Feline coronavirus (FCoV) infects both domesticated and wild cats (African lion, mountain lion, leopard, cheetah, jaguar, lynx, serval, caracal, European wildcat, sand cat and Pallas’s cat) worldwide (1). FCoV exists in two distinct forms: feline enteric coronavirus (FECV), which replicates in the intestinal tract, and feline infectious peritonitis virus (FIPV), the pathogenic variant responsible for feline infectious peritonitis (FIP) (2, 3). Cats that develop FIP experience severe systemic illness with high mortality, resulting in economic burdens from hospitalization and treatment, as well as profound emotional distress for their owners.

FCoV is an enveloped, positive-sense, single-stranded RNA virus with a non-segmented genome and helical symmetry. It belongs to the order Nidovirales, family Coronaviridae, subfamily Coronavirinae, and genus Alphacoronavirus (4, 5). The genome is about 29 Kb in size and contains 11 open reading frames (ORFs). These encode 4 major structural proteins: nucleocapsid (N), membrane (M), envelope (E) and spike (S), (6) and 7 nonstructural proteins, which includes five accessory proteins (3a, 3b, 3c, 7a and 7b) and two replicase proteins (1a and 1b) (2, 7). FCoVs are further divided into two serotypes (I and II) based on antigenicity. Serotype I virus is of feline origin and serotype II virus appears to have arisen from the recombination of FCoV serotype I with canine coronavirus (1, 8–10). The two pathotypes (FECV and FIPV), exist in both serotypes I and II (3, 11). Serotype I FCoV does not grow well in cell culture and grows only in macrophage derived cell lines (12). Antisera to canine coronavirus (CCV) has a weak response to FCoV I. In contrast, serotype II FCoV grows well in cell culture and reacts with antisera to CCV (13).

FCoV is primarily shed in the feces of healthy carrier cats and transmitted through the fecal-oral route. Transmission occurs most efficiently in multi-cat environments, where the infection rate is significantly higher compared to single-cat households. FCoV demonstrates notable environmental stability, remaining infectious on fomites for 3–7 weeks, making contaminated objects potential transmission vehicles (1, 9, 14, 15). Additionally, persistently infected asymptomatic carriers play a crucial epidemiological role, as most shed virus either continuously or intermittently for months to years (15–18).

FIP as a disease in cats was first reported in 1966 (19). After this report, FIPV and FECV were suggested as aetiological agents in FIP between 1978 and 1981 (12, 20). FECV is similar to FIPV in terms of antigenicity, but different in pathogenicity with FIPV being more virulent and may cause death within a few weeks after infection (2, 19, 21). In addition to differences in pathogenicity in vivo, the two biotypes have different cellular tropisms (2). In general, during natural infections, FECV has tropism for mucosal epithelial cells or mesenteric lymph nodes (2, 3, 12), whereas FIPV infects mainly macrophage cell lines as well as lymphocytes, plasma cells and neurocytes (2, 3, 22, 23). FECV has been shown to be present systemically in monocytes of healthy cats (15, 24, 25).

The prevalence of FCoV infections may be up to 90% in multi-cat environments and 10–60% in house-hold cats worldwide (26–31). Primary FCoV infection occurs in enterocytes and passes to blood by monocyte-associated viremia (21, 32, 33). While approximately 20% of FECV-infected cats experience viral mutations, only 12%–13% of these cases progress to FIP. This progression depends on key host and viral factors, including viral virulence and the nature of the host’s immune response particularly strong, rapid cellular immune reactions that may contribute to immunopathological effects (29). The development of FIP correlates strongly with several risk factors including stress, concurrent infections, immunity, high population density. The disease shows particular predilection for young cats aged 3–16 months, when maternal antibody protection wanes and the juvenile immune system remains vulnerable (9, 16, 25, 28, 29). At present, two clinical forms of FIP are well documented: a ‘wet’ or effusive form (polyserositis and vasculitis) and a ‘dry’ or non-effusive form (pyogranulomatous lesions in organs) (21, 32). Infiltration of ascites from tissues into the pleural cavity, peritoneal cavity and pericardial cavity is the most prominent manifestation of ‘wet’ FIP, while lethargy, anorexia, weight loss and fever refractory to antibiotics are common and non-specific signs of FIP (29, 32, 34, 35). Non-effusive FIP is characterized by granuloma formation involving the central nervous system, eyes and abdominal organs (especially kidneys, liver, mesenteric lymph nodes and intestinal wall), and does not produce body cavity effusion (21, 34).

