on the tenth of April with FPHCV. Ria was brought in on October 8th for a dental cleaning procedure. On Oct 12 Ria returned with lethargy, anorexia, fever, and slight swelling over the dorsal muzzle. Hair over the right side of muzzle was epilated revealing 5 mm erythematous patch with a dark center. Ria was sent home for observation but returned two days later with additional focal crusting, erythema epilation over right and left medial canthi and margins of pinnae. Ria also had diffuse cutaneous edema of the face extending down the limbs. A biopsy of the muzzle and pinna revealed multifocal neutrophilic/lymphoplasmacytic perivascular dermatitis, extensive ulceration, superficial dermal necrosis, with underlying vasculitis. No infectious organisms were cultured. Ris was treated with prednisone and antibiotics. Over the next couple of days her appetite was normal again, and her lesions were beginning to heal.




Ari:

Ari was the son of Ria, 3.5 year old neutered male indoor only, vaccinated on tenth of April with FPHCV. Ari was brought in on Oct 19th with history of acute lethargy, anorexia of two days with right forelimb lameness noted 2 days prior but had since resolved. Physical exam detected a fever, crusty lesion on lower lip. Ari was sent home for observation but returned on Oct 21st with diffuse facial edema, dehydration, anorexia, and central ulceration over muzzle and left pinna. Focal crusting lesions were also noted on lower and upper lips. Over the next two days Ari stayed afebrile had facial swelling, forepaw edema, and the ulcerative lesion had less exudative discharge. Ari was transferred to UC Davis VMTH on Oct 23. Blood work showed an elevation in bilirubin, a coagulopathy, moderate decrease in protein, and an increase creatine phosphokinase (CPK). FCV was isolated in cell culture from the blood and nasal samples taken. On Oct 24 Ari’s entire face became edematous, the lesions on his face coalesced to form large crusts on both sides of the muzzle, and his mucous membranes were icteric. A nasoesophageal feeding to was placed as Ari was still anorectic. On Oct 26th Ari was given 1 unit of blood and started on low heparin therapy to combat DIC. A blood analysis later that day still showed decreased HCT, hypoproteinemia, and increased ACT but Ari was alert and responsive. On Oct 27th he was given another unit of cross matched blood, he also had increased RR. Thoracocentesis yielded yellow transudate. On Oct 28th Ari was given a 3rd unit of blood and had a thoracostomy tube placed to continuously remove pleural fluid. Ari’s condition slowly declined and he died Nov 8th from complications of Pneumothorax, shock and arrest. FCV was recovered from blood and tissue samples post mortem.



These cases were reported in 1998, but VSFCV has been seen in some private practices since then. If VSFCV is suspected it is important to take extreme care and caution not to spread the virus to other felines in the clinic. Whatever exam is used for the suspect case should be bleached and closed for at least 24 hours (N.C. Pedersena, 2000). If the patient must be hospitalized an isolation ward should be devoted to that patient. If the resources are not available then the pet should be taken to a facility that can properly isolate. The main signs that will help point to VSFCV are edema of the face and limbs, crusty lesions over face, muzzle, and pinna, treatment is more chronic than with traditional FCV and lung involvement is a greater possibility.

Works Cited 

N.C. Pedersena, J. E. (2000). An isolated epizootic of hemorrhagic-like fever in. Veterinary Microbiology , 73, 281-300.

Vaccination and Control of Feline Calicivirus

Erin Mathews

Vaccination 

There are three types of vaccines available against feline calicivirus. These include modified-live and killed parenteral vaccines and a modified-live intra-nasal vaccine. It is often included in a combination vaccine with feline herpes and panleukopenia viruses. Unlike most modified-live vaccines, the calicivirus vaccine must be boostered to confer maximum protection. Therefore, there may not be much benefit of the modified-live vaccine over a killed vaccine. The intra-nasal vaccine has a shorter onset of immunity than injectable vaccines. Vaccination for calicivirus produces a “non-sterile” immunity, meaning that it does not eliminate infection or development of a carrier state, but lessens the severity of clinical signs in infected cats and decreases shedding of the virus. There are numerous field strains of calicivirus, though the vaccine likely provides cross protection among strains.

Vaccine protocol for the average cat begins at around 9 weeks of age. The vaccine should be boostered twice, 3-4 weeks apart. The kitten should be at least 15 weeks old at the time of the last booster, since maternal antibodies may interfere with development of an appropriate immune response prior to this age. Adult cats should be vaccinated 1 year after their initial series and every 3 years thereafter.

