An update on feline infectious peritonitis: Virology and immunopathogenesis

Abstract

Feline infectious peritonitis (FIP) continues to be one of the most researched infectious diseases of cats. The relatively high mortality of FIP, especially for younger cats from catteries and shelters, should be reason enough to stimulate such intense interest. However, it is the complexity of the disease and the grudging manner in which it yields its secrets that most fascinate researchers. Feline leukemia virus infection was conquered in less than two decades and the mysteries of feline immunodeficiency virus were largely unraveled in several years. After a half century, FIP remains one of the last important infections of cats for which we have no single diagnostic test, no vaccine and no definitive explanations for how virus and host interact to cause disease. How can a ubiquitous and largely non-pathogenic enteric coronavirus transform into a highly lethal pathogen? What are the interactions between host and virus that determine both disease form (wet or dry) and outcome (death or resistance)? Why is it so difficult, and perhaps impossible, to develop a vaccine for FIP? What role do genetics play in disease susceptibility? This review will explore research conducted over the last 5 years that attempts to answer these and other questions. Although much has been learned about FIP in the last 5 years, the ultimate answers remain for yet more studies.

The nucleoside analog GS-441524 strongly inhibits feline infectious peritonitis (FIP) virus in tissue culture and experimental cat infection studies

“…FIPV infection has a complex immunopathogenesis, a feature shared by other coronavirus infections (de Wilde et al, 2017), and has become one of the most researched infectious diseases of cats since its discovery over a half century ago (Kipar and Meli, 2014;Pedersen, 2014aPedersen, , 2014bTekes and Thiel, 2016). Despite these advances, modern treatment options for FIP remain palliative and vaccines have proven either unsafe or ineffective (Pedersen, 2014b).…”

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

“…In spite of many decades of studies on experimental FIPV infection, there is very little information on how the virus and host interact over an entire disease course. Many experimental FIPV infection studies have also been limited to the final disease outcome, e.g., the testing of vaccine candidates for efficacy or testing of various types and biotypes of feline coronavirus isolates for disease potential (Pedersen, 2009(Pedersen, , 2014a. Still other experimental studies have concentrated on specific virus-or host-related inflammatory or immune responses, also measured mainly Twenty specific pathogen free cats were experimentally infected with a virulent catpassaged type I field strain of FIPV.…”

“…in terminally ill cats (Pedersen, 2014a). There are several longitudinal studies which have followed the entire disease course, but these studies were concerned mainly with disease signs such as fever, antibody responses and cytokine expression and not with viral loads in various tissues (Pedersen and Boyle, 1980;Weiss and Scott, 1981;Gunn-Moore et al, 1998a).…”

Canine bicavitary carcinomatosis with transient needle tract metastasis diagnosed by multiplex immunocytochemistry

“…This case demonstrates the diagnostic utility of multiplex ICC for cytokeratin and vimentin in a clinical setting, allowing further characterization of cells on cytology. Co‐expression in dogs can be expected in normal and neoplastic mesothelial cells, and has been documented in other neoplasms, particularly those with anaplastic variants and suspicion of epithelial to mesenchymal transformation . The antemortem diagnosis of carcinomatosis can be challenging and, typically, is achieved through a combination of imaging modalities, cytology of cavitary effusions, and histopathology.…”