An update on feline infectious peritonitis


Feline infectious peritonitis (FIP) remains a daunting disease-its pathogenesis is unclear, it can be difficult to diagnose, especially in the dry form, and it is uniformly fatal.

Feline infectious peritonitis (FIP) remains a daunting disease—its pathogenesis is unclear, it can be difficult to diagnose, especially in the dry form, and it is uniformly fatal. While research into this disease and its causative agent has not answered all the questions, more is being learned, diagnostic tests are improving, and treatment may be on the horizon. This review offers an update on our current knowledge about FIP.

Illustration by Paul Petersen


FIP is caused, at least in part, by feline coronavirus. This virus is related to the enteric canine coronavirus as well as the agent of transmissible gastroenteritis in swine. It is an enveloped virus, which is unusual for enteric pathogens, and contains a large RNA genome. This large genome is correlated with a high virus mutation rate through nucleotide substitutions, deletions, and recombination events. The virus's mutability may play a role in the development of virulence.

Feline coronavirus is divided into two serotypes based on virus antigenicity. Most field strains are type 1; type 2 is a recombinant of feline and canine coronaviruses.1 FIP may be caused by either serotype, although most cases are associated with type 1.2 However, most feline coronavirus infections produce no or only mild disease that typically manifests as diarrhea.

Feline coronavirus infections are common, especially in multicat situations. The virus is widespread, occurring worldwide and in domestic and nondomestic felids. Serologic studies indicate high prevalence rates in most feline populations. The virus is spread primarily by fecal-oral transmission, and infected cats may remain chronically infected, shedding the virus continuously or intermittently for long periods.3 Indirect transmission of the virus may occur; the virus is easily inactivated with detergents used on nonporous surfaces but may persist in the environment for several weeks. Kittens born into populations in which feline coronavirus is endemic may become infected by 4 to 6 weeks of age.4

FIP is an uncommon manifestation of feline coronavirus infection, occurring in only 5% to 10% of infected cats.5 Why most cats suffer no serious consequences of feline coronavirus infection, while some develop a lethal disease, remains uncertain. Virus factors are important in FIP development, as some strains are highly virulent and cause FIP in experimentally infected cats. In addition, FIP outbreaks have occasionally occurred.6,7 It has been speculated that a mutation in the infecting virus leads to a change in the virus's biotype, from one causing mild enteritis to one causing FIP.8,9 However, no genetic mutation that consistently correlates with FIP production has been identified. So why do only certain cats progress to FIP?


The pathogenesis of FIP is complex and still not completely understood. The feline coronavirus is required but may not alone cause the disease. This virus is spread via fecal-oral transmission and survives transit through the gastrointestinal tract. It enters the intestinal epithelia from the lumen, with replication leading to the death of the epithelial cells that may manifest as diarrhea.3 From the intestines, the virus may spread to infect monocytes and macrophages. This acquisition of monocyte/macrophage tropism by the virus is a critical factor for FIP development—in cats that develop FIP, it appears that the virus replicates efficiently in these cells, achieving high viral levels in the blood.10

One study found that the feline coronavirus spike protein provides target cell specificity and is the critical determinant for macrophage infection.11 The region of the spike protein that mediates viral envelope fusion with the cell membrane during virus entry is the critical domain that determines macrophage tropism. Regardless of how the monocyte/macrophage tropism arises, the efficient replication of feline coronavirus in these cells is a key factor in FIP development. High levels of viral RNA have been detected in blood and tissue of cats with FIP.10,12 However, this property alone does not appear to be sufficient to lead to FIP development, as another study found that high viral load was not associated with clinical signs or pathology.13 Thus, systemic spread and replication are not unique to FIP.

Other viral genes speculated to play a role in FIP development are those encoding the coronavirus nonstructural proteins, in particular the 3c and 7b genes.8,9 The function of these gene products is unknown, but they are theorized to be important in the virus's virulence. The evolution of the FIP-causing ability may in fact involve multiple mutations. On the other hand, at least one study found no evidence of mutation in the virus identified in FIP lesions.14 Thus, consensus on the precise nature of the viral contribution to FIP development has not been reached.

