Читать книгу Canine and Feline Epilepsy - Luisa De Risio - Страница 266

Feline infectious peritonitis (FIP) and viral non-FIP encephalitides (i.e. non-suppurative encephalitides of unknown, although probable viral, aetiology based on histological findings) are the two most commonly recognized infectious CNS disorders of cats (Gunn-Moore and Reed, 2011).

FIP is a highly fatal, progressive and immune-augmented disease of cats caused by infection with feline coronavirus (FCoV). Although the terms feline infectious peritonitis virus (FIPV) and feline enteric corona-virus (FECV) have been used to refer to the virus causing FIP and the ubiquitous benign enteric virus, respectively, the term FCoV should be used to describe all coronaviruses in cats. FCoV is an RNA virus and belongs to the genus Coronavirus of the family Coronaviridae. It has been proposed that FCoV along with swine and canine coronaviruses becomes part of a new species called Geselavirus (Addie, 2012). FCoV causes a ubiquitous enteric infection in cats, which leads to FIP in approximately 1–3% of cats. The etiopathogenesis of FIP is complex and still unclear. A widely cited patho-genetic hypothesis is the ‘in vivo mutation transition hypothesis’ also called the ‘internal mutation hypothesis’. This postulates that viral mutations occur in healthy FCoV-infected cats giving rise to virulent virions that are able to replicate within macrophages and disseminate systemically leading to FIP (Pedersen, 2009). The precise nature of the mutation responsible for this pathogenetic hypothesis has not been identified yet. An alternative ‘circulating avirulent and virulent FCoV hypothesis’ suggests that distinctive benign and pathogenic strains of FCoV circulate in a population, and susceptible individuals exposed to the virulent strains develop FIP (O’Brien et al., 2012). It is likely that FIP etiopathogenesis is more complex than either hypothesis alone would suggest.

FCoV has a worldwide distribution and therefore cats worldwide are susceptible to developing FIP (Kent, 2009). FCoV is endemic especially in environments in which many cats are kept together in a small space (e.g. catteries, shelters, pet stores). Although cats of any age can develop FIP, the risk is higher in kittens and cats up to 2 years of age or older than 10 years of age. The risk to develop FIP appears greater in young and immune-compromised cats as well as in cats with a high viral load (Hartmann, 2005). In addition, pure-breed cats (such as the Abyssinian, Bengal, Birman, Himalayan, ragdoll, rex) have a greater risk of developing FIP than non- pure-breed cats (Pesteanu-Somogyi et al., 2006). Infection usually takes place by ingestion (or, rarely, by inhalation) of material contaminated by infected faeces shed by a cat with FCoV infection or by a cat with FIP (Hartmann, 2005). Many healthy cats shed FCoV intermittently or continuously for up to 10 months post-infection or longer, serving as chronic carriers and thereby perpetuating reinfection of other cats (Hartmann, 2005).