History
A 2-month-old 17.0-kg (37.4-lb) black and white crossbred gilt (Sus scrofa; 1/130 pigs) was found dead on the premises of a grower-finisher operation. There were no reported signs of sickness, and no other pigs were reported dead or ill at that time. Recently, the producer had changed the operation's feed supplier.
Gross Findings
On gross examination, the pig's pericardial sac contained approximately 20 mL of serous fluid mixed with a few strands of fibrin (Figure 1). The heart was pale brown with linear or splotchy subepicardial hemorrhages. The trachea contained white to pale pink foam from the thoracic inlet to the carina. The lungs were mottled red to dark red, wet, and heavy with expansion of interlobular septa by clear edema fluid. The abdominal cavity contained approximately 25 mL of serosanguineous fluid. On cut section, the myocardium was pale pink to tan with irregularly shaped and poorly demarcated hemorrhages.
Photographs of the thoracic cavity and heart of a 2-month-old gilt (Sus scrofa) found dead at a grower-finisher operation. A—The epicardial surface of the heart has splotchy hemorrhages. The opened pericardial sac contains serous fluid and aggregates of fibrin. Bar = 2.5 cm. B—In a cross-section of the heart midway between the base and apex, the myocardium is pale pink to tan, with multiple irregularly shaped and poorly demarcated hemorrhages. LV = Left ventricle. RV = Right ventricle. Bar = 1 cm.
Citation: Journal of the American Veterinary Medical Association 253, 6; 10.2460/javma.253.6.719
Photographs of the thoracic cavity and heart of a 2-month-old gilt (Sus scrofa) found dead at a grower-finisher operation. A—The epicardial surface of the heart has splotchy hemorrhages. The opened pericardial sac contains serous fluid and aggregates of fibrin. Bar = 2.5 cm. B—In a cross-section of the heart midway between the base and apex, the myocardium is pale pink to tan, with multiple irregularly shaped and poorly demarcated hemorrhages. LV = Left ventricle. RV = Right ventricle. Bar = 1 cm.
Citation: Journal of the American Veterinary Medical Association 253, 6; 10.2460/javma.253.6.719
Photographs of the thoracic cavity and heart of a 2-month-old gilt (Sus scrofa) found dead at a grower-finisher operation. A—The epicardial surface of the heart has splotchy hemorrhages. The opened pericardial sac contains serous fluid and aggregates of fibrin. Bar = 2.5 cm. B—In a cross-section of the heart midway between the base and apex, the myocardium is pale pink to tan, with multiple irregularly shaped and poorly demarcated hemorrhages. LV = Left ventricle. RV = Right ventricle. Bar = 1 cm.
Citation: Journal of the American Veterinary Medical Association 253, 6; 10.2460/javma.253.6.719
Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn the page →
Histopathologic Findings
Multifocal hemorrhages were present in the myocardium, epicardium, and endocardium. In multiple foci of myocardial necrosis, especially adjacent to or within hemorrhagic foci, cardiomyocytes had condensed and hyperchromatic nuclei (Figure 2). Cardiomyocytes with more advanced necrosis were fragmented with hypereosinophilic sarcoplasm, loss of cross-striations, and karyorrhexis. In a few vessels, mostly arterioles, the tunica media and tunica intima were disrupted and hypereosinophilic with fibrinoid change. Some vessels had hypertrophied endothelial cells and perivascular edema. Within the lungs, the pulmonary parenchyma was congested, scattered alveoli contained lightly eosinophilic edema residue, and interlobular septa were expanded by edema.
Photomicrographs of sections of the heart from the pig in Figure 1. A—In coalescing foci of hemorrhagic myocardial necrosis, the cardiomyocytes have pyknosis and hypereosinophilic sarcoplasm. H&E stain; bar = 200 μm. Inset— Higher-magnification image of a necrotic cardiomyocyte with fragmented sarcoplasm and karyorrhexis. H&E stain; bar = 25 μm. B—An arteriole (center) has disrupted and fragmented tunica media and intima and is surrounded by extravasated erythrocytes and edema. H&E stain; bar = 50 μm. C—In an area of myocardial hemorrhage, periodic acid–Schiff reaction highlights fibrinoid change in arterioles. Periodic acid–Schiff stain; bar = 50 μm.
Citation: Journal of the American Veterinary Medical Association 253, 6; 10.2460/javma.253.6.719
Photomicrographs of sections of the heart from the pig in Figure 1. A—In coalescing foci of hemorrhagic myocardial necrosis, the cardiomyocytes have pyknosis and hypereosinophilic sarcoplasm. H&E stain; bar = 200 μm. Inset— Higher-magnification image of a necrotic cardiomyocyte with fragmented sarcoplasm and karyorrhexis. H&E stain; bar = 25 μm. B—An arteriole (center) has disrupted and fragmented tunica media and intima and is surrounded by extravasated erythrocytes and edema. H&E stain; bar = 50 μm. C—In an area of myocardial hemorrhage, periodic acid–Schiff reaction highlights fibrinoid change in arterioles. Periodic acid–Schiff stain; bar = 50 μm.