While most FCoV-infected cats remain asymptomatic, clinical cases typically present with gastrointestinal manifestations, most commonly vomiting and diarrhea. The clinical presentation of FIP varies significantly between its effusive (‘wet’) and non-effusive (‘dry’) forms. However, both forms typically share several hallmark clinical features including anorexia, lethargy, dehydration, icterus, and neurological manifestations such as ataxia, paresis, and hyperesthesia (21, 36). Neurological signs are more frequent in non-effusive FIP (3). In addition, fever, weight loss, diarrhoea, ocular lesions and kidney disorders are also prominent in cats with non-effusive FIP. In effusive FIP, abdominal distention, ascites, pleural and pericardial effusion, dyspnea are the main clinical signs of disease (35–38).

Currently, no commercially available vaccine exists for FIP. Vaccine development has been hindered by significant genetic variability among circulating FCoV strains (3). Furthermore, effective treatment of FIP remains challenging due to the complex pathogenesis of the disease. A 3C-like protease inhibitor (GC376) was used in the experimental treatment of FIP cats in 2016. This was subsequently developed to treat naturally occurring FIP, but recurrences of disease were observed (39). A nucleoside analog (GS-441524) was found to be a safe and effective treatment of FIP, and interfered with virus replication (21, 40, 41). The protease inhibitors have been used in clinical treatment recently, but their usage is limited because of the high price, long treatment period and relatively low cure rate (3, 21).

In the absence of effective vaccines or reliable treatments for FIP, establishing accurate diagnostic protocols for FCoV infection becomes crucial for case management and disease control. However, FIP diagnosis remains challenging, requiring comprehensive evaluation of multiple parameters including clinical presentation, hematological and biochemical abnormalities, serological testing, virological analysis, and histopathological examination. FIP remains a frequent diagnostic challenge in feline medicine, with misdiagnosis rates exceeding 40% in first-opinion practice (3, 29, 42–46). This is important since some veterinarians start corticosteroids after diagnosis (35). This might increase the manifestation of latent herpesvirus and toxoplasma if present in cats with FIP (3). Therefore, the aforementioned diagnostic parameters need to be collected and evaluated together (3, 9, 45, 47, 48). For virological analyses, virus isolation and molecular tests like RT-PCR and real time RT-PCR are used and are very helpful, particularly when using abdominal or pleural fluid or tissue biopsy or aspirates (1, 45, 49). Results from RT-PCR tests should be evaluated together with clinical findings and postmortem samples (1, 29, 40, 44, 45, 49). Also there are rapid tests and ELISAs for antigen detection in faeces to monitor cats carrying FCoV as well as to check antibody response. However, serological tests have low specificity and sensitivity and may fail to detect recent infections and cross-reactions occur between FIPV and low pathogenic FECV strains (9, 45). While hematological and biochemical alterations in FIP lack pathognomonic specificity, a constellation of the findings (e.g., CBC abnormalities, Serum protein changes, Acute phase reactants, liver function tests, kidney function tests, Hyperbilirubinemia) should raise clinical suspicion. These parameters exhibit 78% combined diagnostic accuracy when ≥4 abnormalities are present, though none are definitive alone (3, 29, 36, 47). Histopathological analysis is considered the gold standard for diagnosing FIP. Currently, definitive confirmation of FIP can only be achieved through immunohistochemistry to detect FCoV antigen in biopsy samples, affected tissues, and macrophages present in effusion fluids (3).

