Feline Infectious Peritonitis, Slides of Veterinary

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FELINE

INFECTIOUS

PERITONITIS

History

➢ First discovered in Boston in 1963 as a syndrome in cats characterized as an immune-mediated Vasculitis & Pyogranulomatous inflammatory reactions ** ➢ 1978 a virus identified as etiologic agent ➢ 1979 classified as a Coronavirus labeled as Feline Infectious Peritonitis Virus, Immune mediated disease triggered by infection with Feline Corona Virus (FCoV) Meaning an imbalance response of the immune system; immune system may overreact by attacking the body ex. Autoimmune diseases

Etiology & Pathogenesis

➢ Two Hypothesis: The Internal Mutation Theory; The existence of distinct circulating virulent and avirulent strains in a population along with exposure to the pathogenic strain, viral load and the cat’s immune response. ** ➢ The internal mutation theory: cats are infected with the primarily avirulent (nonpathogenic strain) FCoV that replicates in enterocytes (cells of intestinal lining); In some cats, a mutation happens in a certain region of the FCoV genome that creates a new phenotype with the ability to replicate within macrophages. Researchers have speculated suggesting that circulating Feline Enteric Coronaviruses are closer to making the mutations necessary for FIP development ** ➢ The Circulating virulent and avirulent strains theory suggests that there are several factors “a perfect storm” such as virulence of strains, exposure to virulent strains, viral load, and immune response. ➢ For both Hypothesis's, the key to development of FIP is the massive replication of FCoV in macrophages. ***** If the cat does not eliminate the macrophages infected with replication- competent virus early in infection, the presence of the virus within the circulating macrophages initiates a fatal arthus-type (antigen-antibody complexes, moderate excess of antigen) immune mediated reaction.

Geographic Distribution

➢ FCoV and FIP are known worldwide in both domestic & wild populations; Of those infected with FCoV only a few < 5% develop FIP. ➢ Among FCoV strains isolated in the field in the USA and Europe, 70%–95% are serotype I ➢ In Japan serotype II is most prevalent ** ➢ Most cats with FIP are infected with FCoV serotype I. However, both serotypes can cause FIP and both can cause clinically inapparent FCoV infections ➢ FCoV is pathogenic and is susceptible to nondomestic animals as well; In South Africa, a study was done that included wild & captive animals. Cheetahs were more prone to developing FIP due to their lack of genetic diversity along with a deficiency in their cellular immunity which predisposes them to FIP ➢ Similar findings were also noted in USA and Europe for nondomestic cats in captivity ➢ Domestic cats in catteries, multi cat households, and shelters are at higher risk for FIP ➢ FIP is closely tied to genetics and the least understood of all cat diseases **

Ascites Anterior Uveitis seen with noneffusive cases Aqueous Flare Fibrin Formation Blood ocular barrier breakdown (mild uveitis) Severe Iritis Chronic Granulomatous disease Uveitis inflammation of the uveal coat of the eye

Previously Categorized as three Forms of FIP

I. Effusive Exudate “wet form” Characterized by ➢ Fibrinous peritonitis ➢ Pleuritis and/or Pericarditis with effusion in abdomen, thorax and/pericardium

• Effusion (abnormal collection of fluid in hollow spaces or between tissues of the body)
• Pleuritis (inflammation of tissues that line lungs & chest cavity)
• Pericarditis (swelling, irritation of the thin saclike membrane surrounding the heart) II. Non-effusive, non-exudative, granulomatous, parenchymatous “Dry Form” Characterized by ➢ Granulomatous changes in various organs including eyes & CNS
• Granulomatous (area of inflammation) III. Mixed form of both ** Differentiation between these forms is not useful and the value is only for diagnostic approaches. Feline Enteric Coronavirus Type 1 is the strain most likely to mutate

Cat kidneys ( A ) Multifocal to coalescing granulomatous inflammation (white, rough appearance) following the superficial blood vessels. ( B ) Cut section also shows the vascular-oriented distribution Spleen with Yellowish- white Raised nodule Jejunum with multiple granuloma serosa

Diagnosis

➢ FIP is difficult to diagnose!! FCoV is highly contagious ➢ The viral DNA of feline enteric coronavirus can be detected in feces by RT-PCR ➢ Histopathology exam of affected tissue; Biopsy (Gold Standard) Immunohistochemistry ➢ Blood Chemistry abnormalities can be found in routine blood work but none specific to FIP * ➢ Serum Chemistry: shows increase in total serum protein concentration increase globulins decreased albumin/globulin ratio show <0.8 High chance (92% PPV) of FIP If >0.8 Likely no FIP (61% NPV) * ➢ Effusion Analysis * ➢ Rivalta’s Test PPV86% NPV 97% Analysis of cerebrospinal fluid (a drop of effusion fluid delicately on the surface of distilled water & acetic acid mixed in reagent tube) If the drop disappears or solution remains clear then its neg, if it retains its shape, sinks, or stays attached at the surface it’s positive * ➢ X-rays, ultrasounds (visualize effusion) ➢ PCR Detects a very small amount of the FCoV; downside false +/ false – * ➢ FIP can be a challenge to Diagnose because clinical signs are similar to many diseases. It can be a diagnosis of exclusion ruling out other diseases first. *

Titers (^) RT-PCR

Biopsy of a mesenteric lymph node from a 1-year-old Burmese cat diagnosed with feline infectious peritonitis. Note the three macrophages in the center with intact erythrocytes in their cytoplasm, depicting erythrophagocytosis. Haematoxylin (Stain) an eosin (x 330 magnification) Photo courtesy of Dr. Patricia Martin. Australian Veterinary Journal Clinicopathological findings associated with FIP in Sydney Australia: 42 cases 1990-2002 (see references)

Risk Factors for developing FIP

➢ Younger cats 3months to 2yrs of age; any can still develop it ➢ Sexually intact males ➢ Cats are at greatest risk of developing FIP in the first 6–18 months after infection with FCoV; the risk decreases to ~4% at 36 months after infection. ➢ Purebreds such as Abyssinian, Bengal, Birman, Himalayan, Ragdoll & Rex are at higher risk due to the genetic background; FIP is a mutation and because there isn't a lot of genetic diversity then there is susceptibility with mutations. Tom cats are also a concern because they’re used over and over ➢ Shelters, Catteries and multi cat homes are at higher risk of infection due to crowed conditions * ➢ Shared and contaminated litter boxes *

Treatment

➢ FIP is almost always fatal Euthanasia is the most humane treatment ➢ FCoV while highly contagious * the rate of mutation is <5% * ➢ Many cats are asymptomatic ➢ Most cases do not require therapy FCoV ➢ Supportive care may be needed in both FIP & FCoV fluid therapy, oral electrolyte solutions, antiemetics, nutritional support ➢ Control and prevention of FECV are usually a concern only in breeding catteries and rescue shelters ➢ Supportive treatment for FIP is aimed at suppressing the immune overreaction * *Corticosteroids, Immunosuppressives Prednisolone, cytotoxic drugs cyclophosphamide ➢ Cats with large effusions benefit from removal of the fluid; injection of dexamethasone into the abdominal or thoracic cavity may follow (1 mg/kg/day until no effusion is present) ➢ If a cat has been euthanized or has died due to FIP, the owner should wait 2 months before obtaining another cat. FCoV can remain infectious for at least 7 wks. in the environment, particularly where litter boxes are in use ➢ Housing and husbandry practices that reduce exposure to feces and contaminated environments have a tremendous influence on the number of cats exposed to FCoV **

Questions?