Feline Infectious PeritonitisFeline Infectious PeritonitisFIPFIP

Accession: 11114 and 13858Accession: 11114 and 13858

SkeeterSkeeter1.5 yo DSH with central vestibular 1.5 yo DSH with central vestibular

signssigns

ThorThor14 yo DSH; history of bicavitary 14 yo DSH; history of bicavitary

effusion and heart murmureffusion and heart murmur

FIP-ReviewFIP-Review

1/200 new feline cases to American VTH1/200 new feline cases to American VTH FIP is a fatal immune-mediated dz triggered FIP is a fatal immune-mediated dz triggered

by infection with a mutated feline coronavirusby infection with a mutated feline coronavirus 5% of FCoV infected cats develop FIP in a cattery 5% of FCoV infected cats develop FIP in a cattery

situation, although infection rates are 50-90%situation, although infection rates are 50-90% Non-mutated FCoV replicates in enterocytes and Non-mutated FCoV replicates in enterocytes and

may cause diarrhea or transient resp signsmay cause diarrhea or transient resp signs Single virulent mutation allows virus to replicate in Single virulent mutation allows virus to replicate in

macrophagesmacrophages

FIP-ReviewFIP-Review Over half of the cats with FIP are younger than Over half of the cats with FIP are younger than

12 months of age12 months of age Transmission of non-mutated FCoV:Transmission of non-mutated FCoV:

Oronasal infectionOronasal infection Most commonly transmitted through virus-Most commonly transmitted through virus-

containing fecescontaining feces Rarely transmitted through saliva (salivary shedding Rarely transmitted through saliva (salivary shedding

early in infection), by mutual grooming, by sharing early in infection), by mutual grooming, by sharing the same food bowl, or through close contact. the same food bowl, or through close contact.

Sneezed droplet transmission possibleSneezed droplet transmission possible Transplacental transmission can occur, but is rareTransplacental transmission can occur, but is rare

FIP-ReviewFIP-Review

Mutated FIP-causing FCoV has not Mutated FIP-causing FCoV has not been found in secretions or been found in secretions or excretions of cats with FIPexcretions of cats with FIP

Transmission of the mutated FIP Transmission of the mutated FIP causing FCoV not likely naturally, can causing FCoV not likely naturally, can be iatrogenicbe iatrogenic

PathophysiologyPathophysiology

Viral mutation leads to changes in the Viral mutation leads to changes in the surface structures of the virus that surface structures of the virus that allow the virus phagocytized by allow the virus phagocytized by macrophages to bind to the ribosomes macrophages to bind to the ribosomes in these monocytes/macrophages and in these monocytes/macrophages and replicate therereplicate there

Clinical signs manifest 2 wks to 2 Clinical signs manifest 2 wks to 2 years after mutationyears after mutation

Proposed mechanisms of Proposed mechanisms of pathogenesispathogenesis

1.1. FCoV-infected macrophages leave the FCoV-infected macrophages leave the bloodstream and enable virus to enter bloodstream and enable virus to enter the tissues, where attracts antibodies the tissues, where attracts antibodies and fixes complement. Secondary and fixes complement. Secondary inflammatory cell recruitment result in inflammatory cell recruitment result in granuloma formationgranuloma formation

2.2. Immune complexes exit circulation into Immune complexes exit circulation into vascular walls, fix complement, vascular walls, fix complement, granuloma formationgranuloma formation

PathogenesisPathogenesis

Complement fixationComplement fixation Release of vasoactive aminesRelease of vasoactive amines Endothelial cell retraction Endothelial cell retraction Increased vascular permeability w/ Increased vascular permeability w/

exudation of plasma proteins and exudation of plasma proteins and development of modified transudate development of modified transudate effusionseffusions

Forms of FIPForms of FIP

Effusive, exudative, wet formEffusive, exudative, wet form fibrinous peritonitis, pleuritis, or pericarditis fibrinous peritonitis, pleuritis, or pericarditis 60% of cats with ascites have FIP60% of cats with ascites have FIP 14% of cats with pericardial effusion have FIP14% of cats with pericardial effusion have FIP

Noneffusive, nonexudative, dry form Noneffusive, nonexudative, dry form granulomatous changes in visceral organs, eye, and CNSgranulomatous changes in visceral organs, eye, and CNS

Mixed formMixed form Differentiating forms has no prognostic Differentiating forms has no prognostic

significance, one form can progress to the significance, one form can progress to the other formother form

Sites of diseaseSites of disease CNS: ataxia, nystagmus, seizures most CNS: ataxia, nystagmus, seizures most

common common 75% have hydrocephalus75% have hydrocephalus

Ocular: Retinal cuffing, uveitisOcular: Retinal cuffing, uveitis Abdomen: Mesenteric LN, visceral organs Abdomen: Mesenteric LN, visceral organs

or just bowel wall, esp ICJor just bowel wall, esp ICJ

DiagnosisDiagnosis

CBC-incr/decr WBC; anemia (AIHA, Heinz CBC-incr/decr WBC; anemia (AIHA, Heinz bodies); decr platelets (DIC)bodies); decr platelets (DIC)