Immune response

The disease of FIP is predominantly immune-mediated. Lesions are distributed along the vasculature, particularly along veins.15 Emigration of infected monocytes/macrophages from blood vessels into perivascular regions incites local inflammatory responses. Type II and type III hypersensitivity responses occur, with complement activation and cellular destruction. This destruction may occur widely throughout an infected cat's tissues, leading to increased vascular permeability, extensive pyogranulomatous lesions, and the classic signs of the effusive, or wet, form of FIP. Alternatively, focal lesions may be confined to one or more organ systems in the noneffusive, or dry, form of FIP.

The cells involved in the inflammatory process are primarily macrophages and neutrophils; however, B lymphocytes play a critical role in producing disease.16 In cats that develop FIP, a strong humoral response to infection occurs, with inadequate cell-mediated response by cytotoxic T cells.17 This antibody production is ineffective in clearing the virus and contributes to the immune-mediated disease.18

Potential causes of immune-mediated effects

The factors responsible for the unsuccessful immune response described above are unknown. Various mechanisms appear to be at work.

Cytokines. A great deal of work has centered on cytokine responses in affected cats. Unfortunately, here, too, the results are not consistent. Much focus has been placed on interferon gamma because of its role in enhancing the cell-mediated immune response. While serum interferon gamma concentrations were not found to differ between cats with FIP and healthy cats with feline coronavirus in catteries with a low prevalence of FIP, higher serum interferon gamma concentrations were seen in healthy cats with feline coronavirus as compared with cats with FIP in catteries with a high prevalence of FIP.19 In addition, interferon gamma concentrations were significantly higher in the effusions than in the serum of cats with FIP, indicating that, at least at the tissue level, cell-mediated immunity may contribute to lesion development.19 In particular, it indicates that local activation of macrophages by interferon gamma may be occurring, leading to enhanced viral replication.20 In contrast, a systemic increase in interferon gamma concentrations, as indicated by elevated expression in blood, may protect infected cats from disease.19,21

Other studies have examined the expression of various cytokines in blood, tissue, or both, often comparing cytokine production between cats with FIP and healthy cats with feline coronavirus. Tumor necrosis factor alpha (TNF-alpha) expression increases in infected macrophages and may increase expression of the receptor for feline coronavirus on macrophages, enhancing viral replication.22 Interleukin-10 and interleukin-12 concentrations have been shown to be lower in cats with FIP as compared with healthy cats with feline coronavirus infection.10 The decreased levels of these cytokines may lead to excessive macrophage activation and inhibition of the cell-mediated immune response. While the virus is not cleared, macrophage infection continues, also leading to activation. These activated monocytes/macrophages adhere to vascular endothelium and infiltrate the perivascular region, causing vasculitis and secreting pro-inflammatory cytokines, a key contributor to the pathology associated with FIP.15,23

T lymphocyte depletion. Another finding in cats with FIP is lymphocyte depletion, particularly of T lymphocytes,24 through apoptosis. The virus does not replicate in lymphocytes, so some other mechanism must be responsible for this process. The resultant depletion of T lymphocytes contributes to enhanced viral replication, as these cells are important in cell-mediated immunity. Soluble mediators released from infected monocytes and macrophages may be responsible for this phenomenon. In particular, TNF-alpha may lead to apoptosis, primarily of CD8+ T cells, the cytotoxic T cells, which are critical to cell-mediated immunity.22 At least one group of investigators propose that the virus-driven T cell depletion occurring in infected cats that do not mount a quick and effective cell-mediated immune response leads to loss of immune control and unchecked viral replication.12

Genetic and environmental factors. The ability of an animal to mount an effective immune response may lie at least in part in its genetic make-up. Studies have shown a genetic predisposition to disease occurrence. Certain breeds, including Bengals, Birmans, and Himalayans, are more likely to develop FIP.25 In addition, susceptibility along familial lines has also been documented.26 It is not known what specific host genetic factor or factors may be involved, but these factors may include major histocompatibility complex haplotype or T lymphocyte receptors.27

Environmental factors may also play a role. Stressors, such as crowded housing, trauma, surgery (e.g. ovariohysterectomy, orchiectomy), or other conditions, may precipitate FIP development.28 It has been shown that concurrent infection with other agents, particularly the feline retroviruses, also predisposes cats to develop FIP, probably through immunosuppression.