Currently, there is limited data on the epidemiology, clinicopathological features, and molecular characteristics of FCoVs in Türkiye. This study aimed to investigate FCoV seroprevalence, perform molecular and phylogenetic analyses, and evaluate associations with signalment (including habitat), clinical and biochemical parameters, and histopathological findings in cats from Istanbul, Türkiye. Additionally, we sought to generate novel data on circulating FCoV strains in Istanbul, which could serve as a reference for future prevention and control strategies against FCoV infections.

FCoV infections have been reported worldwide. The increase in cat population and crowding are important risk factors since FCoV is less frequently seen in housed, stray and feral cats compared to shelter cats (2, 3, 21, 36). The immune status, viral load, undergoing surgery, being subjected to environmental stress like crowding and bad living conditions increase the risk of developing FIP (38). Detection of FCoV antibodies and/or FCoV-RNA in the early stage of infection can be a useful indicator to help minimize the spread of FCoVs in a breeding cattery, multi-cat household and FCoV-free household (16, 17, 33, 55). Therefore, it is important to monitor cats living in multi-cat environments in order to reduce and control FCoV infections.

FCoV prevalence may vary depending on the region/country, inclusion criteria (healthy or ill), selection bias, analytical errors and low specificity of the diagnostic tests. The results of this study indicate that FCoV infections are widespread in cats from Istanbul and this agrees with the results of other studies (27, 30, 31, 56, 57). In the present study, overall seropositivity for FCoV was found to be 90.9%, and was similar over two years (2018 and 2019). However, FCoV seroprevalence was found to be higher in this study compared to a previous study performed in Istanbul (36). This might be associated with an increase in the cat population in recent years and this finding suggests that it will be difficult to find FCoV-seronegative cats in the future. High FCoV seroprevalence (up to 84%) has also been reported in other countries (31, 44, 56, 58). A much lower seroprevalence in chronically ill (19.3%) and healthy cats (10.1%) was reported in Korea (59). The high seroprevalence found in many countries might be attributed to the presence of maternal antibodies but the percentage FCoV seropositivity was also found to be high particularly in this study. Because of the presence of maternal antibodies in younger ages, detection of FCoV RNA by PCR is a better indication of FCoV infection. However, PCR analysis cannot discriminate between FCoV and FIPV at present, although there are some trials aimed at developing specific tests to differentiate them by nucleotide polymorphisms. However, compared to seropositivity, detection of FCoV-RNA in pleural effusion and ascites has a better diagnostic value (42, 60).

In the present study, the overall detection rate of FCoV-RNA in faecal swabs was 37.9% (79/208). Intestinal colonization by FCoV has been investigated by RT-PCR and found to be 37% in Japan (31), 47.5% in Portugal (61), 76.5% in Germany (62) and 84% in Malaysia (30). A high prevalence (84.4%) of FCoV infection in faeces in cat populations in some areas of China has also been reported. They found no significant difference in FCoV-RNA positivity between body cavity effusion from sick cats and faeces from healthy cats (62). In the Fujian Province of China, the overall prevalence of FCoV-RNA positivity in the faeces of cats was 67.9% (63). However, fecal detection is not correlated with ongoing FIP infection (49). Ascitic fluid from 854 cats with suspected FIP was analysed by RT-PCR in Japan and FCoV-RNA was detected in 377 samples (64). In another study performed in Türkiye, 14 (54%) of healthy and sick cats were positive for FCoV-RNA in blood (24).

Results of a retrospective study from 24 American veterinary teaching hospitals showed that FIP prevalence was 0.4% (1,420 cats from 397,182) over a 10-year period (65). The percentage of FCoV-infected cats that subsequently developed FIP was found to be between 8 and 10% in two studies (66, 67). In the present study, the number of FIP cats was most likely about 22 that are PCR positive, and effusions were found as well as histopathological lesions suggestive of FIP. However, limitation of this study is that immunohistochemistry was not performed on these cats died of FIP suspicion.