For cats in high risk environments or during outbreaks, the vaccine can be administered as early as 2-4 weeks of age and boostered at 2 week intervals. Intra-nasal vaccines may be advantageous in these situations, since they may offer some protection within 72 hours of administration. It is important to note that intra-nasal vaccines may induce sneezing, which may be confused with active infection. For adult cats, vaccination prior to the 3 year recommendation may be beneficial if they are to be boarded at a kennel or exposed to new cats (such as foster kittens).

There is now a two strain vaccine available that incorporates a strain known to cause virulent-systemic disease. A study has proven its effectiveness when cats were challenged with the same strain they were vaccinated with. However, most strains that have been isolated from infected cats have arisen from new mutations and are not serologically cross reactive. The two strain vaccine does seem to provide better cross protection for traditional calicivirus infections.

Control

Feline calicivirus is non-enveloped, and therefore resistant to many common disinfectants. 5% bleach at a dilution of 1:32 has proven to be effective and should be used routinely to clean surfaces and instruments that come into contact with cats, especially those showing clinical signs. Other acceptable cleaners include potassium peroxymonosulfate (Trifectant) and chlorine dioxide. Without disinfection, the virus can survive for 28 days at room temperature.

An attempt should be made to minimize factors that predispose cats to infection with calicivirus. Among these are concurrent disease, poor nutrition, parasitism, stress, over crowding, and poor ventilation.

Suspected cases should be kept in strict isolation. Calicivirus can be transmitted on fomites, so these cats should be handled by a limited number of staff members. Gowns, gloves, and shoe covers should be utilized.

Outbreaks of virulent-systemic calicivirus pose an extreme challenge to shelters. All exposed cats must be considered at risk of transmitting the disease. There is no defined quarantine period, because the duration of viral shedding and for how long the virus maintains the mutation causing increased virulence is unknown. It is suggested that up to 3 months may be necessary. This period can be shortened by using viral culture and PCR to determine when quarantined cats are no longer shedding the virus. Due to intermittent shedding, 3 oropharyngeal swabs at 1 week intervals are required. This is not always the most effective allocation of a shelter's resources and many shelters may opt to euthanize these cats.

Often suspected cases of virulent-systemic calicivirus turn out to be an unrelated primary disease (such as panleukopenia) that is confounded by co-infection with traditional FCV. It is possible these diseases will be more amenable to treatment. Before extreme measures are enacted, care should be taken to rule out this scenario. The likelihood that virulent-systemic calicivirus is involved increases when otherwise healthy adult cats or well-vaccinated cats are affected.

References:

American Association of Feline Practitioners: Feline Vaccination Advisory Panel Report. Dec 29, 2006.

Huang C, Hess J, Gill M, Hustead D. “A dual-strain feline calicivirus vaccine stimulates broader cross-neutralization antibodies than a single-strain vaccine and lessens clinical signs in vaccinated cats when challenged with a homologous feline calicivirus strain associated with virulent systemic disease.” J Feline Med Surg. 2010 Feb;12(2):129-37

Rothrock, Kari. VIN Associate Database: Feline Calicivirus. Last updated on 5/25/2012.

UC Davis Koret Shelter Medicine Program. http://sheltermedicine.com/node/38#vacs

Diagnosis and Treatment of Feline Calicivirus

Emily Thornton

Diagnosis

Diagnosis of calicivirus by veterinarians is often based solely off clinical signs. Although certain clinical signs (i.e. severe oral ulceration) tend to suggest calicivirus more so than other diseases, it is important in some cases to obtain a definitive diagnosis. Cats that become infected with calicivirus tend to become chronic shedders of the virus (some may shed for weeks to months, others may be life-long shedders), so in cases where there is more than one cat present in a household or in cattery situations, a definitive diagnosis is desired to prevent rapid spread of disease. The clinical signs of FCV can often mimic clinical signs of other diseases such as Feline Herpes Virus, Chlamydophila infection, or Bordatella infection. On initial presentation, the cat may show mixed clinical signs as secondary bacterial infections are possible with FCV infection. A definitive diagnosis is preferred in areas where there may be increased exposure/spread, if there is no response to symptomatic treatment of FCV, or if the virulent strain of FCV is suspected.