Antemortem diagnosis of FIP can be difficult. Arriving at a diagnosis involves a combination of elements, with no single test providing a definitive diagnosis, except for histologic examination or immunohistochemistry (Figure 1).

1. Metaphorically speaking, diagnosing FIP is like building a brick wall. The patient's history, signalment, and clinical signs as well as findings from multiple tests must all be assessed to reach a diagnosis; only histologic examination or immunohistochemistry provides a definitive diagnosis.

History and signalment

Diagnosing FIP starts with obtaining an animal's history and noting its signalment: most cases occur in young cats (usually < 1 year of age), it occurs more frequently in purebred than it does in mixed-breed cats, and affected cats usually originate from or are currently housed in multicat situations.29 In breeding catteries, examination of records may reveal a genetic connection among cases. A history of a stressful event may precede the onset of signs by several weeks, such as surgery, adoption from a shelter, or trauma.

Clinical signs, physical examination findings, and effusion analysis

The cat may present with weight loss, fever, and inappetence. The fever may wax and wane and is not responsive to antibiotics. Abdominal palpation of affected cats may reveal thickened bowel loops, mesenteric lymphadenopathy, or irregular serosal surfaces of abdominal organs. Cats with the effusive form may not present as much of a diagnostic challenge as those with the noneffusive form do. With the noneffusive form, signs may be referable to virtually any organ, singly or in combination. Granulomatous lesions may occur in the eye (e.g. retinal changes, uveitis), central nervous system (multifocal lesions), or abdominal organs, including the intestines. In addition, a combination of effusive and noneffusive forms may occur, and transition between the two can occur in any cat with FIP.

For cats with effusion, evaluation of this fluid can be informative. The fluid has been described as straw-colored and is usually viscous because of the high-protein content. It usually has a relatively low cellular content that is pyogranulomatous (macrophages and neutrophils; usually no toxic changes in the latter). Detection of feline coronavirus antigen by immunofluorescence within inflammatory cells (macrophages) in effusive fluid correlates with a diagnosis of FIP.30 (Viral antigen detection by immunofluorescence is offered by many diagnostic laboratories and can be done on sediment from submitted abdominal fluid.) A high protein concentration and a low albumin-globulin ratio in the fluid are also indicative of FIP.30

Serum chemistry profile, acute phase protein, CBC, and immunophenotyping findings

Serum chemistry profiles reveal that many cats with FIP have elevated serum total protein concentrations because of the high globulin concentrations; however, even with normal total protein concentrations, a decreased albumin-globulin ratio may be evident. As this ratio approaches 0.5, a diagnosis of FIP becomes more likely.30 Other abnormalities may be evident depending on the tissues involved (e.g. elevated hepatic enzyme activities or renal function values).

In addition to high globulin concentrations, elevation in acute phase proteins also occurs. Elevations in alpha-1 acid glycoprotein in serum have been noted in cats with FIP and may aid diagnosis. In one study that evaluated the usefulness of measuring alpha-1 acid glycoprotein to diagnose FIP, it was found that high alpha-1 acid glycoprotein concentrations are a discriminating marker for FIP.31 Measurement of this serum protein can be specifically requested from some commercial labs. But keep in mind that other inflammatory conditions can lead to alpha-1 acid glycoprotein increase.

