Feline Infectious Peritonitis Flashcards
Main source of infection for FCoV
- faeces
- most transmission is faecal-oral
Shedding of FCoV post infection
- can shed FCoV in faeces as early as 2d post-infection
- shedding continues for d/w/m, a few can be persistently infected
- shedding then stops, or is detected intermittently, and can recur due to re-infection in an endemic environment
Immunity to FCoV
- short-lived, hence why cats can undergo multiple cycles of infections
Signalment for FIP
- any breed or age
- particularly seen in pedigree cats and those under 2y/o
- some studies show males are more likely to develop FIP than females
Prevalence of FCoV & FIP
- FCoV infection occurs worldwide
- very common, particularly in multi-cat households
- FIP only arises in a small % of FCoV infected cats
FCoV pathogenesis
- infection occurs following ingestion of the virus
- the virus replicates in the epithelial cells of the small intestinal villi, resulting in faecal shedding
- enteric FCoV 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
- then FCoV infection is thought to spread to the mesenteric LN before sometimes resulting in viraemia
FIP pathogenesis
- 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 junction allows plasma to leak out of the vessels
- this can appear clinically as an effusion in the the abdominal/thoracic/pericardial cavities
- in more chronic forms of FIP, fewer blood vessels are affected, but larger perivascular pyogranulomata result on affected organs
Horizontal transmission of FIP
- rare
Immunity
- maternally derived antibodies are thought to provide protection until kittens are about 5-6w/o, until they decline by 6-8w/o
- antibody development to FCoV takes 7-28d post-infection
- following natural infection, antibody titres can decline to 0 over a period of several months-years
CS of FCoV
- usually subclinical
- occasionally d+ ± v+ and poor growth (in kittens)
CS of FIP
- varied depending o distribution of vasculitis (which can lead to effusions) and/or (pyo)granulomatous lesions (which can lead to mass lesions) in the body
- lots of overlap between wet & dry forms
- CS can change over time
- non-specific: lethargy, anorexia, weight loss (or failure to gain weight / stunted growth in kittens)
- fever that is refractory to tx is common
- effusions are common, esp in the abdomen
- pleural effusions and pericardial effusions also seen, sometimes concurrently
- when effusions are present, dz progression is often quick, within a few days or weeks
- when effusions aren’t present it tends to be more chronic, progressing over a few w-m
- non-effusive signs
– depend on organ affected but can include CNS, eyes +/- abdominal organs (e.g. liver, abdominal LN [esp mesenteric LN], kidney [incl. renomegaly], pancreas, spleen +/- GIT
— abdominal lymphadenomegaly or intestinal masses - jaundice can occur, more commonly in cats with effusions, but the degree of hyperbilirubinaemia is often not high enough to result in clinical jaundice
- other less common signs including URT signs and CS associated with pneumonia and myocarditis
Neurological signs seen with FIP
- ataxia (with varying degree of tetra- or paraparesis)
- hyperaesthesia
- nystagmus
- seizures
- behavioural and mental state changes
- CN deficits
- central vestibular CS include
– head tilt
– vestibular ataxia
– nystagmus
– obtunded appearance
– postural reaction deficits - fever shown to be less common in cats with neurological FIP cf those without neuro signs
Ocular CS of FIP
- unilateral or bilateral uveitis
- changes in iris colour
- dyscoria or anisocria secondary to iritis
- sudden loss of vision and hyphaema
- keratin precipitates can appear as ‘mutton fat’ deposits on the ventral corneal endothelium
- aqueous flare
on ophthalmic exam:
- chorioretinitis
- fluffy perivascular cuffing = retinal vasculitis
- dull perivascular puffy areas of pyogranulomatous chorioretinitis
- linear retinal detachment
- vitreous flare
- fluid blistering under the retina
Diagnosis of FIP
- sampling effusions
– FIP effusions are usually clear, viscous/sticky and straw-yellow in colour - cases with neurological ocular signs
– sampling of CSF or aqueous humour
There is no non-invasive, confirmatory test for cats without effusions.
Haematology & biochemistry of FIP
Haematology - common abnormalities:
- lymphopaenia
- neutrophilia, sometimes with left shift
-mild to moderate normocytic, normochromic anaemia
Biochem:
- hyperglobulinaemia
- hypoalbuminaemia or low-to-normal serum albumin
- low albumin to globulin ratio of less than 0.4
- increased bilirubin levels in the absence of haemolysis or elevations of liver enzyme activity
- moderately-marked increase in APPs
Cytology and biochem of FIP effusions
- Highly proteinaceous with TP concentration greater than 35g/L -> consistent with exudate
Cytology:
- pyogranulomatous, with macrophages, non-degenerate neutrophils and few lymphocytes
- sometimes neutrophilic inflammation predominates
- thick eosinophilic (pink-red) proteinaceous backgrounds on cytology slides are often described
Rivalta’s test
- crude point of care assay to identify proteinaceous inflammatory exudates which occur in FIP, but also septic peritonitis and lymphoma
- a negative Rivalta’s test is helpful to rule out FIP
Diagnostic imaging in FIP
- no specific US or radiographic findings exist for FIP
- US (esp of the abdomen) and radiography can show the presence of effusions
- pneumonia due to FIP is sometimes reported and can be associated with radiographic changes
US can reveal:
- abdominal lymphadenomegaly or lymphadenopathy +/- LN hypoechogenicity +/- abnormalities of the liver, intestines, spleen +/- kidneys (which can include a medullary rim sign or hypoechoic sub capsular rim), depending on which organs are affected
for those showing neurological signs MRI can be useful
How to directly detect FCoV
- FCoV antigen by immunostaining from immunohistochemistry on biopsies or immunocytochemistry or immunofluorescence on cytology samples
- FCoV RNA detected by RT-PCR on blood samples, effusion, CSF, tissue or aqueous humour
Epidemiology considerations int he management of cats following FIP diagnosis
- likely safe to take an FIP diagnosed cat into a household with other cats that have already had contact with it as they are likely to be already FCoV infected.
- in households where a cat with FIP has been PTS with no remaining cats in the household it is recommended that the O waits 2 months before getting new cats as it has been suggested that FCoV might preserve it’s infectivity for days to a few weeks
- there’s no need to keep cats with FIP in isolation in a vet practice
Prognosis for FIP
- disease progression seems to be quicker in younger cats and cats with effusions
FIP tx
Non-specific:
- correction of dehydration
- appetite stimulation
- vitamin supplements
Specific tx:
- drainage of pleural effusions if present
- abdominal effusions should not be drained unless causing dyspnoea or discomfort, and then only partially (to the point of relief from CS) due to the risk of dehydration & electrolyte disturbances
- antiviral agents (nucleoside analogs that interfere with the activity of RNA-dependent RNA polymerases; protease inhibitors that limit cleavage of the large poly protein) are effective in curing 70-80% of cats with effusive disease and a smaller % of cats with non-effusive dz
– remdesivir
