The aim of this study was to evaluate haematological indices commonly used as inflammatory markers in human medicine in relation to disease severity in cats diagnosed with FIP. In cats suffering from FIP, we observed a marked increase in neutrophil counts that correlated with the severity of the disease, a finding that was statistically significant. This is in contrast to the neutropenia typically induced by viral agents including feline panleukopenia
16, feline leukemia virus
17 and feline immunodeficiency virus
18. Notably, this deviation is consistent with recent human studies reporting neutrophilia in severe acute respiratory syndrome caused by coronaviruses
19,20, highlighting its unique manifestation among coronaviruses. In addition, research suggests that cytokines delay the apoptosis of neutrophils in FIP cats, thereby prolonging their lifespan within lesions. It has also been suggested that neutrophilia in cats with FIP is probably related to the infiltration of neutrophils into granulomatous lesions
21. The increase in neutrophil count with increasing disease severity in FIP cats reflects these findings. Consequently, neutrophilia emerges as a significant inflammatory marker in coronavirus-induced infections in cats. Consequently, further large-scale studies are highly recommended to further investigate neutrophilia in cats with FIP.
We observed a trend of lower lymphocyte counts in cats with FIP compared to the control group, although this decrease did not reach statistical significance. This finding is in aggrement with the previous studies on feline viral infections22,23 and FIP 24, which have reported lymphopenia as a common symptom. Previous research proposes a model for FIP pathogenesis wherein virus-induced T-cell depletion and antiviral T-cell responses act as opposing forces, with the efficacy of early T-cell responses crucially influencing infection outcomes25,26. While this study did not analyse lymphocyte subtypes, study findings are consistent with this model. However, it is important to note the lack of statistical significance, possibly attributable to the small sample size. Therefore, conducting larger-scale studies to further investigate lymphopenia in cats with FIP is strongly recommended in this context.
The increase in NLR levels observed in cats with FIP, as compared to healthy cats, highlights its central role in signalling inflammation, similar to recent breakthroughs in human studies infected with coronavirus infection27,28. This increase in NLR may be related to the immune response in cats, characterised by a paradoxical combination of neutrophilia and lymphopenia, as revealed in these studies. In contrast to viral infections characterised by haematological responses typically associated with neutropenia (feline panleukopenia virus, feline immunodeficiency virus, and feline leukemia virus), the unexpected neutrophilia in FIP, due to the nature of coronaviruses, highlights the remarkable efficacy of NLR as an important haematological marker for monitoring infection in coronavirus-induced infections.
The count of PLT exhibited a notably lower statistical significance in felines afflicted by late-stage FIP when compared with their healthy counterparts. Nevertheless, this decrease did not reach statistical significance in cats with early stage FIP compared to the control cohort. This observation mirrors the occurrence of thrombocytopenia in human research, particularly in cases of coronavirus-induced lung injury in the critically ill patients29. Furthermore, human studies highlight thrombocytopenia as a hallmark of critical illness, signalling severe organ dysfunction and the onset of intravascular coagulopathy, often culminating in disseminated intravascular coagulation30,31. In this framework, it is rational to posit thrombocytopenia as a late marker of inflammation to measure the severity of inflammation in cats with FIP. However, unexpectedly, there was a lack of variation in PLR both in cats affected by FIP and in relation to the severity of FIP. We did not observe any statistical variance in PLR levels between groups, probably due to lymphocyte responses rather than PLT counts. Based on study results, it is conceivable that PLR may not serve as a reliable marker for monitoring inflammation or its severity in FIP-affected cats.
In the present study, we observed a decrease in MPV levels attributed to FIP. Furthermore, this decrease persisted with worsening severity of FIP. We also observed an increase in the MPV/PLT ratio associated with FIP, but neither of these findings reached statistical significance. The reduction in MPV was consistent with findings from previous research32,33. In addition, consistent with studies highlighting the MPV/PLT ratio as a key metric in infection surveillance34, we documented an increase in the MPV/PLT ratio in cats with FIP. It's reasonable to attribute this to a decreased platelet count rather than an escalation in MPV. However, the statistically insignificant variation identified in analysis cautions against using MPV and the MPV/PLT ratio as robust indicators for monitoring infection in cats with FIP. Further investigation is essential to resolve this question. The major limitation of the study is that other viral agents that may affect A:G could not be tested in all cats due to economic constraints.
In conclusion, this study investigated the potential benefits of haematological indices in monitoring inflammation and its severity in cats infected with FIP. In particular, the NEU, NLR and PLT count emerged as promising metrics in this regard. Given the cost-effectiveness, accessibility, and widespread use of haematological indices, they hold the promise of becoming key parameters in monitoring inflammation and its severity in cats with FIP.
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