Cats with FIP may also have evidence of an anemia of chronic disease and a lymphopenia, despite elevated total white blood cell counts.32 Immunophenotyping shows T lymphocyte depletion in particular; in fact, a normal T lymphocyte count has a significant negative predictive value for FIP (immunophenotyping or flow cytometry is often offered by laboratories associated with academic institutions).12

Serum antibody and virus detection assays

Feline coronavirus-specific assays can generally be categorized as antibody measurement or virus detection assays. Because of the inability to identify a consistent mutation correlating with FIP production, no FIP virus-specific test exists.

Serum antibody. Serologic analysis detects only antibody to the coronavirus and does not reflect the virus's biotype. While a high antibody titer is consistent with a diagnosis of FIP, it is not confirmatory; in addition, some cats with FIP have low antibody titers or are seronegative.33 This latter situation may occur in fulminant cases or may be due to high virus levels that bind antibody, making it undetectable in the serologic assay.

Serologic assays for antibody to a single virus-specific protein (as opposed to antibody to multiple virus proteins) have been developed. In particular, a serologic test for antibody to the 7b protein has been offered as a diagnostic aid to FIP. This protein is a viral nonstructural protein whose function is unknown, but, as described above, it may play a role in disease development. It has been theorized that this protein is not expressed in all feline coronavirus infections; when expression does occur, perhaps because of a viral mutation allowing 7b expression, FIP may develop. Cats with high concentrations of antibody to the 7b protein would, by definition, be infected with the FIP viral biotype. However, subsequent studies have shown that 7b expression occurs in most infections; 7b-specific antibodies, while consistently present at high concentrations in cats with FIP, are also present in healthy cats with feline coronavirus.34 Thus, while 7b seronegative status would lessen the likelihood of a diagnosis of FIP, this test (offered by Antech Diagnostics) cannot be used to confirm FIP.

Virus detection. Virus detection assays also suffer from this nonspecificity for FIP virus. That is, finding the virus by antigen detection (e.g. immunofluorescent staining of ascitic macrophages) or genetic detection (e.g. real-time polymerase chain reaction [PCR] testing of whole blood) is consistent with a diagnosis of FIP but is not necessarily confirmatory. At least one laboratory (The Molecular Diagnostics Laboratory at Auburn University's College of Veterinary Medicine) offers a real-time PCR assay that quantitates the level of viral mRNA in the monocytes of cats. While it is not known precisely how the cutoff levels were determined, high levels of viral mRNA do reflect efficient viral replication in circulating monocytes.35 As stated above, high viral loads in the blood are consistent with FIP, especially in the end stage; however, high viral loads in the blood are also found in healthy cats in endemically infected populations.10,36 Virus detection and quantitation is, thus, not confirmatory for FIP but does offer diagnostic information.

In addition, detecting virus in the feces by using PCR testing is the optimal method for identifying viral shedding. PCR testing without quantitation is offered at many commercial laboratories. Testing multiple samples from an animal over time can identify chronic shedding.3 Because these animals may shed the virus intermittently, test at least two, or preferably more, samples collected at a monthly interval. An example regimen would be three samples collected daily, followed by three samples daily one month later. Some laboratories may offer pooling of samples to reduce costs.

Histologic examination and immunohistochemistry

The gold standard for FIP diagnosis remains histologic examination and immunohistochemistry for feline coronavirus antigen.15,16 Granulomatous lesions are vascular and perivascular, involving small and medium veins primarily. Cellular composition is mainly monocytes and macrophages with a minority of neutrophils. B lymphocytes and plasma cells may be found at the periphery of lesions, while T lymphocytes are few. Detection of viral antigen (immunohistochemistry) or nucleic acid (in situ hybridization) in infected cells within lesions is confirmatory; this testing is offered by some pathology laboratories.


