Myocarditis in an FIP-Diseased Cat with FCoV M1058L Mutation: Clinical and Pathological Changes.

Simple Summary: Feline infectious peritonitis (FIP) is a very common coronavirus (FCoV) infectious disease in the feline population. FIP infection is a cause of death in cats and is widespread in domestic cats. FIP can have an acute or chronic clinical form, also known as effusive or non-effusive FIP, respectively. The typical lesion found in the acute form is an effusion in the thoracic and/or abdominal cavities, while collection in the pericardial sac is rare. The chronic form is characterized by pyogranulomatous necrotizing lesions in organs such as the kidney, liver, intestine, lung, eyes, skin, and central nervous system. FIP does not represent a zoonotic risk. The reported case is an uncommon pyogranuloma found in the myocardium in a cat with clinical heart dysfunction. The most important histopathological finding was the myocarditis/myocardial necrosis associated with the presence of S gene-mutated FCoV (M1058L biotype). This is the first described case of myocarditis in an FCoV/FIP M1058L biotype-positive cat. An 8-month-old intact male domestic shorthair cat was referred to the Emergency Service of the Veterinary Teaching Hospital (VTH) of the Department of Veterinary Science of the University of Parma (Italy) from the Parma municipal multi-cat shelter, during the winter season (January 2023), for lethargy, anorexia, hypothermia, and hypoglycemia. At the VTH, upon cardiologic examination, an increase in heart rate, under normal blood pressure conditions, was detected. Signalment, clinical history, basal metabolic panel (BMP), ultrasound investigations, and cytological findings were all consistent with a diagnosis of feline infectious peritonitis (FIP). FIP was confirmed in the effusive abdominal fluid by a molecular genetic test (real-time PCR for feline coronavirus RNA). The molecular genetic investigation also detected an FCoV S gene single-nucleotide mutation: biotype M1058L. At necropsy, an effusive collection was recorded in the abdomen, thoracic cavity, and pericardium sac. White parenchymal nodules, of about 1 mm diameter, were found on the surface and deep in the lungs, liver, kidneys, and heart. Histopathology revealed the typical FIP pyogranulomatous vasculitis and IHC confirmed the presence of the FIP virus (FIPV) antigen. The most relevant histopathological finding was the myocarditis/myocardial necrosis associated with the presence of the S gene-mutated FCoV (M1058L biotype). This is the first case of myocarditis in a cat positive for the FCoV/FIP M1058L biotype. Further studies are necessary to support the mutated FCoV M1058L biotype, as an uncommon, but possible, causative pathogen of myocarditis in FCoV/FIP-positive cats. Studies including several FCoV/FIP M1058L-positive cases could allow us to make a correlation with heart gross pathology, histopathology, and immunolocalization of the FCoV/FIP M1058L biotype in the myocardium. The investigation will potentially allow us to determine the effective tropism of the FCoV/FIP M1058L biotype for myocardiocytes or whether myocardiocyte lesions are evident in the presence of concomitant causes related to the patient, its poor condition, or external environmental distress such as cold season, and whether the aforementioned concomitant events are correlated. [ABSTRACT FROM AUTHOR]