The influence of selenium deficiency on chosen biochemical parameters and histopathological changes in muscles of goat kids.

The research was conducted on 40 young alpine goats (kids) divided into two groups. First group consisted of 20 kids demonstrating clinical signs of muscular dystrophy. Second group was a control and consisted of 20 animals that received intramuscular injection (2ml per animal) of vitamin E and selenium preparation containing in 1ml 50 mg of tocopherol acetate, 0.5mg of sodium selenite and solvent on 2nd day of life. The kids were clinically examined and blood for laboratory analyses was sampled three times from day 5 of their life in 10 day intervals. In addition, six 24 days old kids demonstrating clinical signs of muscular dystrophy and six control kids were subjected to biceps femoris biopsy. Serum total protein, glucose, triglycerides, cholesterol as well as AST, CK and LDH were determined in all the animals. In addition, the activity of glutathione peroxidase (GSH-Px) was determined in whole blood and serum concentrations of selenium and vitamin E were deter-mined in 6 kids from each group. Total lactate dehydrogenase activity and its separation into isoenzymatic fractions were determined in the collected biopsy material. The muscle samples collected were additionally subjected to histopathological examination consisting of HE staining and HBFP staining to detect necrotic muscle fibers. Symptoms of muscular dystrophy began to appear in the first group between 17 and 23 days of age and included tremors of the limbs, poor posture, stilt gait and increased time of laying. The control animals did not show any symptoms of the disease during the experiment. Hypo-proteinemia, hypoglycemia, cholesterol reduction and elevated triglycerides level associated with lipolysis of adipose tissue have been found in the sick kids. A significant decrease in selenium, vitamin E and activity of glutathione peroxidase levels was observed in the kids with symptoms of muscular dystrophy. The activity of AST, CK and LDH was significantly higher in the animals with symptoms of the disease as well. Five isoenzymes were obtained in the electrophoretic separation of lactate dehydrogenase into isoenzymatic fractions in the muscle tissue. LDH4and LDH5 isoenzymes were dominating, and a significant increase in LDH5 fraction of the sick animals was also observed. Histopathological examination of muscle samples from sick animals revealed changes characteristic for the presence of Zenker necrosis.

White Matter High Signals Interfere with Noncontrast Computed Tomography in the Early Identification of Cerebral Infarction.

BACKGROUND: We developed an image patch classification-based method to detect early ischemic stroke. The accuracy of this method was >75%. We aimed to analyze patients' image data to identify interference factors that would affect its accuracy. METHODS: We conducted a retrospective analysis of 162 patients who were hospitalized with acute ischemic stroke. Factors related to the noncontrast computed tomography (ncCT) determination results were analyzed according to the patient's sex, age, clinical symptoms, cerebral infarction volume, cerebral infarction location, and whether or not the white matter high (WMH) signal was combined. RESULTS: The volume of cerebral infarction was positively correlated with the predicted results. The correct percentages of patients with volumes >1 and <1 mL were 59.18 and 83.19%, respectively, and the difference was statistically significant (p = 0.001). The correct percentage of the internal capsule region (47.1%) was significantly lower than that of the other groups (p = 0.011). The correct percentage of lateral ventricular paraventricular infarction was significantly lower than that of non-lateral ventricle patients (70.8 vs. 85.7%). In patients with lateral ventricular paraventricular infarction, if the WMH was combined, the correct percentage will decreased further as the Fazekas level increased. The correct percentage of lateral ventricle infarction combined with Fazekas 3 was 40.0%, which was statistically significant compared with the patient having Fazekas 0 with lateral ventricular infarction (p = 0.01). CONCLUSIONS: WMH had a similar computed tomography appearance to cerebral infarction and could interfere with the prediction of the cerebral infarction region by ncCT. This result provides a reference for clinicians to choose imaging methods for identifying acute cerebral infarction areas.

Two-photon microscopic imaging of capillary red blood cell flux in mouse brain reveals vulnerability of cerebral white matter to hypoperfusion.

Despite the importance of understanding the regulation of microvascular blood flow in white matter, no data on subcortical capillary blood flow parameters are available, largely due to the lack of appropriate imaging methods. To address this knowledge gap, we employed two-photon microscopy using a far-red fluorophore Alexa680 and photon-counting detection to measure capillary red blood cell (RBC) flux in both cerebral gray and white matter, in isoflurane-anesthetized mice. We have found that in control animals, baseline capillary RBC flux in the white matter was significantly higher than in the adjacent cerebral gray matter. In response to mild hypercapnia, RBC flux in the white matter exhibited significantly smaller fractional increase than in the gray matter. Finally, during global cerebral hypoperfusion, RBC flux in the white matter was reduced significantly in comparison to the controls, while RBC flux in the gray matter was preserved. Our results suggest that blood flow in the white matter may be less efficiently regulated when challenged by physiological perturbations as compared to the gray matter. Importantly, the blood flow in the white matter may be more susceptible to hypoperfusion than in the gray matter, potentially exacerbating the white matter deterioration in brain conditions involving global cerebral hypoperfusion.