In the past, treatment has focused on two areas—suppressing the immune response or modulating the immune response. The former generally involves administering immunosuppressive drugs to inhibit the immune response, while the latter attempts to enhance the cell-mediated response through the administration of cytokines such as interferon. Immunosuppression by using prednisolone or cyclophosphamide will sometimes slow disease progression but will not provide a cure.37 While human and feline recombinant interferon have been shown to inhibit feline coronavirus replication in vitro, in vivo studies have shown no effect on survival time or quality of life.37

Recently, a new drug tested in three cats with the dry form of FIP demonstrated efficacy in prolonging life and alleviating signs.38 The drug, a polyprenyl immunostimulant, is an investigatory veterinary biologic that upregulates mRNA expression of T helper lymphocytes responsible for effective cell-mediated immunity. In this study, two cats with FIP were still alive two years after diagnosis, while one cat survived 14 months. Further studies are under way to assess this drug's potential for FIP treatment.38


Preventing FIP is challenging since the only effective means of control is preventing infection with feline coronavirus. The widespread nature of the virus and its ease of transmission, as well as the existence of persistent infections, make prevention difficult in a multicat situation. If one cat in a population dies of FIP, the other members are likely already infected with the circulating virus. The likelihood that other cats in the population will develop FIP is not high, but it can occur, especially if there are genetic links to the affected cat.39 There may be some risk to introducing a new cat to this population, but generally, FIP outbreaks are not observed.

Isolating queens and kittens

Various strategies have been used to eliminate or prevent feline coronavirus infection in a cat population. In breeding catteries, isolating pregnant queens nearing parturition and queens and kittens after parturition, as well as early weaning, has been advocated.39 This prevention method, which requires strict quarantine measures and low (< 5) numbers of cats in the population, is designed to delay infection until the kitten is older and can more easily eliminate the virus after exposure.

Removing affected cats from a population

Other means of control involve removing chronic shedders from the population. As mentioned above, this may be done most accurately by using PCR tests to detect virus in feces. Serology may also be helpful, as cats that maintain high antibody levels are likely shedding high levels of virus.39 One of the most important measures that can be used in a breeding cattery is to maintain complete breeding records. Heritability of FIP susceptibility is known to exist; thus, continued breeding of parents, particularly sires that have produced kittens that developed FIP, is not recommended.26,39


At least one commercially available feline coronavirus vaccine exists. It is an intranasal vaccine containing a temperature-sensitive mutant of feline coronavirus that allows replication in the upper respiratory tract but not systemically. While this vaccine appears to be safe, its efficacy has been questioned. A small reduction in the number of FIP cases was noted in one study when the vaccine was given to seronegative cats.40 However, in cats with pre-existing antibody, the vaccine showed no protection.

In households in which feline coronavirus is endemic or in which FIP has occurred, most cats are seropositive and, thus, not aided by vaccination. Kittens at highest risk for FIP are those born into colonies in which the virus is endemic, where infection often occurs by 4 to 6 weeks of age.4 However, the vaccine is not given until 16 weeks of age; thus, the vaccine is of dubious usefulness in those situations in which the risk is greatest. It may provide some protection for seronegative cats entering an infected population, but currently, this vaccine is not recommended as part of core vaccines for routine use.41


FIP is an enigmatic disease that can frustrate clinicians and distress cat owners. It remains the focus of intense research, and the findings hold promise for understanding the pathogenesis, improving diagnostic tests, and developing effective treatment and control strategies.

Melissa A. Kennedy, DVM, PhD, DACVM (virology, immunology, bacteriology/mycology)

Department of Comparative Medicine

College of Veterinary Medicine

The University of Tennessee

Knoxville, TN 37996


1. Herrewegh AA, Smeenk I, Horzinek MC, et al. Feline coronavirus type II strains 79-1683 and 79-1146 originate from a double recombination between feline coronavirus type I and canine coronavirus. J Virol 1998;72(5):4508-4514.

2. Benetka V, Kübber-Heiss A, Kolodziejek J, et al. Prevalence of feline coronavirus types I and II in cats with histopathologically verified feline infectious peritonitis. Vet Microbiol 2004;99(1):31-42.

3. Pedersen NC, Allen CE, Lyons LA. Pathogenesis of feline enteric coronavirus infection. J Feline Med Surg 2008;10(6):529-541.

