Summary of Section 4: Pathogenesis:  FCoV infection occurs following the ingestion of the virus, which then replicates in the epithelial cells of the small intestinal villi, resulting in faecal shedding. This enteric FCoV infection is often subclinical but can result in enteritis. FCoV is then found in the colon, which is the main site of viral replication alongside the ileum. Thereafter, FCoV infection is thought to spread to the mesenteric lymph nodes before sometimes resulting in viraemia. Whilst low-level FCoV viraemia in monocytes can occur in cats that do not go on to develop FIP, efficient and high-level FCoV replication in activated monocytes and macrophages (which may well be mediated by viral mutations) is believed to be a key event in FIP pathogenesis, alongside the nature of the immune response mounted by the cat in response to FCoV infection.  When FIP develops, there is a reaction between replicating FCoV in monocytes and blood vessel walls, allowing the extravasation of the monocytes, where they differentiate into macrophages. The breakdown of the endothelial tight junctions allows plasma to leak out of the vessels; this can appear clinically as an effusion in the abdominal, thoracic and/or pericardial cavities. In more chronic forms of FIP, fewer blood vessels are affected, but larger perivascular pyogranulomata result on affected organs.  The horizontal transmission of FIP, via an FIP-associated FCoV strain, is believed to be a very unlikely occurrence.