Cerebrovascular reactivity as a determinant of deep white matter hyperintensities in migraine.

OBJECTIVE: To evaluate the association between the cerebrovascular reactivity to carbon dioxide (CO2-CVR) and the deep white matter hyperintensity (WMH) burden in patients with migraine. METHODS: A total of 86 nonelderly patients with episodic migraine without vascular risk factors and 35 headache-free controls underwent 3T MRI. Deep WMHs were quantified with a segmentation method developed for nonelderly migraineurs. The interictal CO2-CVR was measured with transcranial Doppler with the breath-holding method. The mean breath-holding index of the bilateral middle cerebral arteries (MCA-BHI) was square root transformed and analyzed with univariate and multivariate logistic regression models to determine its association with the highest tertiles of deep WMH burden (number and volume). RESULTS: A low MCA-BHI was independently associated with the highest tertile of deep WMH number in patients with migraine (adjusted odds ratio [OR] 0.02, 95% confidence interval [CI] 0.0007-0.63, p = 0.026). In controls, the MCA-BHI was not associated with deep WMH number. Interaction analysis revealed that migraine modified the effect of MCA-BHI on deep WMH number (p for interaction = 0.029). The MCA-BHI was not associated with increased deep WMH volume in both patients and controls. Age was independently associated with deep WMH volume in patients (adjusted OR 1.07, 95% CI 1.004-1.15, p = 0.037). CONCLUSIONS: In this study, we found a migraine-specific association between a reduced CVR to apnea and increased number of deep WMHs in healthy, nonelderly patients with migraine. A dysfunctional vascular response to apnea may predispose migraineurs to an increased risk of WMHs.

Detection of Se, Vit. E, Vit. A, MDA, 8-OHdG, and CoQ10 Levels and Histopathological Changes in Heart Tissue in Sheep with White Muscle Disease.

This study was carried out to determine vit. E, Se, vit. A, malondialdehyde (MDA), 8-hydroxy-2-deoxyguanosine (8-OHdG), and ubiquinone-10 (CoQ10) levels and histopathological changes in sheep with white muscle disease (WMD). A total of 30 sheep were used; 20 sheep with WMD were brought to our clinic for diagnosis and treatment at various times, and 10 healthy sheep were in the control group. The Se, vit. E, vit. A, MDA, 8-OHdG, and CoQ10 values of the healthy and WMD sheep were as follows: 0.917 ± 0.037, 0.790 ± 0.067; 1.190 ± 0.011, 1.090 ± 0.021; 5.400 ± 0.275, 5.200 ± 0.173; 1.602 ± 0.264, 2.636 ± 0.576; 0.656 ± 0.197, 1.485 ± 0.271; and 0.280 ± 0.044, 1.753 ± 0.551 respectively (p < 0.05). According to histopathological and immunohistochemical findings in the WMD group, hyaline degeneration, Zenker's necrosis, and dystrophic calcification were observed in the muscle fibers. Immunohistochemically, 8-OHdG staining of the heart tissue determined a severe 8-OHdG expression in the WMD group. The findings of this study suggest that MDA, 8-OHdG, and CoQ10 values could be used as diagnostic and prognostic biomarkers in sheep affected with WMD.

Development and clinical consequences of white matter lesions in Fabry disease: a systematic review.