Several risk factors have been found to be associated with FCoV infection and development of FIP, which include stress, surgery, age, breed, gender, multi-cat environment, different housing conditions and the frequency of litter box disinfection (28–30, 36, 57, 68, 69). While our study identified several significant associations, we caution that some marginal results (e.g., hematological variables) could reflect Type I error. Future replication in larger cohorts with pre-specified hypotheses is warranted.

FCoV infections are usually seen in cats less than 2 years old and especially during the first year of life (1, 28, 31, 36, 49). However, older cats may also be affected (70, 71). In a previous study performed in Istanbul, FCoV serological status was significantly associated with age, FIP serological status and habitat variables. In contrast, age exhibited a bimodal distribution in our study, with cats aged 23–59 weeks showing a lower risk of PCR positivity compared to both younger and older cats. There was no association with age and FCoV-RNA positivity in Malaysian, Australian and Chines studies (28, 30, 63, 69). This could be due to increased cat-to-cat contact in young cats before their immune system reaches maturity, facilitating efficient virus replication and favoring mutation from FECV to FIPV and lack of natural and protective immunity at young ages (49, 63). Young cats may also experience stress due to various factors, including weaning, vaccination, dietary changes, neutering, separation from the queen, and living in a multi-cat environment (36, 55, 72). Stress provokes the release of glucocorticoids, which may cause suppression of cell-mediated immunity and facilitate FCoV replication (49, 72).

No difference in FCoV seroprevalence was found between females and males in previous studies (16, 28, 30, 31, 36, 58, 63, 73). Similar results were found in a previous study in Istanbul (36). In contrast, in Australia and the USA, FCoV prevalence was higher in male cats compare to females (49, 57, 68). Similarly, FIP occurred significantly more often in male cats as reported by others (35, 68, 74). which may be due to regional differences. In Japan, PCR positivity in ascitic fluids was significantly higher in males (51.5%) than in females (35.7%). However, gender was not significantly associated with presence of antibody which indicate the development of FIP in male cats is higher than females (64). In the present study, no significant association was found between gender and FCoV-RNA positivity or seropositivity. At present, there is no biological evidence supporting gender-associated susceptibility and resistance to FCoV. The difference shown in previous studies could be related to males and females having different lifestyles, facilitating FCoV exposure and living in different regions. Alternatively, sex-based differences may be related to androgens, which may negatively affect the immune system, increasing the risk of virus replication (75). However, results of another study indicated that male and female cats had similar risks of developing FIP (47).

Breed was not associated with FCoV seropositivity in either this study or a previous study conducted in Istanbul (36). Multiple international studies have reported higher FCoV seroprevalence in pedigree cats compared to non-pedigree cats (28, 31, 49, 57, 58). In a Japanese study of 17,392 cats, FCoV antibody prevalence was significantly higher in pedigree cats (67%) than in non-pedigrees (31%) (31). In another study, Norwegian forest cats and Birmans had a lower risk of FCoV infection (69). Similarly, FIP disproportionately affects pedigree cats (57, 74, 76). In contrast, no specific breed has been identified as a risk factor for FCoV infection in cats in Germany (12), Fujian Province China (63), and in Türkiye (36). In the present study, 55 of 162 cross breed and 24 of 46 purebred cats were found to be positive for FCoV-RNA and this was statistically significant in cross breed cats. This finding contrasts with the results reported from others since the PCR positivity in ascitic fluids was significantly higher in purebreds (62.2%) than in crossbreds (34.8%) in Japan (64). The reason for this can be because of the higher number of cross breed cats than pure-breed cats analyzed in this study.

