Most cats infected by FCoV either develop an asymptomatic infection or show minor signs of enteritis. Only a proportion (see above) of these cats goes on to develop FIP, a pyogranulomatous disease [Pedersen et al, 1981; Pedersen, 1987].
The precise cause of FIP is unclear but there are two main hypotheses. First, that a mutation occurs which favours viral replication in monocytes and macrophages [Poland et al, 1996; Vennema et al, 1998; Cornelissen et al, 2007 Haijema et al, 2004; Rottier et al, 2005]. This has been called the internal mutation theory although no consistent mutation has yet been identified. In support of this hypothesis is the presence of highly virulent strains of FCoV that are capable of consistently inducing FIP, albeit under experimental conditions [Poland and Venemma 1996]. The second hypothesis for the development of FIP is that any FCoV can cause FIP but that the viral load and the cat’s immune response determines whether or not FIP will develop [Addie et al, 1995, Dewerchin et al, 2005; Dye & Siddell, 2007; Meli et al, 2004, Rottier et al, 2005; Kipar et al, 2006]. It is likely that both factors, namely viral genetics and host immunity, play a role in the development of FIP.
FIP occurs in two major forms: an effusive form which is characterized by polyserositis (e.g. thoracic and abdominal effusion) and vasculitis as a consequence of injury of blood vessels wall by extravasating macrophages [Kipar et al, 2005] and a non-effusive form characterized by granulomatous lesions in organs. These two forms probably reflect clinical extremes of what is in reality a continuum, with many cats having signs and lesions consistent with both forms.
A rare nodular enteric form described in young cats with diarrhoea and vomiting was associated with intestinal pyogranulomatous lesions [Van Kruiningen et al, 1983; Harvey et al, 1996].
All forms of FIP are lethal and the disease progression may be the consequence of severe immunodepression by T-cell depletion [de Groot-Mijnes et al, 2005].
Whether a cat develops the wet or dry form of the disease is thought to depend on strength of the T-cell-mediated immune response, which is probably the only efficient immune response against disease progression [Pedersen, 1987; Cornelissen et al, 2007]. The wet forms are presumed to be the consequence of a weak cell-mediated immune response [Pedersen, 1987].
Attempts to identify a tissue distribution of FCoV that is diagnostic for FIP have proved difficult. In cats with FIP, virus replicates to high titres in monocytes and can be found in many organs [Kipar et al, 2005]. In asymptomatic cats, FCoV is mainly confined to the intestine. However a low-level monocyte-associated viraemia can also be detected by RT-PCR [Gunn-Moore et al, 1998b; Herrewegh et al, 1995; Meli et al, 2004] and a high-level of replication has also been demonstrated in organs of asymptomatic cats, at least within the first month after an experimental infection with FCoV type I [Meli et al, 2004]. A significant difference in viral replication in haemolymphatic tissues has been demonstrated between cats that died from FIP and healthy long-term infected cats [Kipar et al, 2006].
Monocytes and macrophages remain infected by FCoV even in the presence of high levels of antibodies. The mechanism of this immune evasion has not yet been elucidated but one hypothesis could be an escape from antibody-dependent lysis due to absence of viral antigens on the surface of infected cells triggered by FCoV specific antibodies [Dewerchin et al, 2006; Cornelissen et al, 2007]. The direct consequence may be a quiescent infection state and a long incubation period. Activation of monocytes and perivascular macrophages may lead to the development of typical widespread pyogranulomatous and vasculitis/perivasculitis lesions in various tissues and organs, including lung, liver, spleen, omentum, and brain of cats with FIP [Kipar et al, 2005; Berg et al, 2005].