BACKGROUND: Fabry disease (FD) is a rare lysosomal storage disorder that might result in, amongst other complications, early stroke and white matter lesions (WMLs). More insight in WMLs in FD could clarify the role of WMLs in the disease presentation and prognosis in FD. In this systematic review we assessed the prevalence, severity, location and course of WMLs in FD. We also systematically reviewed the evidence on the relation between WMLs, disease characteristics and clinical parameters. METHODS: We searched Pubmed, EMBASE and CINAHL (inception to Feb 2018) and identified articles reporting on FD and WMLs assessed with MRI. Prevalence and severity were assessed for all patients combined and divided by sex. RESULTS: Out of 904 studies a total of 46 studies were included in the analyses. WMLs were present in 46% of patients with FD (581 out of 1276 patients, corrected mean age: 38.8 years, range 11.8-79.3) and increased with age. A total of 16.4% of patients (31 out of 189 patients, corrected mean age: 41.1 years, range 35.8-43.3 years) showed substantial confluent WMLs. Men and women showed comparable prevalence and severity of WMLs. However, men were significantly younger at time of WML assessment. Patients with classical FD had a higher chance on WMLs compared to non-classical patients. Progression of WMLs was seen in 24.6% of patients (49 out of 199 patients) during 38.1 months follow-up. Progression was seen in both men and women, with and without enzyme replacement therapy, but at an earlier age in men. Stroke seemed to be related to WMLs, but cerebrovascular risk factors, cardiac and renal (dys)function did not. Pathology in the brain in FD seemed to extend beyond the WMLs into the normal appearing white matter. CONCLUSIONS: A significant group of FD patients has substantial WMLs and male patients develop WMLs earlier compared to female patients. WMLs could be used in clinical trials to evaluate possible treatment effects on the brain. Future studies should focus on longitudinal follow-up using modern imaging techniques, focusing on the clinical consequences of WMLs. In addition, ischemic and non-ischemic pathways resulting in WML development should be studied.

Expression of ADAMTS-7 in myocardial dystrophy associated with white muscle disease in lambs.

The aim of the present study was to investigate the role of ADAMTS-7 gene in the pathogenesis of myocardial dystrophy associated with white muscle disease (WMD) in lambs. A total of 217 cardiac tissue samples from lambs with WMD were used in the study. Histopathological sections of the samples were stained with hematoxylin-eosin (HE) and examined using Western-blot, real-time PCR (RT-PCR) and immunohistochemistry for ADAMTS-7 gene expression, and the findings were statistically evaluated. Histopathological examinations revealed fibrosis associated with hyalinization, necrosis and granular calcifications in cardiomyocytes. Western blot and RT-PCR showed a statistically significant upregulation of ADAMTS-7 (p<0.05) (p<0.05). Immunohistochemical analyses showed that immunopositive cell numbers significantly high for ADAMTS-7 (p<0.05). The study has revealed that ADAMTS-7 gene is significantly expressed in myocardial dystrophy associated with WMD in addition to its role in the pathogenesis of this disease.

White muscle disease in foals: focus on selenium soil content. A case series.

BACKGROUND: White muscle disease (WMD) is a nutritional myopathy caused by selenium (Se) deficiency. In most soils, Se is present in low concentrations, sometimes even below 0.2 mg/kg, a trend which is seen in many countries. Apart from total soil Se concentrations, soil conditions may be such that the bio-availability of Se is so low that it causes very low uptake in plants which can ultimately lead to deficiency problems in animals. This is the first case series to report clinical WMD in foals in areas deficient in Se, in the Netherlands. The aim of the current report is to provide an overview of the clinical history, symptoms and (clinical) pathology of 8 newborn foals living at 4 different premises and suffering from WMD together with the effectiveness of Se and vitamin E (Vit E) supplementation in the affected foals, their dams and herd members. Hands on practical information is provided to apply a correct and effective Se supplementation management in horses and which pitfalls need to be avoided for a successful approach. CASE PRESENTATION: Case features and history were mapped out for all foals. Se and Vit E status were assessed for the foals, their dams and herd members, at admission and after 3 months of Vit E/Se supplementation. Common symptoms were muscle weakness, inability to rise, lethargy and inadequate suckle reflex together with increased serum muscle enzymes and low glutathione peroxidase (GSH-Px) and low to normal serum vit E levels. Necropsy revealed necrosis of skeletal muscles consistent with nutritional myopathy. Se status of the dams and herd members correlated well with the Se status of the foals. All surviving foals (n = 6) showed normal Vit E and GSH-Px levels after supplementation, likewise, all horses tested at premises 1, 3 and 4. However, dams and herd members in premises 2 showed no normalization. Horses of that premises were diagnosed with pyrrolizidine intoxication one year prior to the study. CONCLUSIONS: Certain regions in the Netherlands are sufficiently Se deficient to predispose newborn foals to develop WMD, especially when they are being fed a diet that mainly consists of locally harvested roughage.

CONGENITAL NUTRITIONAL MYODEGENERATION (WHITE MUSCLE DISEASE) IN A GIRAFFE ( GIRAFFA CAMELOPARDALIS) CALF.

