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| Acute stomatitis associated with FCV |
Feline calicivirus (FCV), a non-enveloped, positive-sense,
and single-stranded RNA virus, is one of the two feline viral diseases (including
FHV-1) responsible for the disease 'Cat Flu.' The two virus can infect
separately or together. The incidence of calicivirus is believed to be lower
than FHV although the clinical symptoms are often confused. The presence of the
virus does not necessarily lead to disease. Caliciviruses are among the most
common problematic infectious agents of cats, with extraordinarily high rates
of infectivity, morbidity and death. Although vaccination against caliciviruses
is practised commonly, these vaccines have incomplete efficacy and can
contribute to minor morbidity. Caliciviruses are responsible for diseases
ranging from acute nuisances and cattery problems to chronic debilitating
problems to peracute fatal emerging problems.
At least six different outbreaks of similar disease
characterized by high mortality have since been recognized in the United
States, but the lesions have not previously been described in detail.
Clinical signs
Caliciviruses appear to have a predilection for the
epithelium of the oral cavity and the deep tissues of the lungs. Some
caliciviruses are non-pathogenic. Some induce little more than salivation and
ulceration of the tongue, hard palate, or nostrils; others produce respiratory
disease such as pulmonary oedema and interstitial pneumonia. Clinically, it is
often impossible to differentiate FHV from FCV infection. Two strains may
produce a transient “limping syndrome” without signs of oral ulceration or
pneumonia. These strains produce a transient fever, alternating leg lameness,
and pain on palpation of affected joints. Signs occur most often in 8- to
12-wk-old kittens and usually resolve without treatment. The syndrome may occur
in kittens vaccinated against FCV because no vaccine protects against both of
the strains that produce the “limping syndrome.” Serous rhinitis and
conjunctivitis also can occur.
Acutely affected cats often develop fever, conjunctivitis,
rhinitis (although both conjunctivitis and rhinitis are more typical of FHV
infection than FCV), and vesicular stomatitis, including glossitis, faucitis
and palatitis. Vesicles rupture within hours or days; therefore observation of
small inflamed, painful erosions is more typical.
About 25% of FCV-infected cats develop chronic infection,
whereas as many as 50% appear to shed virus chronically after infection. Some
of the variance in clinical severity could be due to genetic differences in the
infecting viruses, in addition to the individual cat's immune system's response
to infection. In all endemically infected populations of cats, the FCV isolates
exhibit a large amount of genetic variation, often with some isolates that
cluster genetically with the vaccine strain.
A number of clinical forms of FCV can present, including:
Respiratory tract infection - FCV infection commonly causes
an upper respiratory infection in cats. Following infection of nasal and oral
mucosa via aerosol, a viremia ensues and the virus begins to be shed from nasal
and oral orifices for approximately 2 weeks afterwards and, commonly in
catteries and shelters, for months. Concurrently, cats develop lymphopenia and
neutropenia.
Polyarthropathy/Stomatitis.
Virulent systemic disease (FCV-VSD)
Even more severe disease may occur in cats that have
experienced chronic, high-titre FCV infection. These cats can develop progressive
immune complex-mediated glomerulonephritis, with chronic renal disease
characterised by high urine protein concentrations and high urine
protein:creatinine ratios. Many cases occur exclusively in overcrowded,
multicat households with marginal management (August, 2006).
Diagnosis
Diagnosis of FCV is based on primarily based on clinical
signs, which include ocular and nasal exudates, conjunctivitis, oral ulcers and
stomatitis, and varying degrees of upper respiratory distress. In virulent
systemic disease (FCV-VSD), facial and limb oedema and ulcerative dermatitis
may also be seen, in conjunction with respiratory distress.
Exclusion of FHV (most common differential) and isolation of
FCV virus using reverse transcriptase PCR (now commercially available worldwide
at relatively low costs).
Treatment
Kittens born to vaccinated Queens have minimal protection
against the virus due to the rapid genetic mutations which occur within
caliciviruses. As cats mature to 3 years of age, some innate immunity develops
and helps improvement in clinical signs. Vaccination for FCV does not prevent
infection consistently, although in many instances, the vaccine mitigates signs
of severe disease. Vaccines can also stimulate oral shedding of vaccine-strain
virus.
Broad-spectrum antibiotics are the normal medical treatment
and supportive therapy such as mucolytic agents, good food supplements. Lysine
is not useful as it is with FHV infection. Cats that develop chronic LPS
gingivitis or glomerulonephritis require more aggressive therapy with acyclovir
or other antiviral medications. The prognosis in these cases is guarded.
Quarantine is useful to isolate infected cats and thus
minimise spread of the disease. Breeding from chronically infected cats is not
recommended.
Recent in vitro reports suggest the efficacy of soybean β-conglycinin
(7S-peptides) acylated with myristic and palmitic acids potently inhibited FCV
replication.
Prevention
Vaccinations using core vaccines have shown the highest
efficacy at preventing disease when given at 8 and 12 weeks of age, although
vaccination offers, at best, a 75% protection from this genetically-mutable
virus (August, 2006).
References
Rabbits
