Spontaneous Dilated Cardiomyopathy and Right-Sided Heart Failure as a Differential Diagnosis for Hepatosis Dietetica in a Production Pig

Abstract

An experimentally naïve 37.7-kg Yorkshire-crossbred gilt died unexpectedly 2 d after arrival. Necropsy revealed severe dilated cardiomyopathy characterized grossly by markedly dilated ventricles and thinned ventricular walls and interventricular septum. Histologically there was multifocal myofiber attenuation and patchy loss of myofiber cross striations. The liver contained submassive to massive, diffuse hepatic centrilobular hemorrhage and degeneration. These lesions supported a diagnosis of dilated cardiomyopathy with right heart failure and secondary hepatic degeneration due to marked acute passive congestion. To our knowledge, this case is the first report of spontaneous dilated cardiomyopathy in swine and represents a potential diagnostic challenge regarding the differentiation of the cardiac-associated liver lesion from hepatosis dietetica. The diagnosis of dilated cardiomyopathy and right-sided heart failure was supported by the character of the hepatic lesion, absence of typical gross or histologic lesions of mulberry heart disease, and normal selenium levels.

Figure 1.

(A) The atria and ventricles of the heart from the current case were enlarged and flaccid, compared with (B) a heart from an age-, weight-, and sex-matched control pig. (C) The left and right ventricles were markedly dilated and the ventricular walls and interventricular septum severely thinned on cross-section compared with (D) the control sample. All panels, Bar = 1 inch.

Figure 2.

(A) Locally extensive myofiber atrophy and prominence of supporting stromal elements (bar, 50 μm). (B) Myofibers are markedly thinned, irregular, and wavy in appearance (bar, 25 μm). Hematoxylin and eosin stain. (C) Masson trichrome staining revealed little to no collagen deposition (bar, 25 μm), and (D) phosphotungstic acid–hematoxylin stain showed focal loss of cross-striations in affected myofibers (arrows; bar, 25 μm).

Figure 3.

(A) Focal thrombus formation along the endocardial surface of the right papillary muscle (bar, 50 μm). (B) Locally extensive intraalveolar hemorrhage and fibrin deposition with the presence of macrophages undergoing erythrophagocytosis (arrows; bar, 25 μm). (C) Marked centrilobular congestion affected all hepatic lobules (bar, 200 um) and was characterized by (D) expansion of sinusoids and secondary degeneration and loss of hepatic cords (bar, 50 μm).