FIP Flashcards

1
Q

What is the structure of coronaviruses?

A
  • Enveloped
    • ssRNA
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2
Q

How many feline coronaviruses are there?

A
  • 2 serotypes (I and II)
    • Based on antigenicity (S protein) of a virus
      • resulting from recombination of feline and canine coronavirus genomes including the S gene
    • Serotype I: predominant in the field
    • Either serotype can cause enteric disease or FIP
  • 2 biotypes
    • Based on clinical presentation
      • Feline enteric coronavirus (FECV)
      • Feline Infectious peritonitis virus (FIPV)
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3
Q

What are the outcomes of Feline enteric coronavirus?

A
  1. Infection of enterocytes and blunting of the villi
  2. Inapparent clinical signs or self-limiting diarrhea
  3. Most recover
    1. <5% FIP
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4
Q

What is Feline Enteric Coronavirus Infection?

A
  • Infects felids (domestic cats, cheetah, mountain lion)
  • No clinical signs or self-limiting small bowel diarrhea
  • Spreads by fecal-oral route:
    • very common fecal pathogen
  • High prevalence in multi-cat environments
    • ~30% are chronic shedders
    • Immunity is short-lasting - reinfection possible
    • Feline coronavirus can survive for months in a dry environment
    • Viruses are transmitted by direct contact and fomites
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5
Q

When was FIP discovered?

A
  • first described in 1963
  • Cause-and-effect relationship with feline enteric coronavirus first reported in 1981
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6
Q

How common is FIP?

A
  • 1 in 100-200 cats under 2 years old will develop FIP
  • Most common in cats of 4 months to 2 years old
  • Higher incidences in multi-cat environments
  • Sporadic occurrences - outbreaks uncommon
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7
Q

Why is FIP important

A

almost always fatal

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8
Q

What are the theories of FIP development? Which one is most widely accepted?

A
  • Two different biotypes circulating theory
  • Internal mutation theory:
    • widely accepted
    • Ubiquitously present feline enteric coronavirus mutates into FIPV within each cat
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9
Q

How does the Internal mutation theory work?

A
  • FECV tropism change through mutations - from enterocytes to monocyte/macrophages
  • Impaired T-cell immunity - Humoral (Ab) immune response is NOT protective
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10
Q

What virus mutations are implicated in FIP?

A
  • S (spike) protein: viral attachment and entry
    • 96% FIPV had 2 mutations at the fusion peptide of S gene
    • Commercial RT-PCR test based on these mutations
      • 4% of FIPV does not have mutations & FECV may also have these mutations
  • Mutations in accessory genes 3c and 7b

Multiple viral genes, including S gene and others, are likely to be involved in FIP development

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11
Q

Is there immunity to FIP?

A
  • Humoral immunity (antibodies) is not protective and may be harmful
    • Antibodies to FIPV may facilitate the uptake of the virus into macrophages
    • In experimental FIP studies, cats that have antibodies to FECV progressed faster than naive cats
    • Cats with FIP usually develop strong antibody responses
  • Protective immunity to FIPV is largely cell-mediated
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12
Q

What are the clinical forms of FIP?

A
  • Wet (effusive) form:
    • up to ¾ of cases
    • Chest or abdominal fluid
    • Progress rapidly
    • Average survival time from Dx to euthanasia is about a week
    • Rarely survive more than several weeks
  • Dry (non-effusive) form:
    • About ¼ cases
    • Survival time is weeks to months, rarely one year
  • Dry form may develop effusion at a later stage (dry-to-wet form) Wet form can turn into dry form (wet-to-dry from)
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13
Q

What is the Pathogenesis of FIP?

A
  • Immune-mediated
  • Virus infects macrophages ⇢ activated macrophages secret inflammatory mediators and triggers inflammatory response ⇢ tissue damage
  • Once infected, cytokines, such as Tumor necrosis factor (TNF)-a, secreted by activated macrophages and other immune cells induce T-cell apoptosis leading to lymphopenia ⇢ weaker cellular immunity ⇢ more virus replication
    *
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14
Q

What lesions are common with FIP?

A
  • Granulomatous vasculitis
  • (pyo)granulomatous lesions (granuloma) in organs
  • “Granuloma” - focal area of immune cell aggregates formed in response to chronic inflammation
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15
Q

What is Granulomatous vasculitis associated with FIP?

A
  • Accumulation of activated and FIPV-infected circulating monocytes/macrophages in the blood vessel wall or perivenous spaces
  • Serosal surfaces (peritoneum or pleura)
    • Serositis (peritonitis or pleuritis)
    • Leakage of protein-rich fluid with fibrin
    • Chest or abdominal effusion
  • May affect organs such as brain, eyes, lungs, liver, kidneys ⇢ damage their functions
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16
Q

Where are the pyogranulomas associated with FIP?

A
  • Parenchymatous abdominal organs
    • intestine, liver, kidney, spleen, omentum, pancreas, mesenteric lymph nodes
  • Eyes/central nervous system
  • Lungs
17
Q

What ocular signs are associated with FIP?

A
  • ~68% bilateral involvement
  • Mostly with dry FIP - either alone or with systemic signs
  • FIP is most frequent cause of uveitis
  • Also:
    • keratin precipitates
    • change in coloration of the iris
    • retinal hemorrhage
    • retinal detachment
18
Q

What are the neurological signs associated with FIP?