The effect of a multi-cat environment and housing density on the prevalence of FCoV has been investigated in many studies. Significantly increased risks have been found for cats living in a multi-cat environment, which could lead to virus mutation and development of FIP. Household cats living alone had the lowest risk of being FCoV seropositive (29, 36, 55, 69). The number of cats in a house hold or cattery was significantly associated with the occurrence of FIP in one study (77) but not in another (14). In another study, the majority of cats (75.7%) analysed shed FCoV at least once (69). Results of a previous study performed in Istanbul indicated that household cats that cohabitated with other cats had a high risk of being FCoV seropositive (36), as has been previously shown (14, 18, 26, 27, 30, 57). In contrast to previous findings, most FCoV-RNA positive cats in our study were household cats. Among these, FCoV-RNA positivity showed significant associations with being home-raised, cohabitation with other cats, and outdoor access. This pattern suggests that environmental factors—particularly outdoor exposure and multi-cat households—may facilitate viral transmission and potentially contribute to FCoV mutation and FIP development. These observations align with established literature documenting higher FCoV prevalence in multi-cat environments (62, 69, 78). A previous Istanbul study reported significantly lower FCoV seroprevalence in stray cats (30%) compared to household cats (57%) (36). While prior research suggests household cats with outdoor access and multi-cat cohabitation are disproportionately susceptible to FCoV infection, our study revealed comparable seroprevalence rates (∼90%) across groups, with no statistically significant differences observed.

FCoV infection typically causes mild to moderate clinical signs, primarily diarrhea and lethargy. In cases progressing to FIP, the disease manifests as either effusive (‘wet’) or non-effusive (‘dry’) forms, with clinical signs reflecting disease severity. The most common FIP symptoms include persistent fever (often fluctuating), anorexia, and profound lethargy. Ocular manifestations of non-effusive FIP may include uveitis and retinitis. Neurological involvement can present with seizures, nystagmus, progressive ataxia, and paresis (2, 3, 21). Our study found significantly higher prevalence rates of fever, lethargy, diarrhea, ascites, and pleural effusion in FCoV-PCR positive cats compared to PCR-negative controls (p < 0.05). Notably, pleural effusion showed particularly strong association in seropositive cases. These findings align with previous research that additionally identified weight loss and vomiting as clinical markers significantly associated with FCoV seropositivity (36). Consistent with previous reports (73), weight loss and pleural effusion were identified as predominant clinical signs in FIP cases, often accompanied by ascites, lethargy, and anorexia. Recent findings further characterize the FIP presentation profile, reporting abdominal distension (68%), depression (60%), dehydration (58%), anorexia (53%), and dyspnea (42%) as common manifestations (35).

Although the following hematological and biochemical blood parameters are not specific for FIP, thrombocytopenia, normochromic anemia, lymphopenia particularly in cats with effusions, neutrophilia and microcytosis were frequently reported (3, 36, 70, 79–81). No association was found with anemia and occurrence of effusions in one study (82). However, a difference between FIP and microcytosis has been previously reported (70). A decrease in red blood cell count has been reported but attributed to poor prognosis of FIP (80, 83). In a recent study, lymphopenia developed in 75% of cats with FIP, while 45.5% showed neutrophilia, and 13.6% had monocytosis (35).

Characteristic serum biochemical abnormalities in FIP cases include hyperbilirubinemia, hyperproteinemia, hyperglobulinemia, and hypoalbuminemia (3, 21). Particular diagnostic significance lies in the identification of hyperglobulinaemia accompanied by hypoalbuminaemia or low-to-normal serum albumin (3, 41, 70, 73). In addition, low albumin to globulin (A:G) ratio can have a better diagnostic value than either total serum protein or globulin (3, 36). In the present study, as also reported previously, a decrease in serum A/G ratio was detected in most of the cats suspected of having FIP (3, 42, 73). In a recent study, blood profiles revealed mild anemia, lymphopenia, thrombocytopenia, hypoalbuminemia, hyperglobulinemia, and an albumin to globulin ratio of 0.4 in FIP cases (35).

In the present study, the deletion of specific nucleotides was observed in S gene sequences of FCoV type 1. Spike protein is crucial for the virus’s ability to enter host cells. It plays a significant role in the virus’s infectivity and is a primary target for neutralizing antibodies. The implications of S gene variations in FCoV for virulence, transmission, and strain evolution are complex and can significantly impact disease dynamics. S gene deletions (e.g., in the 3′ end) are associated with the transition from feline enteric coronavirus (FECV, low virulence) to feline infectious peritonitis virus (FIPV, high virulence). Loss of certain regions (e.g., furin cleavage sites) may alter cell tropism, allowing systemic spread and macrophage infection, a hallmark of FIP. In addition, S gene deletions may increase or decrease enteric replication, environmental persistence and cat-to-cat transmission. Furthermore, clustering of S gene variants may reflect immune selection pressure, leading to escape mutants that evade neutralizing antibodies (virus evolution).

