The virus enters via the nasal, oral or conjunctival routes. It causes a lytic infection of the
nasal epithelium with spread to the conjunctival sac, pharynx, trachea, bronchi and
bronchioles. Lesions are characterised by multifocal necrosis of epithelium, with neutrophilic
infiltration and inflammation. A transient viraemia associated with blood mononuclear cells
can be observed rarely after natural infection. This may be observed exceptionally in neonates
or hypothermic individuals as viral replication is usually restricted to lower temperature
tissues (Gaskell et al., 2007).
Viral excretion starts as soon as 24 hours after infection and lasts for 1 to 3 weeks. Acute
disease resolves within 10 to 14 days. Some animals may develop chronic lesions in the upper
respiratory tract and ocular tissues.
During infection, the virus spreads along the sensory nerves and reaches neurons, particularly
in the trigeminal ganglia, which are the main sites of latency. Almost all cats experiencing
primary infection become lifelong latent carriers. There are no direct diagnostic methods to
identify latency, because the virus persists as genomic DNA in the nucleus of the latently
infected neurons without virus replication. Reactivation of virus shedding can be induced
experimentally by glucocorticoid treatment in approximately 70% of cats. Other stressors that
may cause reactivation include lactation (40 %), and the cat moving into a new environment
(18%) (Gaskell and Povey, 1977; Ellis, 1981; Gaskell and Povey, 1982; Pedersen et al., 2004).
Some adult cats may show acute lesions at the time of viral reactivation. Disease at
reactivation is referred to as recrudescence.
Conjunctivitis may be associated with corneal ulcers, which may develop into chronic
sequestra. Stromal keratitis is a secondary immune-mediated reaction due to the presence of
virus in the epithelium or the stroma. In some cases damage to the nasal turbinates in acute
disease is thought to predispose some cats to developing chronic rhinitis (Gaskell et al., 2007)