A
  • Up to 30% of dry FIP develop neurological signs
  • More common for dry FIP - either alone or with systemic signs
  • Pyogranulomatous inflammatory infiltrates:
    • meningitis, ependymitis or periventriculitis
  • Abnormal behavior, personality changes
  • Seizures, ataxia, paresis, paralysis
  • Deficits in cranial nerve function:
    • head tilt
    • nystagmus
    • postural reaction deficits
    • anisocoria
19
Q

What are the common clinical manifestations of FIP?

A
  • Clinical signs and time of appearance are dependent on the organs/tissue involved and attributed to the immune status of the cat
  • Persistent, undulating fever unresponsive to antibiotics
  • Weight loss/failure to grow
  • Effusions in abdomen/chest (wet form)
  • Anorexia
  • Lethargy
  • Anemia
  • Jaundice
  • Ocular lesions
  • CNS signs
  • Abdominal lymphadenopathy
  • Irregular/asymmetrical kidneys
  • Ileocolic mass
20
Q

How is FIP diagnosed?

A
  • Can be challenging in dry form - definitive dx usually post-mortem because:
    • no clinical signs specific for FIP
    • No lab values specific for FIP
    • Detection of virus or antibody in ‘blood’ does NOT mean FIP
  • Dx made through exclusion of other diseases
21
Q

What signalment, clinical and physical features align with a dx of FIP?

A
  • Age: most common for 4 mo - 2yr old cats
  • Environment: higher incidences in multi-cat environment
  • Clinical findings:
    • Fever, lethargy, weight loss, effusions, abdominal palpation/ultrasound (enlarged lymph nodes, intestines or kidney masses), ocular signs, neurological signs, etc
22
Q

What are the common blood abnormalities that align with a dx of FIP?

A
  • ⇡ globulin
  • ⇡ Total protein
  • Low - low-normal albumin
  • ⇡WBC
  • lymphopenia
  • Non-regenerative anemia
  • Hyperbilirubinemia
  • Others (eg elevated liver enzymes)
23
Q

How is the Albumin/globulin ratio helpful for a FIP dx?

A
  • helpful for ruling out FIP (when A/G >0.8)
  • Cats w/ FIP are highly likely to have A/G ration of < 0.8
  • Other diseases can also show A/G of <0.8
    • Of cats showing FIP-like symptoms and having A/G < 0.8:
      • FIP - 12.5%
      • Other disease - 87.5% (may be treatable)
24
Q

What are the characteristics of the effusion that are associated with a dx of FIP?

A
  • Clear to yellow, viscous fluid
  • Protein-rich (High total protein >3.5g/dL)
  • A/G ratio < 0.8
  • Cytology - modified transudate with low-moderate cellularity < 5,000 cells/uL
    • macrophages, neutrophils, and some lymphocytes
  • Rivalta test:
    • Acetic acid reacts with protein in effusion.
      • add one drop of 98% acetic acid (vinegar) to a tube of distilled water, then add a drop of effusion - Positive = drop remains
    • Positive results include FIP, bacterial peritonitis, lymphoma, etc
    • Consider False positives/False negatives!
25
Q

Should dx of FIP be based on RT-PCR on blood or stool?

A
  • No
  • Blood - can be negative in FIP cats, can be positive in FECV cats
  • Stool - FIPV typically not shed in stool; FECV will be positive for RT-PCR
26
Q

What dx can be done to confirm FIP?

A
  • IHC or RT-PCR on biopsy or aspirates of tissues
  • Positive is confirmatory
  • Lesions can be missed!
27
Q

Why are serology test for feline coronavirus Ab unreliable for FIP diagnosis?

A
  • Titers of > 1 : 1600 may suggest FIP
  • ~10% of cats with low titers have FIP
28
Q

Do cats with FIP need to be isolated?

A
  • FIPV loses the ability to infect the enterocytes
  • FIP cats shed no/low titers of virus in stool
  • The risk of FIPV transmission is very low
  • Cats in the same household are likely to have already been exposed to feline enteric coronavirus
29
Q

How can FIP be controlled/prevented?

A
  • Routine strict hygiene to reduce FECV contamination
30
Q

What are the challenges in controlling FECV infections

A
  • Chronic shedders - cats may shed viruses for weeks to several months
  • Reinfection
  • Feline coronavirus can survive for months is a dry environment
  • Easily spread by direct ingestion of feces or contaminated litter or fomite (clothes, gloves, carpet, etc)
31
Q

What are the risk factors for FIP?

A
  • Multi-cat environment - continued exposure to FECV
  • Young age
  • Stress - surgery, change in environment, other infections
  • Immune suppression - coinfection with FeLV or FIV
  • Certain FECV strains have a propensity to mutate into FIPV
  • Certain breed have higher incidences of dry FIP:
    • Burmese, Birman, Himalayan, ragdoll, Abyssinian
  • Bloodline is more important than breed
    • Multiple gene are likely to play into genetic susceptibility
32
Q

Is there a FIP vaccination?

A
  • NO FECV vaccine
  • FIP vaccine:
    • temperature-sensitive modified-live intranasal, FIPV vaccine for kittens of 16 weeks or older
    • Not a core vaccine
    • NOT recommended by the AAFP
    • Limitations:
      • cats are usually exposed at an early age
      • Diverse field strains of feline coronavirus