Eto zamechatelno chto vi s takoi nastoichivost'u otstaivaete "svoiu" a tochnee skazat' prochitannuiu gde to informaciu.Ya prochel bolshuiu chast' polemiki vokrug voprosa FIP na zoovet.ru,poimite eto vse pustoe iz razr'ada "Odna baba skazala". Informacia ne proverennaia i v uvajaemoi literature ne ukazana,bolee togo ya utochnil etu informaciu u Board Certified Internist Virusologist, doctor kotoriy 4 extra goda izuchal tolko virusologiu,vi bi videli ego glaza! Ya viju u vas mnogo vremeni i lubite igrat' v "doctora" vot vam poslednaia informacia iz uchebnika po voprosu FIP(nadeius s English problem net,u men'a pri vsem uvajenii net vremeni na perevodi)
Feline infectious peritonitis (FIP), caused by a feline coronavirus, is seen worldwide. Although a large number of cats may be infected with the feline coronavirus, only a few develop clinical FIP. The disease is progressive and may manifest clinically as a continuum between the effusive (serositis or wet) and noneffusive (granulomatous or dry) forms. A distinct clinical form of noneffusive FIP affecting only the eyes or brain (or both) may be seen. Mortality, even with therapy, approaches 100%. Although primarily a disease of domestic cats, FIP has been recognized in exotic Felidae, including the large and small wild cats. Among larger cats, FIP is seen in lions, leopards, jaguars, mountain lions, and especially cheetahs. Smaller cats susceptible to FIP include the sand cat, lynx, caracal, and pallas cat.
Field strains of feline coronavirus vary in their ability to induce FIP. Some isolates cause FIP (feline infectious peritonitis virus [FIPV]); others cause more localized GI disease ( Feline Enteric Coronavirus). Mutations from feline enteric coronavirus to FIPV occur. The exact relationship between low virulence FIPV strains and feline enteric coronavirus, which is relatively nonpathogenic, is not clear. FIPV is antigenically related to and serologically cross-reacts (by current ELISA and immunofluorescent antibody tests) with a subgroup of mammalian coronaviruses, including transmissible gastroenteritis virus of swine, human coronavirus 229-E, canine coronavirus, and feline enteric coronavirus. FIPV and canine coronavirus are very closely related antigenically and may have crossed between hosts. Strains of FIPV may differ considerably in antigenicity.
Feline coronaviruses are fairly stable in the environment and, once dry, can survive for 4-6 wk. They are enveloped viruses and are destroyed by most household disinfectants, particularly household bleach at a 1:32 dilution.
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Transmission, Epidemiology, and Pathogenesis:
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.
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The acute or primary infection often is asymptomatic, but in some cases, fever of unknown origin, conjunctivitis, and other upper respiratory signs and diarrhea may occur. This stage may last several days or weeks or longer before signs of effusive or noneffusive FIP develop. Cats with effusive FIP are often presented after the owner notices progressive distention of the abdomen due to ascites. About one-third of cats with effusive FIP have pleural involvement and dyspnea, often accompanied by chronic fluctuating fever (102-106Â°F [39-41Â°C]) lasting 2-5 wk, anorexia, weight loss, and depression.
Cats with noneffusive FIP may have a history of vague illness, including chronic fever, malaise, weight loss, and occasionally major organ system failure (renal, hepatic). Overt ocular and CNS signs may occur simultaneously or independently. About 50% of all cats with noneffusive FIP have signs related to intra-abdominal involvement (kidney, liver, spleen, pancreas, lymph nodes); ~60% of cases exhibit either CNS or ocular signs, or both; and ~15% present with ocular signs only. Only 10-15% of noneffusive cases have lesions of the pleural cavity. Many cats have elements of both the effusive and noneffusive forms of FIP.
Ocular disease may manifest as a bilateral anterior uveitis with iritis or iridocyclitis, hyphema, aqueous flare, hypopyon, or keratic precipitates in the anterior chamber. Posterior chamber involvement may include chorioretinitis with subretinal fluid exudation or hemorrhage and secondary bullous or linear retinal detachment. Fundic lesions may include perivascular cuffing, engorgement of retinal veins, and retinal hemorrhage.
Involvement of the CNS in the noneffusive form may cause focal or diffuse lesions in the brain or spinal cord; ~40% of these cases have CNS signs occurring either alone (25%) or in combination with other organ involvement. Clinical signs are variable and may reflect primary spinal cord, cranial, or cerebellar disease. The most common neurologic signs, in order of decreasing frequency, are posterior incoordination and paresis progressing to generalized ataxia, dorsal hyperesthesia, convulsions, personality changes, and hyperesthesia.
