Causes of FIP
Most FIPV infections probably result from ingestion of the virus; however, aerosol transmission is also possible. Close contact with an infected cat or its excreta, most likely feces and saliva, is required for virus transmission. Because cats shed viral particles in feces, litter box exposure and mutual grooming are important sources of infection. Cats living in multiple cat households are at greater risk of contracting feline coronavirus and developing FIP because of sharing multiple strains of the virus and stress-associated immunosuppression. Transplacental transmission is suggested by the occasional observation of FIP in stillborn kittens, but the frequency with which this occurs is unknown. In the past, up to 50% of cats with FIP were co-infected with feline leukemia virus (FeLV); FeLV potently suppresses cell-mediated immunity, which is required for resistance to FIP. Currently, the co-infection rate is only 5%, due to FeLV testing and vaccination.
Cats of all ages and either sex can develop the disease, but incidence is highest in cats 6-24 mo old, decreased in cats 5-13 yr old, and increased in those 14-15 yr old. Kittens raised in infected colonies may contract the virus from their mothers or asymptomatic carriers when their maternal immunity wanes at 5-10 wk of age. These kittens typically may develop FIP weeks or months after they are placed in new homes. The prevalence of clinical FIP is <1% of cat-containing households, even though 20-35% of cats are infected with coronavirus. Losses are often sporadic and unpredictable, and morbidity and mortality may be greatly increased, sometimes up to 35% or more in some breeding catteries and households with multiple cats. Generally, the morbidity rate in cattery-bred kittens is 10%. The prevalence of FIPV infection in the general cat population is difficult to determine because current serologic tests for detecting FIPV antibodies cannot discriminate between FIPV and other feline coronaviruses that do not produce disease and that may be more prevalent.
After ingestion of virus or aerosol exposure, FIPV initially replicates in tonsil or intestinal epithelium and then is transported via macrophages and monocytes to primary target organs such as liver, spleen, and visceral lymph nodes. The development of FIP, and the particular clinical form of disease (ie, effusive or noneffusive) depends on the intrinsic immune responses of the cat. Cats with a strong humoral immunity and a weak or absent cell-mediated immune response against FIPV develop a persistent viremia and effusive FIP. The effusive disease results from widespread formation and deposition of immune complexes in blood vessels and from complement activation leading to vasculitis, vessel damage, and leakage of serum and protein into body cavities. Cats with partial cell-mediated immune responses along with humoral immunity develop the more chronic noneffusive FIP, which is characterized by immune-mediated (delayed hypersensitivity-like), granulomatous, frequently perivascular lesions in abdominal viscera, lungs, eyes, and brain. Cats with strong cell-mediated immune responses with or without humoral responses can either completely recover or become persistently infected asymptomatic carriers. The latter may infect contact cats and may themselves later develop FIP, usually after periods of stress or co-infection with FeLV. Some asymptomatic, seropositive carrier cats subsequently may become seronegative and stop excreting virus.
Life is more beautiful with cats!
This website is prepared by www.kedimveben.com
© Copyright 2003-2009
All rights reserved.