4. Harpold LM, Legendre AM, Kennedy MA, et al. Fecal shedding of feline coronavirus in adult cats and kittens in an Abyssinian cattery. J Am Vet Med Assoc 1999;215(7):948-951.

5. Addie DD, Toth S, Murray GD, et al. Risk of feline infectious peritonitis in cats naturally infected with feline coronavirus. Am J Vet Res 1995;56(4):429-434.

6. Panzero RA. An outbreak of feline infectious peritonitis in a colony of Cornish Rex cats. Feline Pract 1992;20(4):7-8.

7. Kennedy MA, Boedeker N, Gibbs P, et al. Deletions in the 7a ORF of feline coronavirus associated with an epidemic of feline infectious peritonitis. Vet Microbiol 2001;81(3):227-234.

8. Herrewegh AA, Vennema H, Horzinek MC, et al. The molecular genetics of feline coronaviruses: comparative sequence analysis of the ORF7a/7b transcription unit of different biotypes. Virology 1995;212(2):622-631.

9. Vennema H, Poland A, Foley J, et al. Feline infectious peritonitis viruses arise by mutation from endemic feline enteric coronaviruses. Virology 1998;243(1):150-157.

10. Kipar A, Baptiste K, Barth A, et al. Natural FCoV infection: cats with FIP exhibit significantly higher viral loads than healthy infected cats. J Feline Med Surg 2006;8(1):69-72.

11. Rottier PJM, Nakamura K, Schellen P, et al. Acquisition of macrophage tropism during the pathogenesis of feline infectious peritonitis is determined by mutations in the feline coronavirus spike protein. J Virol 2005;79(22):14122-14130.

12. de Groot-Mijnes JDF, van Dun JM, van der Most RG, et al. Natural history of a recurrent feline coronavirus infection and the role of cellular immunity in survival and disease. J Virol 2005;79(2):1036-1044.

13. Meli M, Kipar K, Müller C, et al. High viral loads despite absence of clinical and pathological findings in cats experimentally infected with feline coronavirus (FCoV) type I and in naturally FCoV-infected cats. J Feline Med Surg 2004;6(2):69-81.

14. Dye C, Siddell SG. Genomic RNA sequence of feline coronavirus strain FCoV C1Je. J Feline Med Surg 2007;9(3):202-213.

15. Kipar A, May H, Menger S, et al. Morphologic features and development of granulomatous vasculitis in feline infectious peritonitis. Vet Pathol 2005;42(3):321-330.

16. Kipar A, Bellmann S, Kremendahl J, et al. Cellular composition, coronavirus antigen expression and production of specific antibodies in lesions in feline infectious peritonitis. Vet Immunol Immunopathol 1998;65(2-4):243-257.

17. Pedersen NC. Virologic and immunologic aspects of feline infectious peritonitis virus infection. Adv Exp Med Biol 1987;218:529-550.

18. Jacobse-Geels HEL, Daha MR, Horzinek MC. Isolation and characterization of feline C3 and evidence for the immune complex pathogenesis of feline infectious peritonitis. J Immunol 1980;125(4):1606-1610.

19. Giordano A, Paltrinieri S. Interferon-gamma in the serum and effusions of cats with feline coronavirus infection. Vet J 2009;180(3):396-398.

20. Berg AL, Ekman K, Belák S, et al. Cellular composition and interferon-gamma expression of the local inflammatory response in feline infectious peritonitis (FIP). Vet Microbiol 2005;111(1-2):15-23.

21. Gelain ME, Meli M, Paltrinieri S. Whole blood cytokine profiles in cats infected by feline coronavirus and healthy non-FCoV infected specific pathogen-free cats. J Feline Med Surg 2006;8(6):389-399.

22. Takano T, Hohdatsu T, Hashida Y, et al. A "possible" involvement of TNF-alpha in apoptosis induction in peripheral blood lymphocytes of cats with feline infectious peritonitis. Vet Microbiol 2007;119(2-4):121-131.