A definitive FCV diagnosis may be done by a variety of mechanisms which include PCR, virus isolation, and serology, although serology is often not recommended for two reasons: There are an increased number of FCV strains that may cause a varying titer response, and FCV vaccines may confound antibody response. Although serology may not be effective in diagnosing most FCV cases, it may have some use in identifying virulent systemic FCV. Virus isolation is another option for diagnosing FCV. Samples should include oropharyngeal, nasal, and/or conjunctival swabs (more swabs for better diagnosis). Virus isolation isn’t as sensitive in cats recovering from FCV infections, so a cat cannot be considered FCV-free from one negative sample taken over a week after the onset of clinical signs. Two or three negative samples on a weekly basis will confirm that the cat has stopped shedding the virus. Feline calicivirus may be diagnosed using PCR, but this may not be the best method of diagnosis due to the fact that FCV frequently mutates and develops new strains which may not all be detected by PCR methods. Something that should be taken into consideration with PCR detection of FCV is that there is an increased risk of false positives if there is contamination of the sample.

A new method to diagnose FCV is currently being researched to increase the sensitivity of PCR. There has been recent development of a nested PCR (nPCR) method which aims to isolate a primer sequence that is more conserved among the different strains of FCV. In a recent study, results have suggested increased sensitivity of nPCR tests compared to RT-PCR and virus isolation. The table below shows the results of the aforementioned study. There was approximately a 20% increase in diagnosis of FCV with nPCR compared to RT-PCR or virus isolation.

                     

Positive diagnostic results for FCV need to be considered in light of clinical signs and other possible infections (concurrent or otherwise). Cats that are FCV positive may be chronic shedders of the virus and may be showing clinical signs due to some other underlying disease which needs to be treated. Therefore, a FCV positive cat that does not respond to symptomatic treatment should be reevaluated.

Treatment

Unfortunately, FCV cannot be cured and treatment is only symptomatic. After a cat is infected, they tend to become chronic shedders, although it is possible for them to clear the virus completely. Severe oral ulcerations may cause the cat to become anorectic, and in those cases fluids and nutritional support are necessary. Often, affected animals need to be put on broad spectrum antibiotics to prevent secondary bacterial infections or treat concurrent infections. The virulent systemic form of FCV should be treated with more aggressive fluid and antibiotic therapy. These cats should also receive oral interferon alpha to boost the protective effects of natural immunity. There is some evidence suggesting that immunosuppressive doses of glucocorticoids may decrease mortality due to the virulent systemic strain, but more research needs to be done to confirm this. Confirmed FCV cases should be isolated to prevent further spread of disease, but strict isolation of virulent systemic cases is required due to the high mortality associated with the disease.

References: 

Hurley, Kate F., and Jane E. Sykes. "Update on Feline Calicivirus: New Trends." Veterinary Clinics of North America: Small Animal Practice 33.4 (2003): 759-72. SciVerse. ScienceDirect, July 2003. Web. 1 May 2013.

Marsillo, Fulvio, Barbara Di Martino, Nicola Dicaro, and Canio Buonavoglia. "A Novel Nested PCR for the Diagnosis of Calicivirus Infections in the Cat." Veterinary Microbiology 105.1 (2005): 1-7. SciVerse. ScienceDirect, 5 Jan. 2005. Web. 1 May 2013.

Virulent Systemic Feline Calicivirus: FCV’s Bigger, Badder Brother

Jessica Yankus

Feline calicivirus (FCV) is a common virus of cats (domestic and wild) that produces a variety of clinical signs including fever, ocular and nasal discharge, conjunctivitis, limping, and most typically oral ulceration. FCV is a small, non-enveloped, single stranded RNA Vesivirus of the family Caliciviridae. It is a highly contagious virus which is transmissible through the secretions of infected cats. This particular virus is difficult to eradicate because of its highly stable, non-enveloped nature and the fact that recovered cats continue to harbor the virus (in their tonsils and oropharynx) and shed it persistently. Being an RNA virus, FCV is also prone to mutation due to the lack of a ‘proof-reading’ ability of its polymerase. This results in various strains of the virus. Adult cats infected with non-virulent strains are typically non-fatal but can have approximately 30% mortality in kittens that subsequently develop pneumonia or severe upper respiratory infection.

