Feline Panleukopenia Virus Is Not Associated With Myocarditis or Endomyocardial Restrictive Cardiomyopathy in Cats

Abstract

Canine parvovirus-2 (CPV-2) is nearly indistinguishable from feline panleukopenia virus (FPV) and is a well-known cause of viral myocarditis in young puppies; however, it is not known whether either FPV or CPV-2 naturally infects feline cardiomyocytes and causes myocarditis. Endomyocarditis (EMC) and left ventricular endomyocardial fibrosis (LVEF), clinically known as "endomyocardial restrictive cardiomyopathy," are important feline heart diseases suspected to have an infectious etiology. A continuum is suggested with EMC representing the acute reaction to an unknown infectious agent and LVEF the chronic manifestation of repair. The purpose of this study was to determine (1) whether there is natural parvovirus infection of the feline myocardium and (2) whether parvoviral infection is associated with feline EMC and/or LVEF. In a retrospective study, polymerase chain reaction and sequencing for the parvovirus VP1/2 gene was performed on archived heart tissue from cats with endomyocardial disease and controls. Similar methods were used prospectively on myocardial tissues from shelter-source kittens. Although 8 of 36 (22%; 95% confidence interval [CI], 11%-40%) shelter kittens had parvoviral DNA in myocardial tissue, VP1/2 DNA was not detected in 33 adult cases or 34 controls (95% CI, 0% to ∼11%). These findings were confirmed by in situ hybridization: adult cats did not have detectable parvovirus DNA, although rare intranuclear signal was confirmed in 7 of 8 shelter-source kittens. In kittens, parvovirus was not significantly associated with myocarditis, and in situ hybridization signal did not colocalize with inflammation. Although infection of cardiomyocytes was demonstrated in kittens, these data do not support a role for parvovirus in EMC-LVEF.

Keywords: cats; endocardial fibrosis; endomyocarditis; feline panleukopenia virus; heart diseases; in situ hybridization; polymerase chain reaction; restrictive cardiomyopathy; viral.

Figures 1–4.

Heart, cat. Figure 1. Necrotizing myocarditis; case No. C7. The endomyocardium of the left papillary muscle is disrupted and expanded by lymphocytes, macrophages, neutrophils, and plasma cells mixed with fibrin and eosinophilic necrotic debris. Hematoxylin and eosin (HE). Figure 2. Left ventricular endocardial fibrosis; case No. C8. The endocardium is markedly thickened by a layer of connective tissue that is >1 mm thick (arrowheads). Inset: The thickened endocardium has areas of matrix alteration that individualizes cells (chondroid metaplasia). HE. Figure 3. Left ventricular endocardial fibrosis; case No. C8. The endocardium is markedly thickened by collagenous connective tissue. Masson’s trichrome. Figure 4. Hybrid endomyocarditis and endocardial fibrosis; case No. C32. The endocardium is expanded by variable loose fibrous proliferation accompanied by macrophages and lymphocytes and lined by plump activated endothelial cells (inset). The endothelial lining is focally disrupted and covered by a mat of amorphous eosinophilic fibrin. HE.

Figures 5–6.

Heart, kitten. Figure 5. Myocarditis, case No. K32. There are multifocal to coalescing aggregates of lymphocytes, macrophages, and plasma cells within the myocardium. Inset: Higher magnification. Hematoxylin and eosin. Figure 6. Case No. K23. Labeling of cardiomyocyte nuclei (arrow) for parvoviral nucleic acid in the heart of a kitten without myocarditis. In situ hybridization.