This complexity arises from the nature of RNA viruses like FCoV, where genetic variation frequently occurs (5, 10, 73, 84–89). In this study, the nucleotide sequence of the S gene of FCoV showed 81.2 to 99.6% nucleotide identity between them. This identity range suggests a high degree of genetic variation between different FCoV strains. The lower end of this range indicates more divergent strains, while the higher end suggests closely related strains. The finding that all 68 FCoV strains sequenced belonged to FCoV-I indicates that these strains share a common evolutionary lineage, which can provide insights into transmission dynamics, virulence, and potential vaccine development. Similar findings were reported from China by Shi et al. (89).

Several unique recombinant events and recombination signals were observed for some FCoV strains in this study by using seven recombination testing methods. Recombination events are indeed a significant aspect of the evolution of coronaviruses, including those affecting both humans and animals. The spike protein gene, in particular, is a critical region for recombination, as it is responsible for viral entry into host cells and plays a key role in determining the virus’s virulence and host range (13, 87, 90–92). FCoV is known for its ability to undergo recombination, which can significantly impact its assembly, invasion, and pathogenicity. Recombination events between different strains of FCoV can lead to increased genetic diversity. This diversity allows the virus to adapt to changing host environments and immune responses, potentially resulting in more virulent strains. For instance, the transition from the less pathogenic FCoV type I to the more pathogenic type II is believed to involve recombination with a canine coronavirus, which may enhance its ability to infect feline hosts. Recombination plays a crucial role in the pathogenesis of FIP, a severe and often fatal disease caused by a mutant form of FCoV. The recombination events may lead to the generation of a more virulent strain that can evade the host’s immune response, resulting in systemic infection and severe inflammatory responses (2). The ability of FCoV to recombine and create variants that can infect macrophages is critical for the development of FIP (93). The assembly of FCoV involves the formation of viral particles through the interaction of structural proteins. Recombination can affect the genes encoding these proteins, potentially altering the efficiency of viral assembly and the virus’s ability to enter host cells. Recombination can lead to the emergence of viral variants that possess mutations in epitopes recognized by the host immune system. This allows the virus to evade neutralizing antibodies generated from previous infections or vaccinations (2, 94). Such immune escape is particularly relevant in the context of FCoV, where previous exposure to less pathogenic strains does not confer protection against the more virulent forms. The recombination of FCoV can also result in variants that are more adept at transmission between cats. Enhanced transmissibility can lead to outbreaks of FIP in multi-cat environments such as shelters or breeding facilities. The ability to recombine and generate new strains that maintain or enhance transmissibility is a key factor in the epidemiology of FCoV infections. Recombination events may facilitate the adaptation of FCoV to new host species, potentially leading to zoonotic spillover or the emergence of new variants that can infect other animals. This host range expansion can complicate control measures and increase the virus’s impact on feline populations.

All FCoV strains identified in this study phylogenetically clustered with type I variants, with no type II strains detected. This finding aligns with global epidemiological patterns, where type I FCoV demonstrates significantly higher prevalence than type II across most geographic regions (59, 62, 73, 95). Our study revealed substantial genetic diversity among type I FCoV strains circulating in Istanbul’s feline population. This high degree of variability presents significant challenges for infection control and eradication, as divergent viral variants may harbor distinct virulence determinants.

