Virulent Systemic Feline Calicivirus in cats

Feline Calicivirus (FCV) is a common infection in cats caused by several strains of calicivirus. It causes flu-like symptoms and more severe disease in some cats.

A particularly virulent strain of FCV – Virulent Systemic Feline Calicivirus (VS-FCV) – emerged in England in 2003. Australia's first outbreak was reported in Sydney in June 2016.

VS-FCV can cause severe generalised diseases through severe vasculitis and ulcerations by epithelial cell cytolysis.

What are the characteristics of VS-FCV disease?

All FCV strains are potentially pathogenic and need to be managed collectively.
VS-FCV is a recognised distinct disease variant with increased pathogenicity. Some specific strains described for some outbreaks such as Ari, Diva, Koas and Ukos-W. However, VS-FCV has no definite diagnostic or virological features that would differentiate it from other strains.
Vasculitis and associated typical clinical feature is suggestive of the VS strain.
A RT-PCR is best used for diagnosis of FCV but it won’t differentiate the VS strain. Don’t rely on PCR for diagnosis – interpret results in combination with clinical presentation and epidemiologic data.
An un-enveloped virus means it is more resistant to environmental exposure and disinfection methods.
High mutation rate leads to the development of virulent strains and resistance against vaccines.
VS-FCV can be associated with co-infection, which can complicate the clinical presentation and management, and can confuse regular strains for VS. Rule out other infections (particularly panleukopaenia, FHV-1, Mycoplasma felis, Chlamydophila felis and Bordetella bronchiseptica).
Incubation period is two to 10 days.
Persistence in the environment at room temperature can be for up to four weeks, with longer persistence in cold conditions.
Caliciviruses are typically species specific and don’t represent a risk to people or other animal species.

Is there a specific risk profile?

Carriage of FCV strains is common in all cats.

Cats are at particularly high risk if they are in a shelter or other intensively managed facilities such as catteries, breeding facilities and clinics.
Stress is an underlying risk factor: factors include co-infection, crowding, social, nutritional, co-mingling, poor hygiene and poor ventilation.
Clinical recovery and/or lack of symptoms does not mean the cat is not potentially shedding the virus, although asymptomatic cats will generally excrete less virus.
F3 vaccine is not completely protective for disease and not protective for carriage.
Kittens appear to be more frequent shedders.
Shedding can persist up to four months in cats recovering from clinical infection.

How is VS-FCV transmitted?

FCV can be spread through cat-to-cat contact. It is highly contagious when a cat is hospitalised for more than 12 hours in the presence of an infected cat; there is a 90 per cent chance of a cat being infected if it is in the same household with an infected cat.

It can be transmitted via:

droplet as mainly URT, but potentially any excretion
no true aerosolisation but possible airborne spread is less than one metre
fomites, especially hands, but including clothing and equipment
surfaces including floors, benches and cages
cat’s fur contaminated by excretions.

What are the clinical signs?

Fever
Anorexia
Limping
Upper respiratory signs
Lower respiratory signs going from tachypnoea to dyspnoea
Icterus
Bleeding tendencies with melena, petechiations
Sudden death
Oral ulcers*
Oedema of face and limbs*
Ulcerative pododermatitis*

* typical for VS-FCV when found concurrently

What is the mortality rate?

Case fatality of 40 per cent, ranging from 25 per cent to 70 per cent, depending on the strain and population described.

Mortality rate is often higher in cats older than 12 months than kittens less than six months old, with respective rates of about 60 per cent and 15 per cent.

How to diagnose VS-FCV

PCR from oropharyngeal swabs or other fluids like pleural effusion.
Virus isolation from oropharyngeal swabs or tissues sampled.
Genetic sequencing can be done to identify specific strains.
Serum virus neutralising titers.
IHC in tissue samples.

What can work-up of these cases identify?

Pleural effusion and most likely a modified transudate with pyogranulomatous component, which can make the disease appear initially similar to FIP.
Increased glycaemia due to associated pancreatitis and pancreatic necrosis.
Increased liver enzymes and bilirubin due to viral liver damage.
Decreased albumin and increased CK.
Neutrophilia common on CBC.

Can VS-FCV be treated?

There is no specific treatment for VS-FCV; you can offer mainly supportive care.

Broad spectrum antibiotics (doxycycline or amoxyclav suggested) for secondary bacterial infection.
Nutritional management through feeding tube and enteral nutrition.
Use intravenous fluids with caution due to the vasculitis component of the disease and risk of aggravating respiratory symptoms of pulmonary oedema; favour the enteral route for rehydration if dyspnoea or tachypnoea present.
Interferon has been reported to be helpful in some cases but literature remains controversial on its use. It has been suggested to use them in the more severe cases and the risk benefit would be favourable as its use is not usually associated with marked side effects.
Sometimes glucocorticoids are needed to help with a potential immune-mediated component for the vasculitis associated with the viral infection. Use it with caution and on a case-by-case basis as it is not considered gold standard for treatment.
Gastrointestinal supportive care with anti-emetics, anti-acids, sucralfate for the GI ulcers.
Adjust plan with each specific case as they might present with various combinations of the symptoms listed above.

Is vaccination protective?

No. The current vaccine does not protect against the virulent strain.

Young unvaccinated animals tend to suffer from the mild form while adult and vaccinated cats tend to suffer from the more severe form.