In classic effusive FIP, there is diffuse peritonitis or pleuritis (or both) characterized grossly by variable amounts of viscous abdominal or thoracic fluid, deposition of gray-white exudate, and disseminated necrotic plaques (0.5-3.0 mm) on the visceral and parietal peritoneum or pleura. Fibrinous adhesions, particularly between the liver and diaphragm and between loops of bowel, can develop in protracted cases; occasionally, the omentum may be contracted into the anterior abdomen as a thickened mass of fibrinous adhesions. Histologically, lesions are characterized by perivascular necrosis and fibrinonecrotizing or pyogranulomatous inflammation; FIPV particles are seen within macrophages at the periphery of lesions.
Gross lesions in noneffusive FIP consist of multiple, gray-white, raised nodules (0.5-2 cm or larger) in kidneys, visceral lymph nodes, liver, intestines, lungs, eyes, and brain. A single, obstructive, granulomatous intestinal mass is seen in some cases. Histologically, the lesions are perivascular granulomas or pyogranulomas with systemic vasculitis or thrombovasculitis. Ocular lesions may affect either anterior or posterior chambers causing anterior uveitis and iridocyclitis or chorioretinitis, retinitis, retinal hemorrhage and detachment, and optic neuritis. Lesions in the CNS affect the brain and spinal cord and can cause either focal granulomatous masses or more diffuse fibrinonecrotizing or pyogranulomatous meningitis and ependymitis. Occasionally, CSF flow is obstructed by inflammatory exudate, and obstructive hydrocephalus develops.
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Presumptive diagnosis of FIP is based on history, clinical signs, and results of laboratory tests. Diagnosis of effusive FIP is based largely on analysis of the characteristic exudate. The fluid typically is sterile, viscous or ropey, and yellow to tan; it may contain fibrin strands, has a high specific gravity (1.017-1.047) and high protein content (5-12 g/dL), and is composed of variable amounts of mixed inflammatory cells (1,600-25,000/ÂµL). Mixtures of neutrophils, lymphocytes, macrophages, and fewer mesothelial cells in a granular, eosinophilic, proteinaceous background are seen on Wrightâ€™s-stained smears. Protein determinations and electrophoresis of the exudate may be useful in diagnosis. Exudates with total protein >3.5 g/dL (of which >50% is gamma globulin) and cytology consistent with FIP have a positive predictive value of >90%. In addition, the albumin: globulin ratio of the effusion is usually <0.8; a ratio <0.45 is usually predictive of effusive FIP. Documentation of a coronavirus infection by either a positive titer or coronavirus RNA by reverse-transcriptase PCR support a diagnosis of effusive FIP.
About 50% of cats with effusive FIP (and up to 70% of cats with noneffusive FIP) have an increased total plasma protein (>7.8 g/dL), often with hyperglobulinemia (>4.6 g/dL) and a hypergammaglobulinemia. Serum protein electrophoresis may show increases in ?2-globulins and polyclonal (occasionally monoclonal) increases in gamma globulin. Hematologic changes in both effusive and noneffusive FIP, although variable, most consistently show a neutrophilic leukocytosis (>19,000 cells/ÂµL) and a relative lymphopenia (>1,500 cells/ÂµL). Forty to 50% of cats develop a progressive normochromic, normocytic anemia (PCV <24%) that may be severe and nonregenerative if FIP is accompanied by FeLV or infection with Haemobartonella felis . Serologic tests (ELISA, immunofluorescent antibody) that detect antibodies against coronaviral proteins are not specific for FIPV and also detect antibodies against feline enteric coronavirus. The coronavirus titer in cats with FIP is usually increased (1:100 to 1:3,200); some cats with clinical FIP have negative or very low titers. PCR does not differentiate between feline coronaviruses and may be interpreted the same as a positive antibody titer.
Noneffusive FIP is a greater diagnostic challenge. Serum protein abnormalities in debilitated cats with nonresponsive fever, weight loss, multisystemic signs (including ocular and CNS signs), and increased coronavirus titers are suggestive of noneffusive FIP. Blood changes in the noneffusive form must be viewed collectively. Cats that have clinical signs of FIP, lymphopenia, and hyperglobulinemia of >5.1 g/dL have an almost 90% probability of having FIP. In cats that do not meet all 3 criteria, there is a 99% probability that FIP is not the diagnosis. A thorough ophthalmic examination is indicated because nearly 40% of noneffusive cases have ocular lesions. Other ancillary laboratory tests may be helpful; clinical chemistries may indicate organ dysfunction in liver, kidney, or pancreas. In cases of neurologic disease with diffuse meningeal involvement, CSF analysis may show increased protein content (90-2,000 mg/dL) and increased numbers of cells (90-9,250 cells/ÂµL), predominantly neutrophils. The most definitive antemortem diagnostic technique is laparotomy and organ punch biopsy of lesions with subsequent demonstration of typical histopathologic changes.