Analyses for virus detection should focus on tissues and effusions presumably containing FIPV-infected macrophages rather than blood since viremia is not always found in FCoV infected cats (81, 96). When FCoV was detected in feces, it was likely to be detected in other organs and tissues, and vice versa (49). Besides, FCoV-RNA can be found in the blood of healthy cats (24). An interesting finding reported by others (49) indicated the high detection rate and viral burdens of FCoV in urine and kidney samples suggesting urine as a convenient and valuable sample for FIP diagnosis. Similarly, a high detection rate of feline morbillivirus in the kidney has been reported (97). However, the association between renal damage and urine positivity needs to be studied in FIP cases.

In this study, qRT-PCR analysis detected FCoV RNA in tissue samples from 33 of 43 postmortem feline cases (76.7%). Among these PCR-positive cats, 22 (66.7%) exhibited gross and/or histopathological lesions consistent with FIP diagnosis. Out of the 22 cats, 12 exhibited the mixed form of the disease (12/22, 54.5%). Although clinical examinations often distinguish between effusive and non-effusive forms of the disease, this finding supports the notion that mixed forms of FIP may be under-reported. This is particularly true when diagnosis is based solely on clinical observations, as postmortem examinations can reveal both granulomatous lesions in organs and effusions in body cavities (55, 93, 98, 99). The number of cats with abdominal effusion was higher than those with thoracic effusion, with the characteristic gross findings predominantly localized in the abdominal cavity, as previously described (1, 100).

The histopathological hallmarks of FIP observed in this study included fibrinous serositis, focal to disseminated granulomas with or without necrosis and, less commonly, perivasculitis. At least two of these findings were present in 22 of the 33 PCR-positive cats. Fibrinous serositis and granulomas were most frequently detected in the liver, followed by the kidneys and the intestines, aligning with previous studies. Perivasculitis was predominantly observed in the liver, followed by lungs, brain and kidneys as described previously (1, 98, 101, 102). Of the 33 cats which were positive for FCoV RNA, 11 did not show macroscopic or microscopic findings specific to FIP. Several factors may explain this discrepancy. One possibility is the high sensitivity of the PCR technique, which may detect FCoV even in the absence of gross and microscopic lesions. Another explanation is that these cats might have been in the early stages of the disease where characteristic lesions had not yet developed. Alternatively, sampling limitations could account for the absence of lesions, as characteristic histopathological findings might be missing in the examined tissues (93, 98, 103). On the other hand, while histopathological findings suggestive of FIP were observed in various organs of 8 cats, PCR testing did not yield positive results. Although histopathological examination can identify lesions indicative of FIP, it is insufficient for a definitive diagnosis. Immunohistochemistry (IHC) improves diagnostic accuracy by detecting FCoV antigen within characteristic lesions, particularly in cases where histopathological findings and PCR results are inconsistent (38, 98, 103). Unfortunately, IHC could not be performed in this study due to project constraints.

In our study, histopathological and PCR findings showed complete diagnostic agreement in 25 cases (22 FIP-positive and 3 FIP-negative). Among the examined tissues (liver, brain, and intestines), the liver demonstrated the highest concordance rate between both diagnostic methods. These results reinforce existing evidence that hepatic tissue provides the most reliable sampling site for FCoV detection when using PCR as a confirmatory diagnostic approach (98). However, recent findings suggest the kidney can also be targeted for sampling to aid diagnosis of FIP (49).

“Our research provided a comprehensive understanding of FCoV and revealed a higher prevalence of FCoV in cats in Turkey. This study might provide an outline for future research on the development of new vaccines and antiviral therapies. It highlights several critical findings and implications: i: The study identifies a higher prevalence of FCoV in Turkish domestic cats, potentially influenced by factors such as multi-cat environments, population density, or limited preventive measures. This underscores the need for targeted interventions in similar settings; ii: Significant genetic mutations observed could affect viral behavior, such as enhanced transmissibility or pathogenicity, possibly contributing to FIP, a severe outcome of FCoV; iii: Evidence of recombination suggests evolutionary dynamics that may lead to noel variants, complicating disease management. Regular epidemiological surveillance for FCoV infections among domestic and stray cats is needed to gain better insights into viral evolution, risk factors, and transmission dynamics, risk assessments and management strategies.”