Levels of feline infectious peritonitis virus in blood, effusions, and various tissues and the role of lymphopenia in disease outcome following experimental infection

Abstract

Twenty specific pathogen free cats were experimentally infected with a virulent cat-passaged type I field strain of FIPV. Eighteen cats succumbed within 2-4 weeks to effusive abdominal FIP, one survived for 6 weeks, and one seroconverted without outward signs of disease. A profound drop in the absolute count of blood lymphocytes occurred around 2 weeks post-infection (p.i.) in cats with rapid disease, while the decrease was delayed in the one cat that survived for 6 weeks. The absolute lymphocyte count of the surviving cat remained within normal range. Serum antibodies as measured by indirect immunofluorescence appeared after 2 weeks p.i. and correlated with the onset of disease signs. Viral genomic RNA was either not detectable by reverse transcription quantitative real-time PCR (RT-qPCR) or detectable only at very low levels in terminal tissues not involved directly in the infection, including hepatic and renal parenchyma, cardiac muscle, lung or popliteal lymph node. High tissue virus loads were measured in severely affected tissues such as the omentum, mesenteric lymph nodes and spleen. High levels of viral genomic RNA were also detected in whole ascitic fluid, with the cellular fraction containing 10-1000 times more viral RNA than the supernatant. Replicating virus was strongly associated with macrophages by immunohistochemistry. Virus was usually detected at relatively low levels in feces and there was no evidence of enterocyte infection. Viral genomic RNA was not detected at the level of test sensitivity in whole blood, plasma, or the white cell fraction in terminal samples from the 19 cats that succumbed or in the single survivor. These studies reconfirmed the effect of lymphopenia on disease outcome. FIPV genomic RNA was also found to be highly macrophage associated within diseased tissues and effusions as determined by RT-qPCR and immunohistochemistry but was not present in blood.

Epidemiological data and a score-based study of renal, hepatic and cerebral lesions in feline infectious peritonitis

“…Most organs evaluated during this investigation had some degree of pyogranulomatous inflammatory reaction with an associated vasculitis; pyogranulomatous inflammation and vasculitis are the hallmarks FIP (KIPAR et al, 2005;PEDERSEN, 2009;DRECHSLER et al, 2011;PEDERSEN et al, 2015). Pyogranulomas in effusive FIP were frequently observed at the serous surfaces of abdominal organs during this study; similar findings were described (KIPAR et al, 2005;ADDIE et al, 2009;PEDERSEN, 2009;DRECHSLER et al, 2011).…”

“…The pathological alterations observed during this investigations are similar to those described in cases of FIP (HARTMANN, 2005;NORRIS et al, 2005;PEDERSEN, 2009;PEDERSEN et al, 2015), considering that a definitive diagnostic of FIP is based on the histopathologic evaluation of the tissues of the affected cat (DRECHSLER et al, 2011). Most organs evaluated during this investigation had some degree of pyogranulomatous inflammatory reaction with an associated vasculitis; pyogranulomatous inflammation and vasculitis are the hallmarks FIP (KIPAR et al, 2005;PEDERSEN, 2009;DRECHSLER et al, 2011;PEDERSEN et al, 2015).…”

“…Cats were divided into two predefined age-related groups: those that were less than and more than one year of age, based on the incidence of this disease (HARTMANN, 2005;ADDIE et al, 2009;PEDERSEN, 2009;SOMA et al, 2013;RIEMER et al, 2016). Clinical variables (gender and breed) related to the age of cats with FIP were determined by using the Chi Square test (P≤0.05), by univariate analysis.…”

“…FIP has been reported predominantly in cats that are less than two years of age (ADDIE et al, 2009;PEDERSEN, 2009;ADDIE, 2012;RIEMER et al, 2016), due to the immature immune systems of these animals (HARTMANN, 2005;ADDIE et al, 2009;PEDERSEN, 2009). …”

“…Epidemiological studies of FIP have been reported from different countries, demonstrating that cats with less one-year-old and cats living in shelters are more predisposed to contracting FIP, including Australia (NORRIS et al, 2005;BELL et al, 2006;WORTHING et al, 2012), Austria (BENETKA et al, 2004), Brazil (OLIVEIRA et al, 2003;SANTOS et al, 2013), Japan (TANAKA et al, 2015), Turkey (TEKELIOGLU et al, 2015), USA (HARTMANN, 2005;PESTEANU-SOMOGYI et al, 2006;PEDERSEN, 2009), and Germany (RIEMER et al, 2016). However, none of these have investigated the degree of tissue destruction associated with FIP.…”