Key result
Foot-and-mouth disease in calves was associated with increased serum cardiac troponin I (14.8 +/- 1.9 ng/ml) and loss of cTnI immunolabeling in cardiomyocytes compared with controls.
Case-Control (n=24)
May indicate myocardial injury in FMD calves; leaves open cTnI utility for diagnosis or prognosis in outbreaks.
The current study was designed to determine the changes of the cardiac troponin I (cTnI) expression in blood and tissue during the myocardial degeneration in calves with foot-and-mouth disease (FMD). Seventeen crossbred calves presenting pathological signs for FMD confirmed by viral analysis were studied. A biochemistry panel and immunohistochemistry were performed on 17 diseased calves and 7 calves used as controls. Creatine kinase (CK), CK-myocardial band (CK-MB), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) activities were analyzed for both groups. Cardiac troponin I levels were measured by a commercially available enzyme-linked immunosorbent assay kit. Mean cTnI (14.8 +/- 1.9 ng/ml) concentration and CK (573 +/- 407 U/l), CK-MB (238 +/- 37 U/l), AST (84 +/- 7), and LDH (298 +/- 29 U/l) activities were higher in FMD cases compared with controls. Immunohistochemistry revealed loss or depletion of cTnI expression in myocardium of all cases. None of the 7 controls showed loss of cTnI expression. Increased serum cTnI concentration correlated with myocardial injury and loss of cTnI immunolabeling in cardiomyocytes of calves with FMD.
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Tunca et al. (2008) conducted a case-control in Foot-and-mouth disease (n=24). Foot-and-mouth disease vs. Healthy controls was evaluated on Mean cardiac troponin I (cTnI) concentration. Foot-and-mouth disease in calves was associated with increased serum cardiac troponin I (14.8 +/- 1.9 ng/ml) and loss of cTnI immunolabeling in cardiomyocytes compared with controls.
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