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In humans, it is acknowledged that dilated cardiomyopathy is also caused by infection-induced myocarditis. To evaluate whether the occurrence of lesions of dilated cardiomyopathy in cattle may be triggered by myocarditis, an adult Holstein-Friesian dairy cow which showed dilated cardiomyopathy associated with myocarditis was examined by histopathology. Traumatic pericarditis or idiopathic congestive heart failure was clinically suspected, and the animal was culled because of unfavorable prognosis. Histopathological examination revealed an intrinsic cardiomyopathic lesion that overlapped with myocarditis. Cardiomyocytes had sarcoplasmic vacuoles containing amorphous materials and/or lipofuscin granules, which were consistent with autophagic vacuoles. Inflammatory cells, such as lymphocytes and neutrophils, infiltrated the myocardium and sub-pericardial regions. Even though the pathogenetical mechanism of dilated cardiomyopathy following myocarditis in humans may not necessarily be applicable to that of the hereditarily determined dilated cardiomyopathy in the cow, the myocardium of latter showed histopathological features similar to some degree to those of the human heart disease. To confirm whether the inflammatory process may have played a role as a trigger (or promoting) factor for initiating cardiomyopathic lesions of this cow, further research of substantial numbers of relevant bovine cases appears warranted. [ABSTRACT FROM AUTHOR]

Occurrence of vacuolar myopathy caused by factors other than inherited glycogen storage condition is uncommon in domestic animals. This preliminary report describes the detection of a vacuolar myopathic lesion in a 13-year-old Holstein- Friesian dairy cow which showed an 8-day history of cardiac disease. Gross inspection after slaughter revealed edema in a variety of tissues, dilatation and hypertrophy of the cardiac ventricles, and hepatic congestion. Histopathology revealed degenerative myocardial lesions and passive hepatic congestion, which were identical to those previously documented in cases of bovine dilated cardiomyopathy. Skeletal muscles represented a vacuolar myopathic lesion characterized by the presence of distinctive vacuoles in atrophic myofibers, which occurred singly in the central zone of each myofiber on transverse sections and showed an irregularly elongated appearance on longitudinal sections. Such vacuoles frequently contained a small amount of weakly eosinophilic, granular, debris-like, or amorphous substances, displaying a feature of autophagic vacuoles. These vacuolated myofibers were more prominently observed in some muscle fascicles of the longissimus thoracis muscle than other muscles examined. The vacuolar myopathic lesion recognized in this cow was similar to some degree to that of autophagic vacuolar myopathy in man. Further studies are necessary to clarify a causal relationship between this vacuolar myopathic lesion and the disorder of bovine dilated cardiomyopathy. [ABSTRACT FROM AUTHOR]

Three Holstein-Friesian dairy cows, aged 5 1/3 to 12 years, showed a history of heart failure and were euthanized on separate days. Commonly observed postmortem findings included edema in many sites of the body, dilatation and hypertrophy of the right cardiac ventricle, hepatic congestion, and swollen pale kidneys. Histopathologically, myocardial lesions were comprised of a variety of degenerative changes in cardiomyocytes and interstitial fibrosis, consistent with those described previously in cases of bovine dilated cardiomyopathy in Holstein-Friesian cattle. Additionally, in one of these three cows, unmyelinated nerve fibers of many intra-cardiac nerve bundles that probably were postganglionic fibers exhibited multifocal segmental degeneration of axons. Degenerated axons were closely associated with Schwann cell pathology, indicating an intimate involvement of axon-Schwann cell interaction. Such an intra-cardiac autonomic neuropathy might have had an adverse effect on the regulation of heart activity. It is not possible to determine if this intra-cardiac autonomic neuropathy was primary or secondary to the dilated cardiomyopathy. [ABSTRACT FROM AUTHOR]

Iron has been identified as a necessary element for the normal development of newborn calves, but on the contrary, milk is considered to be a poor source of iron. This study was designed to investigate the iron requirements of Holstein calves at different time points postpartum. Serum iron (Fe), total iron binding capacity (TIBC), ceruloplasmin, and ferritin were measured in 46 newborn calves. Blood samples were collected before suckling colostrum (T0), after suckling at 1-day-old (T24), 2-day-old (T48), and 2-month-old (T2mon). Blood iron levels in newborn calves, before suckling colostrum, was the same as the mother, but decreased in 1 and 2-day-old calves and continued to decrease until 2 months of age. There were significant differences between serum iron levels at T0, T48, and T2mon ( P<0.001). Blood TIBC levels were significantly higher in newborn calves at T0 ( P<0.001) than in their mothers and continued to show significant increases at T24, T48, and T2mon ( P<0.001). Ceruloplasmin at T2mon was within normal ranges for normal adult cows, suggesting that transport of iron in 2-month-old calves, at least in that part which is related to blood ceruloplasmin, is normal. Blood ferritin levels in newborn calves before suckling colostrum, which was the same as their mothers’, decreased at T24 and T48 but insignificantly increased at T2mon. This data show that commercially reared suckling calves require iron supplements, which are essential for them at birth and may play an important role in their growth, hematopoiesis, and resistance to infections. [ABSTRACT FROM AUTHOR]