FIP should be considered in the differential diagnosis of any condition that causes peritoneal or thoracic fluid accumulation and in any chronic wasting disease of cats. Effusive FIP with peritoneal involvement should be differentiated from ascites due to congestive heart failure or hypoproteinemia (renal and liver disease, glomerulonephritis, malabsorption, parasitism), neoplasia, bacterial peritonitis, pansteatitis, toxoplasmosis, tuberculosis, pregnancy, and trauma. Differential diagnoses of effusive FIP with pleural effusion include cardiac insufficiency, neoplasia (lymphoma), pyothorax, chylothorax, cryptococcosis, lung lobe torsion, diaphragmatic hernia, and trauma (hemothorax). Differential diagnosis of noneffusive FIP includes neoplasia and other systemic infectious diseases such as toxoplasmosis, nocardiosis, actinomycosis, tuberculosis, and deep mycotic disease (cryptococcosis, coccidioidomycosis, histoplasmosis, blastomycosis).
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There is no known treatment that can cure FIP once clinical signs arise. Although spontaneous remission in treated cats has been reported, it is uncommon. The mortality rate of clinical FIP is 95%. Cats with the effusive form progress rapidly, usually within 2 mo. The noneffusive form usually is associated with a more prolonged clinical course, with many cats living several months to a year. Treatment with anti-inflammatory and immunosuppressive drugs, along with supportive care, can make the cat more comfortable; in some cats (probably ?10%), therapy may extend survival time by several months. Treatment is best advised in cats that are in good physical condition, are still eating, have no neurologic signs, and that do not have concurrent FeLV-induced malignancy or bone marrow suppression.
Treatment is directed toward controlling the immune-mediated vasculitis and reducing viral load. The most effective treatments are combinations of prednisolone (4 mg/kg or 50-100 mg/m2, PO, sid) and cyclophosphamide (2-4 mg/kg, PO, sid for 4 consecutive days of each week). Alternatively, the cyclophosphamide can be given at 50 mg/m2, PO, every 48 hr or 200-300 mg/m2, every 2-3 wk. Other cytotoxic agents may be substituted for the cyclophosphamide, such as chlorambucil at 10 mg/m2, PO, every 2-3 wk. Because this cytotoxic therapy may suppress bone marrow cells, the hemogram should be monitored weekly and the cat observed carefully for signs of sepsis. Supportive therapy for FIP is important and includes broad-spectrum antibiotics, adequate nutrition and fluid intake, and high doses of ascorbic acid (125-250 mg, bid). The use of low doses of aspirin (10 mg/kg every 48-72 hr) may be useful as an anti-inflammatory and possibly antithrombotic agent when used along with the steroids and cytotoxic agents. Treatment directed toward controlling the virus includes systemic interferon-a (10,000 U/kg, SC, sid or 1.3 million U/m2, SC, 3 times/wk).
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Prevention and Control:
An intranasal, modified live virus vaccine to help prevent FIP is available. It protects 60-90% of the cats vaccinated as determined by experimental challenge several weeks after vaccination. The protection afforded by the vaccine appears to be related to secretory IgA, which neutralizes the virus before entry. The duration of significant protection is unknown but is thought to be limited. Its use has not been associated with causing FIP or accelerated disease either in the general cat population or in catteries with endemic FIP, and it has shown efficacy in preventing FIP losses in large cat shelters with endemic FIP when given to uninfected cats. Because FIP in the general cat population is relatively rare, vaccination of individual pet cats that live mostly or entirely indoors appears to be unwarranted.
Vaccination alone cannot be relied on to control endemic FIP within a cat facility. Other measures to reduce exposure include frequent removal of feces (the primary source of coronavirus), early weaning, isolation of cats that test positive for coronavirus antibodies, isolation and testing of cats after shows, proper sanitation and cleaning using virucidal disinfectants, and immunization against other feline viruses. These should be combined in an overall preventive health program. Increasing the number of litter boxes to at least 1 litter box per 2 cats and reducing crowding stress will reduce FIP losses. A control program based on the presence of serum antibodies to coronaviruses is not warranted. No healthy cat should be euthanized on the basis of a positive coronavirus serum antibody test. The risk of developing FIP following FIPV infection has been shown to have a strong genetic influence. Thus, prevention programs in catteries should include pedigree analysis of disease incidence so that only FIP-resistant breeding stock are used.
Esli est' voprosi,obrashaites, raz'asnu.