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Case Reports
. 2020 Aug 1;70(4):376-383.
doi: 10.30802/AALAS-JAALAS-19-000162. Epub 2020 Jul 16.

Mulberry Heart Disease and Hepatosis Dietetica in Farm Pigs (Sus scrofa domesticus) in a Research Setting

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Case Reports

Mulberry Heart Disease and Hepatosis Dietetica in Farm Pigs (Sus scrofa domesticus) in a Research Setting

Kristi L Helke et al. Comp Med. .

Abstract

Perioperative complications and deaths occurred while developing a novel surgical model of pediatric kyphosis in 10 to 12 kg male farm-raised Yorkshire piglets. All piglets appeared clinically normal preoperatively. Intraoperative complications included tachycardia, respiratory acidosis, and death. Postoperatively, clinical signs included posterior paresis, head pressing, prolonged anesthetic recovery, difficulty rising, and sudden death. Necropsies were performed on all piglets. Some morbidity and mortality were accurately attributed to the spinal surgery. However, the index piglet for this report died suddenly approximately 16 to 18 h after surgery. Necropsy of this animal revealed clear, serosanguineous pleural and pericardial effusions along with myocardial hemorrhage and hepatic lesions, consistent with mulberry heart disease and hepatosis dietetica, respectively. Serum vitamin E and selenium levels from this animal were below age-specific lab reference ranges. Clinical signs of vitamin E and selenium deficiency are most common in fast-growing weaner piglets. The added stress of major surgery may exacerbate the condition in young piglets. Resolution of morbidity and mortality in both juvenile and adult pigs occurred upon the use of an alternate vendor able to provide feed analyses meeting industry standards, although serum levels of vitamin E and selenium in similar ages and breed of swine were still occasionally slightly below reference ranges.

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Figures

Figure 1.
Figure 1.
(A) Gross image of porcine heart with paintbrush lesions (white arrows) consistent with vitamin E/selenium deficiency (Mulberry Heart Disease). (B) Gross image of cut surface porcine heart with hemorrhagic myocardium consistent with vitamin E/selenium deficiency (Mulberry Heart Disease).
Figure 2.
Figure 2.
(A) Microscopic overview image of left ventricle (Hematoxylin and eosin, 2×). (B) Higher magnification image of panel A. Microscopic image of left ventricle (Hematoxylin and eosin, 20×). There is pronounced mineralization (*) evident within cardiomyocytes. There is loss of cells and abundant hemorrhage separating cells (black arrows).
Figure 3.
Figure 3.
(A) Microscopic overview image of liver (Hematoxylin and eosin, 4×). There is loss of cell detail surrounding central veins (centrilobular necrosis). (B) Higher magnification image of panel A. Microscopic image of liver (Hematoxylin and eosin, 20×). There is pronounced loss of cellular detail (*) surrounding central veins with shrunken hepatocyte nuclei (arrows) and hemorrhage (centrilobular necrosis).
Figure 4.
Figure 4.
Gross image of stomach. The esophagus is at the upper right and pylorus is at the left. There is erosion and ulceration at the pars esophageal region (arrow).
Figure 5.
Figure 5.
(A) Vitamin E values (Lab A) compared with age. Black bar represents regression line. (B) Selenium values (Lab A) compared with age. Black bar represents regression line.
Figure 6.
Figure 6.
Difference in selenium levels in blood values. Samples taken from same animals sequentially on farm and upon arrival at facility (Lab B).

References

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