Citation: Journal of the American Veterinary Medical Association 253, 6; 10.2460/javma.253.6.719
Photomicrographs of sections of the heart from the pig in Figure 1. A—In coalescing foci of hemorrhagic myocardial necrosis, the cardiomyocytes have pyknosis and hypereosinophilic sarcoplasm. H&E stain; bar = 200 μm. Inset— Higher-magnification image of a necrotic cardiomyocyte with fragmented sarcoplasm and karyorrhexis. H&E stain; bar = 25 μm. B—An arteriole (center) has disrupted and fragmented tunica media and intima and is surrounded by extravasated erythrocytes and edema. H&E stain; bar = 50 μm. C—In an area of myocardial hemorrhage, periodic acid–Schiff reaction highlights fibrinoid change in arterioles. Periodic acid–Schiff stain; bar = 50 μm.
Citation: Journal of the American Veterinary Medical Association 253, 6; 10.2460/javma.253.6.719
Additional Laboratory Findings
Hepatic selenium concentration, as assessed by high-pressure liquid chromatography, was 0.34 ppm (reference range, 0.40 to 1.20 ppm). The gross, histologic, and high-pressure liquid chromatography findings suggested that the myocardial and vascular necrosis and hemorrhage in this pig were attributable to dietary selenium deficiency. This was confirmed via feed analysis performed by the producer's feed supplier. Hepatic vitamin E concentration was within reference limits. Bacterial culture of a sample of the pericardial fluid was negative.
Morphologic Diagnosis and Case Summary
Morphologic diagnosis and case summary: hemorrhagic myocardial necrosis consistent with mulberry heart disease (MHD) caused by dietary selenium deficiency in a pig.
Comments
Mulberry heart disease, named for the mottled red gross appearance of the heart in affected animals, results from selenium or vitamin E deficiency (or both). It becomes clinically apparent as sudden and unexpected death (usually because of ventricular dysrhythmia) in pigs that are a few weeks to 4 months of age.1–3 Both vitamin E and selenium are antioxidants. Selenium is a key component in the selenoprotein family of glutathione peroxidases, enzymes that inactivate peroxides and thereby maintain physiologic muscle function.2 Vitamin E (α-tocopherol) works along with selenium as a peroxyl radical scavenger to protect cell membranes from high concentrations of lipid radicals produced in the lipid peroxidation chain reaction.1–4 Animals with high feed-conversion efficiency and substantial muscle mass are susceptible to selenium or vitamin E deficiency because of increased nutritional requirements.3 Additionally, grains from selenium-deficient soils or selenium antagonists in mixed feeds can result in low dietary concentration of selenium.4–6 Certain components in a diet, such as saturated fats and propionic acid–treated corn, can deplete vitamin E content.7
Common gross lesions of porcine MHD principally develop in the thorax and include straw-colored transudate in the pleural cavity, edematous and congested lungs, and pericardial transudate containing strands of fibrin.3 Within the heart, linear and ecchymotic hemorrhages may be extensive and involve the epicardium, myocardium, and endocardium of all cardiac chambers.1,3 Histologically, degeneration and necrosis of cardiomyocytes and hemorrhage may be prominent or negligible. The microangiopathy of MHD in small arteries and arterioles probably develops independently of the myocardial necrosis.7–9 Microangiopathy is nonspecific, given that the same change is associated with many viral infections and bacterial toxemias in pigs.3,6,7 It is, however, a useful indicator of MHD.
White muscle disease is the typical outcome of selenium or vitamin E deficiency in lambs, calves, and chickens.1,3,10 Pallor or streaks of white, gritty mineralization in cardiac or skeletal muscle are often observed.3,10 Microscopic characteristics include necrosis and mineralization of myocytes.10–12 Hepatosis dietetica, a syndrome named for the hepatic lesions and the belief that those lesions are related to a pig's diet, is now a less common result of vitamin E or selenium deficiency because the recommended amount of supplemental selenium in livestock feed has been increased to 0.3 ppm.3,13,14 As with MHD, hepatosis dietetica is associated with sudden death with few or no premonitory signs. In cases of hepatosis dietetica, there is typically submassive to massive hepatic necrosis and hemorrhage; myocardial necrosis and pulmonary edema may be present.1,13 Because the causes of MHD, white muscle disease, and hepatosis dietetica are similar, it is not surprising that lesions associated with these conditions can coexist. Diagnosis can often be made on the basis of the appearance of gross lesions; microscopic examination of lesions in the heart, liver, or muscles; and analysis of vitamin E and selenium concentrations in samples of liver tissue or serum.
Acknowledgments
Dr. Peat is a fellow in the NIH Comparative Biomedical Scientist Training Program supported by the National Cancer Institute.
References
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