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Feline Infectious Peritonitis (view source)
Revision as of 11:31, 27 July 2010
, 11:31, 27 July 2010→Pathogenesis
==Pathogenesis==
==Pathogenesis==
Weeks, months or years may intervene between localized primary FECoV infection and FIP development. FECoV replicates in the gut, but FIP spreads systemically in the circulation. FIP then gains the ability to replicate in [[Monocytes|monocytes]] and macrophages
Weeks, months or years may intervene between localized primary FECoV infection and FIP development. FECoV replicates in the gut, but FIP spreads systemically in the circulation. FIP then gains the ability to replicate in [[Monocytes|monocytes]] and macrophages.
Failure of the [[Adaptive Immune System - WikiBlood|immune system]] to clear antibody-antigen complexes leads to immune-mediated disease and deposited complexes cause [[Inflammation - Pathology|inflammation]] and exudation.
This leads to characteristic [[Oedema - Pathology| oedema]] as fibrin-rich serum escapes to intercellular spaces.
Pyogranulomas reactions can develop in major organs as a result of the immune response and the body's failure to clear away excess [[Neutrophils|neutrophils]].
Cats previously exposed to coronavirus (and therefore with circulating antibody) may be at greater risk as they are more susceptible to taking up virus into mononuclear cells
Cats making a biased [[Adaptive Immune System - WikiBlood #Cellular response: Proliferation and Differentiation|Th-1]] response are more likely to evade infection, whereas cats making a balanced response are at moderate risk and cats making a biased [[Adaptive Immune System - WikiBlood #Cellular response: Proliferation and Differentiation| Th-2]] response are at greater risk, as the virus is best tackled by cell mediation and not antibody.
Cats compromised by immunosuppression (either iatrogenic or disease-related) are at a greater risk of developing FIP.
==History and Clinical signs==
==History and Clinical signs==