Feline calicivirus: clinical signs and treatment
Feline calicivirus (FCV) is a highly contagious RNA virus that is widely distributed among the cat population. It is a common cause of infections in the respiratory tract, digestive tract and ocular conjunctiva.
Epidemiology and pathogenesis
Feline calicivirus (FCV) is a highly contagious RNA virus that is widely distributed among the cat population. The cat is the main reservoir of FCV, although it has also been isolated from dogs. However, it does not seem to have a significant epidemiological role in dogs. Cats of any age are susceptible to FCV infection.
The prevalence of the virus is proportional to the size of the population. The prevalence in small groups of cats is around 10%, but it rises to 25–40% in colonies or animal shelters.
Cats are infected via the nasal, oral or conjunctival routes. The virus initially starts to replicate in the oropharynx. Transient viraemia develops 3–4 days after transmission, at which point the virus can be detected in several locations.
One of the most frequent sites is the tongue, where it causes epithelial cell necrosis and consequently ulcers. In less severe cases, the signs are self-limiting, and patients recover within about 2–3 weeks. In graver cases, the virus may affect other systems, such as the respiratory (causing pneumonia) and/or musculoskeletal (acute synovitis).It rarely follows a fatal course, although very virulent strains (V-FCV) have been described recently that cause alopecia, skin ulcers, subcutaneous oedema and which have a high mortality in cats.
After recovering from the acute infection, most cats clear the infection within an average of 30 days. Cats with FCV can develop a chronic infection and become carriers (10% of domestic cats and 25–75% of those in colonies/shelters). FCV can be reactivated when the animal suffers a stressful event (disease, surgery, etc.). The virus mainly replicates in the nasal, tracheal and conjunctival mucous membranes, but also in the lungs and/or oral mucosa, hence the broad range of clinical signs. Transmission is basically via direct contact.
Association with other viruses
FCV infection is frequently encountered in cats with an upper respiratory tract disease, either as a sole infectious agent or in combination with other pathogens (FHV-1, Chlamydophila felis, Mycoplasma spp.), so it is a potential cause of lesions on the ocular surface in patients with upper respiratory problems.
While feline herpesvirus (FHV-1) is the main cause of eye disease in cats, causing bilateral conjunctivitis and characteristic dendritic corneal ulcers, it is important to remember that feline calicivirus (FCV) is another possible cause. Feline herpesvirus infection generally causes more severe signs, but the clinical picture is similar, whereas FCV also affects the lungs and oral cavity due to its tropism for the lung parenchyma and orolingual epithelium.
However, the only definitive diagnostic method is a PCR test on samples collected from conjunctival, nasal or oral secretions, as well as by means of a corneal scraping or even biopsy.
It has also been shown that virulent FHV-1 and FCV can be found in clinically normal corneas of cats and dexamethasone facilitates viral spread.
Clinical signs of feline calicivirus
Animals with FCV have variable signs depending on the virulence of the virus and host factors.
The most characteristic clinical signs of FCV infection are:
- Ocular involvement in the form of conjunctivitis, which is sometimes erosive.
- Upper respiratory tract disease, especially in young cats. Depending on the cat’s immunisation status, FCV can cause pneumonia. It lasts between 1–2 weeks (for more information on feline viral rhinotracheitis, click here).
- Orolingual involvement with ulcers, blisters and chronic gingivostomatitis. As such, patients have sialorrhoea, halitosis, dysphagia, etc.
- Nasal, ocular and oral secretions (for more information on gingivitis in cats, click here).
- Anorexia secondary to oral pain caused by ulcerous lesions.
- Systemic dissemination may cause arthritis and/or lameness due to the deposition of immune complexes in the synovial membrane.
Prevalence of gingivostomatitis in cats with feline calicivirus
A study conducted at the University of Munich investigated the prevalence of different viruses, including feline calicivirus, in 52 cats with chronic gingivostomatitis and a control group of 50 cats of a similar age. They found that the presence of FCV RNA was significantly more common in cats with chronic gingivostomatitis (53.8%) than in the control group (14%).(2)
A later study looked at the prevalence of calicivirus in cats with chronic gingivostomatitis and feline odontoclastic resorptive lesions (FORL). They found a high correlation between FVC and chronic gingivostomatitis, 60% of the cats with gingivostomatitis also had FCV. However, they did not identify any correlation between FCV and the aetiopathogenesis of FORL.(3)
That same year, researchers at Colorado State University published a study examining the relationship between feline calicivirus and gingivostomatitis. They analysed 42 oral biopsy samples from cats with gingivostomatitis and 19 from healthy cats for FCV RNA, FHV-1 DNA and Bartonella spp. DNA (4)
The results did not reveal any differences between the two cat groups in terms of seroprevalence rates for the Bartonella species, DNA in blood and tissue, and FHV-1 DNA. However, when observed, FCV RNA was more commonplace in cats with gingivostomatitis (40.5%) compared to the control cats, which were free from FCV. The researchers therefore concluded that the two diseases are related.
The origin of gingivostomatitis may lie in an alteration to the local immune system, resulting in an exaggerated response to the presence of chronic antigenic stimuli, such as calicivirus. Given that over 80% of cats with a chronic inflammatory process in the oral cavity test positive for FCV isolated from the oropharynx, it is also believed that calicivirus facilitates the penetration of other agents, causing cell membrane damage.(2,4)
Treatment of feline calicivirus
The treatment of feline calicivirus infections depends on the animal’s condition and the organ systems affected, and it must be adapted to the signs and complemented by other supportive treatments.
Patients with pneumonia, purulent conjunctivitis and gingivostomatitis are indicated antibiotic therapy to prevent secondary bacterial infections.
Although vaccination provides good protection against the acute oral signs and upper respiratory tract diseases, it does not prevent infection and the virus from then spreading. Furthermore, there is no clear evidence that vaccination prevents chronic gingivostomatitis from developing if the patient becomes infected.
Bear in mind that viruses such as FCV evolve through the mutation and selection of variants that evade herd immunity. Thus, variants develop resistance to vaccines that have been in use for some time. A noteworthy example of this point is the observation of the systemic virulent form in previously vaccinated cats.