In recent years, there have been an increase in the number of cases associated with a particularly virulent strain of FCV which, unlike the typical FCV, causes severe systemic disease. First reported in 1998, virulent systemic feline calicivirus (VS-FCV) has been associated with typical FCV ulcerations on the tongue, mouth and nose, and high fever, facial and limb edema, ulceration, crusting and focal hair loss (face, muzzle, paws, and pinnae), multiple organ involvement and damage, and death. The clinical signs of this syndrome manifest from the virus’ tropism for endothelial and epithelial cells. Typically, VS-FCV presents with high mortality and is also highly contagious and seems to more frequently infect healthy, vaccinated adult cats.

Diagnosis of this particularly virulent strain of FCV can be challenging as it is still an emerging disease. Blood chemistries performed on afflicted patients are typically non-specific and diagnosis should be made by clinical signs and ultimately real time polymerase chain reaction (RT-PCR) for viral genome sequencing to differentiate the VS-FCV strain from other FCV strains. Specific clinical signs that differentiate VS-FCV from traditional FCV is the sustained high fever. Cats with traditional FCV are typically febrile for one day and this physical exam finding may no longer be present once the patient is evaluated. Cats infected with VS-FCV will present with a high fever of prolonged duration.


                                    

Feline patient with virulent systemic feline calicivirus (VS-FCV). Clinical signs include facial edema, ulcers present on nose, ocular and nasal discharge, and skin lesions on pinna. 

                                       

A) Peripheral edema and skin lesion of the forelimb B) Ulcers on tongue

C) Alopecia and crusting of the forelimb D) Crusting of paw pads 

Typical FCV vaccines only protect against two or three cross-reactive strains of the virus. These traditional vaccines do not prevent against virulent systemic feline calicivirus. CalciVax produced by Fort Dodge Animal Health is the only vaccine that has been proven effective against VS-FCV (DVM360 Magazine, 2007). The vaccine, which gained licensure in 2007, contains one strain of VS-FCV and traditional FCV strains as well. The vaccine has reportedly proven effective against severe challenges of the vaccine strain with no vaccinated cats showing signs of VS-FCV (DVM360 Magazine, 2007). However, since FCV is prone to frequent mutation, the strain included in the vaccine may or may not be effective against all strains of VS-FCV. Vaccination for traditional strains of FCV is considered a core vaccine for all domestic cats and VS-FCV targeted vaccination is indicated for cats considered at high risk of VS-FCV.

Awareness of this highly virulent strain of FCV and its clinical signs will aid in prompt diagnosis. Ultimately, knowledge of the specific characteristics of VS-FCV will lead to better prevention and control of outbreaks of this deadly newcomer.

Citation 

Hurley, Kate F., Patricia A. Pesavento, Niels C. Pedersen, Amy M. Poland, Erin Wilson, and Janet E. Foley. "An Outbreak of Virulent Systemic Feline Calicivirus Disease." Journal of the American Veterinary Medical Association 224.2 (2004): 241-49. AVMA. Web. 30 Apr. 2013. http://avmajournals.avma.org/doi/abs/ 10.2460/javma.2004.224.241?journalCode=javma.

Klopfleisch, R., A. Meyer, and O. Kershaw. "Feline Calicivirus-associated Virulent Systemic Disease: Not Necessarily a Local Epizootic Problem." The Veterinary Record 168.22 (2011): n. pag. Veterinary Record. Web. 30 Apr. 2013. http:// veterinaryrecord.bmj.com/content/by/year.

Reynolds, Brice S., Hervé Poulet, Jean-Luc Pingret, Dominique Jas, Sylvie Brunet, Celine Lemeter, Mélanie Etievant, and Corine Boucraut-Baralon. "A Nosocomial Outbreak of Feline Calicivirus Associated Virulent Systemic Disease in France." Journal of Feline Medicine & Surgery 11.8 (2009): 633-44. SciVerse. 7 Feb. 2009. Web. 30 Apr. 2013. http://www.sciencedirect.com/science/article/pii/ S1098612X08002787.

Subbiah, E. VM 8124 Veterinary Virology Course Notes, Feline Viruses. Spring 2013; Lecture 27.

"CaliciVax Updated to Cover Virulent System Feline Calicivirus." DVM 360. N.p., 1 Feb. 2007. Web. 01 May 2013. http://veterinarynews.dvm360.com/dvm/Feline Center/CaliciVax-updated-to-cover-virulent-system-feline-/ArticleStandard/ Article/detail/408460.