23. Regan AD, Cohen RD, Whittaker GR. Activation of p38 MAPK by feline infectious peritonitis virus regulates pro-inflammatory cytokine production in primary blood-derived feline mononuclear cells. Virology 2009;384(1):135-143.

24. Haagmans BL, Egberink HF, Horzinek MC. Apoptosis and T-cell depletion during feline infectious peritonitis. J Virol 1996;70(12):8977-8983.

25. Pesteanu-Somogyi LD, Radzai C, Pressler BM. Prevalence of feline infectious peritonitis in specific cat breeds. J Feline Med Surg 2006;8(1):1-5.

26. Foley JE, Pedersen NC. The inheritance of susceptibility to feline infectious peritonitis in purebred catteries. Feline Pract 1996;24(1):14-22.

27. Addie DD, Kennedy LJ, Ryvar R, et al. Feline leucocyte antigen class II polymorphism and susceptibility to feline infectious peritonitis. J Feline Med Surg 2004;6(2):59-62.

28. Kass PH, Dent TH. The epidemiology of feline infectious peritonitis in catteries. Feline Pract 1995;23(3):27-32.

29. Addie DD, Jarrett O. Feline coronavirus infections. In: Greene CE, ed. Infectious diseases of the dog and cat. 3rd ed. St. Louis, Mo: Elsevier, 2006;88-102.

30. Hartmann K, Binder C, Hirschberger J, et al. Comparison of different tests to diagnose feline infectious peritonitis. J Vet Intern Med 2003;17(6):781-790.

31. Paltrinieri S, Giordano A, Tranquillo V, et al. Critical assessment of the diagnostic value of feline alpha1-acid glycoprotein for feline infectious peritonitis using the likelihood ratios approach. J Vet Diagn Invest 2007;19(3):266-272.

32. Sparkes AH, Gruffydd-Jones TJ, Harbour DA. An appraisal of the value of laboratory tests in the diagnosis of feline infectious peritonitis. J Am Anim Hosp Assoc 1994;30(4):345-350.

33. Kennedy MA, Brenneman K, Millsaps RK, et al. Correlation of genomic detection of feline coronavirus with various diagnostic assays for feline infectious peritonitis. J Vet Diagn Invest 1998;10(1):93-97.

34. Kennedy MA, Abd-Eldaim M, Zika SE, et al. Evaluation of antibodies against feline coronavirus 7b protein for diagnosis of feline infectious peritonitis in cats. Am J Vet Res 2008;69(9):1179-1182.

35. Simons FA, Vennema H, Rofina JE, et al. A mRNA PCR for the diagnosis of feline infectious peritonitis. J Virol Methods 2005;124(1-2):111-116.

36. Can-Sahna K, Soydal Ataseven V, Pinar D, et al. The detection of feline coronaviruses in blood samples from cats by mRNA RT-PCR. J Feline Med Surg 2007;9(5):369-372.

37. Hartmann K. Feline infectious peritonitis. Vet Clin North Am Small Anim Pract 2005;35(1):39-79.

38. Legendre AM, Bartges JW. Effect of Polyprenyl Immunostimulant on the survival times of three cats with the dry form of feline infectious peritonitis. J Feline Med Surg 2009 May 23. [Epub ahead of print].

39. Addie DD, Paltrinieri S, Pedersen NC. Recommendations from workshops of the second international feline coronavirus/feline infectious peritonitis symposium. J Feline Med Surg 2004;6(2):125-130.

40. Fehr D, Holznagel E, Bolla S, et al. Placebo-controlled evaluation of a modified life virus vaccine against feline infectious peritonitis: safety and efficacy under field conditions. Vaccine 1997;15(10):1101-1109.

41. Richards JR, Elston TH, Ford RB, et al. The 2006 American Association of Feline Practitioners Feline Vaccine Advisory Panel report. J Am Vet Med Asooc 2006;229(9):1405-1441.

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