Chemistry-reflect organ involvementChemistry-reflect organ involvement Hyperglobulinemia-if serum A/G ratio<0.8 has Hyperglobulinemia-if serum A/G ratio<0.8 has

92% PPV for FIP92% PPV for FIP Cavity fluid-straw-colored modified Cavity fluid-straw-colored modified

transudatetransudate

Splenic US findingsSplenic US findings

2 cases: Pyogranulomatous splenitis 2 cases: Pyogranulomatous splenitis secondary to FIP (2001)secondary to FIP (2001) Abdominal effusionAbdominal effusion Large spleen, normal echogenicityLarge spleen, normal echogenicity Irregular contour in one catIrregular contour in one cat

Compared to dogs, cats have little Compared to dogs, cats have little periarterial lymphatic tissue, with the periarterial lymphatic tissue, with the lymphatic tissue confined to nodules of lymphatic tissue confined to nodules of white pulp.white pulp.

MRI findings in Neuro FIPMRI findings in Neuro FIP

Pachymeningeal enhancement, especially Pachymeningeal enhancement, especially of brainstem and spinal cordof brainstem and spinal cord

Hydrocephalus-obstructiveHydrocephalus-obstructive Marked ependymal enhancement Marked ependymal enhancement Periventricular contrast enhancementPeriventricular contrast enhancement The 4th ventricle was the most The 4th ventricle was the most

consistently affected (4/4), and the lateral consistently affected (4/4), and the lateral ventricles were the least affected (1/4).ventricles were the least affected (1/4).

Clinical features of Clinical features of neurologic FIPneurologic FIP

Histopathologic lesions in the brain Histopathologic lesions in the brain consisted of meningitis, ependymitis consisted of meningitis, ependymitis or periventriculitis, and choroiditis of or periventriculitis, and choroiditis of varying severity varying severity

Lesions most severe at the base of Lesions most severe at the base of the cerebellum and brain stem, the cerebellum and brain stem, including the medulla oblongata.including the medulla oblongata.

Diagnosis?Diagnosis? Antibody tests-cannot differentiate Antibody tests-cannot differentiate

enteric form and mutated form!enteric form and mutated form! PCR tests cannot differentiate two PCR tests cannot differentiate two

forms!forms! Possibly helpful on CSF or effusion? Possibly helpful on CSF or effusion? Not adeq studied, may be very helpfulNot adeq studied, may be very helpful

DiagnosisDiagnosis IFA-FIP antigen-effusion or tissueIFA-FIP antigen-effusion or tissue

100% PPV on effusion, 57% NPV100% PPV on effusion, 57% NPV “… “… intracellular FCoV antigen by intracellular FCoV antigen by

immunofluorescence or immunohistochemistry is the immunofluorescence or immunohistochemistry is the only way to diagnose FIP definitively. This tool should only way to diagnose FIP definitively. This tool should be used whenever possible.” (Hartmann, 2005)be used whenever possible.” (Hartmann, 2005)

Histopathology/NecropsyHistopathology/Necropsy Pathognomonic lesions: localized Pathognomonic lesions: localized

perivascular mixed inflammation perivascular mixed inflammation w/macrophages, neutrophils, lymphocytes, w/macrophages, neutrophils, lymphocytes, and plasma cellsand plasma cells

ReferencesReferences

1.1. Foley JE, Lapointe J, Koblik PD, Poland A, Pedersen Foley JE, Lapointe J, Koblik PD, Poland A, Pedersen NC. Diagnostic features of clinical neurologic feline NC. Diagnostic features of clinical neurologic feline infectious peritonitis. J Vet Intern Med 1998;415-423.infectious peritonitis. J Vet Intern Med 1998;415-423.

2.2. Hanson, JA, et al. Ultrasonographic appearance of Hanson, JA, et al. Ultrasonographic appearance of splenic disease in 101 cats. Veterinary Radiology & splenic disease in 101 cats. Veterinary Radiology & Ultrasound, Vol. 42, No. 5, 2001, pp 441-445.Ultrasound, Vol. 42, No. 5, 2001, pp 441-445.

3.3. Hartmann K. Feline Infectious Peritonitis. Hartmann K. Feline Infectious Peritonitis. Vet Clin Vet Clin Small Anim, 35, 2005. pp 39–79.Small Anim, 35, 2005. pp 39–79.

4.4. Mellema, JM et al. Meningeal enhancement on Mellema, JM et al. Meningeal enhancement on magnetic resonance imaging in 15 dogs and 3 cats. magnetic resonance imaging in 15 dogs and 3 cats. Veterinary Radiology Veterinary Radiology & Ultrasound, Vol. 43, No. I , & Ultrasound, Vol. 43, No. I , 2002. pp 10-15.2002. pp 10-15.