FIP Flashcards
What is the structure of coronaviruses?
- Enveloped
- ssRNA
How many feline coronaviruses are there?
- 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
- Based on antigenicity (S protein) of a virus
- 2 biotypes
- Based on clinical presentation
- Feline enteric coronavirus (FECV)
- Feline Infectious peritonitis virus (FIPV)
- Based on clinical presentation
What are the outcomes of Feline enteric coronavirus?
- Infection of enterocytes and blunting of the villi
- Inapparent clinical signs or self-limiting diarrhea
- Most recover
- <5% FIP
What is Feline Enteric Coronavirus Infection?
- 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
When was FIP discovered?
- first described in 1963
- Cause-and-effect relationship with feline enteric coronavirus first reported in 1981
How common is FIP?
- 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
Why is FIP important
almost always fatal
What are the theories of FIP development? Which one is most widely accepted?
- Two different biotypes circulating theory
-
Internal mutation theory:
- widely accepted
- Ubiquitously present feline enteric coronavirus mutates into FIPV within each cat
How does the Internal mutation theory work?
- FECV tropism change through mutations - from enterocytes to monocyte/macrophages
- Impaired T-cell immunity - Humoral (Ab) immune response is NOT protective
What virus mutations are implicated in FIP?
- 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
Is there immunity to FIP?
- 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
What are the clinical forms of FIP?
- 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)
What is the Pathogenesis of FIP?
- 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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What lesions are common with FIP?
- Granulomatous vasculitis
- (pyo)granulomatous lesions (granuloma) in organs
- “Granuloma” - focal area of immune cell aggregates formed in response to chronic inflammation
What is Granulomatous vasculitis associated with FIP?
- 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