It is well known that vitamin E and selenium deficiencies in domestic ruminants can lead to white muscle disease. After a clinically normal gestation period at Ouwehand Zoo in the Netherlands, a newborn giraffe ( Giraffa camelopardalis) calf showed clinical signs of white muscle disease almost immediately after birth. The calf was rejected by the mother and was euthanized 3 days later because of deterioration of clinical signs. At necropsy, pulmonary edema and pallor of skeletal and heart muscles was noted. Histologically, there was hyaline degeneration of skeletal muscle myocytes and pulmonary edema. Blood concentrations of vitamin E were ≤ 0.7 mg/L. Based on clinical, biochemical, and gross and microscopic pathological findings, congenital nutritional myodegeneration was diagnosed. This case of neonatal white muscle disease is particularly remarkable given that the diet of the dam contained more than the recommended amount of vitamin E.

White matter lesions reduce number of brain metastases in different cancers: a high-resolution MRI study.

Brain metastases are major complications of common cancers. Tumor type and proneness to the CNS are thought to define the number and size of brain metastases. It is not known if intrinsic vascular factors can also have an effect. Restricted perfusion due to cerebral small vessel disease is frequent in elderly patients and causes white matter lesions (WML). The aim of this analysis was to evaluate a possible negative effect of WML and patient age on the number and size of brain metastases (BM) of different tumor entities. Pre-therapeutic 3 T brain magnetic resonance imaging (MRI) of 200 patients with BM were analyzed. Location, size and number of BM (NoM) were determined. T2 hyperintensive WML were scored according to Fazekas-Score (grade I-III). Patients with WML grade 1 (NoM: 5.59; p = 0.009) and grade 2 (NoM: 3.68; p = 0.002) had significantly less BM than patients without WML (NoM: 6.99). This effect was present in subgroups of different tumors: NSCLC (p = 0.05), other tumors than NSCLC (p = 0.048). Age (≤65 or >65 years) was positively correlated with the degree of WML but not with number (pNoM = 0.832) or mean diameter (pmDM = 0.662) of brain metastases. While patient age did not appear to be relevant, increasing WML were associated with lower number of brain metastases in different tumor types.

Apcdd1 stimulates oligodendrocyte differentiation after white matter injury.

Wnt signaling plays an essential role in developmental and regenerative myelination of the CNS, therefore it is critical to understand how the factors associated with the various regulatory layers of this complex pathway contribute to these processes. Recently, Apcdd1 was identified as a negative regulator of proximal Wnt signaling, however its role in oligodendrocyte (OL) differentiation and reymelination in the CNS remain undefined. Analysis of Apcdd1 expression revealed dynamic expression during OL development, where its expression is upregulated during differentiation. Functional studies using ex vivo and in vitro OL systems revealed that Apcdd1 promotes OL differentiation, suppresses Wnt signaling, and associates with ß-catenin. Application of these findings to white matter injury (WMI) models revealed that Apcdd1 similarly promotes OL differentiation after gliotoxic injury in vivo and acute hypoxia ex vivo. Examination of Apcdd1 expression in white matter lesions from neonatal WMI and adult multiple sclerosis revealed its expression in subsets of oligodendrocyte (OL) precursors. These studies describe, for the first time, the role of Apcdd1 in OLs after WMI and reveal that negative regulators of the proximal Wnt pathway can influence regenerative myelination, suggesting a new therapeutic strategy for modulating Wnt signaling and stimulating repair after WMI.

Mechanisms of white matter damage in multiple sclerosis.

Glia cells are mediators as well as targets of the chronic inflammatory process in the central nervous system of multiple sclerosis (MS) patients. They are involved in the control of autoimmunity, in the propagation and termination of the inflammatory reaction, in the induction of demyelination and neurodegeneration, and in remyelination and scaring. Demyelination, as well as neuronal and GLIA cell damage are induced by different immunological mechanisms including components of the adaptive and innate immune system. Oxidative injury resulting in mitochondrial dysfunction is one important mechanism of tissue injury. It is in part driven by the inflammatory response and the production of oxygen radicals mainly in microglia and macrophages. With increasing age of the patients and disease progression, oxidative injury is further amplified by additional mechanisms including central nervous system damage related microglia activation, progressive mitochondrial damage, and age-dependent iron accumulation within the human central nervous system. The inflammatory mechanisms associated with lesion formation in MS are to a large extent reflected in experimental models of inflammatory demyelination, such as autoimmune encephalomyelitis. This is not the case for the amplification mechanisms of oxidative injury, which mainly operate in the progressive stage of the disease.

Depressive symptoms predict cognitive decline and dementia in older people independently of cerebral white matter changes: the LADIS study.

OBJECTIVE: Depressive symptoms (DS) have been associated with increased risk of cognitive decline. Our aim was to evaluate the longitudinal influence of DS on cognition in independent older people, accounting for the severity of white matter changes (WMC). METHODS: The LADIS (Leukoaraiosis And DISability in the elderly) prospective study evaluated the impact of WMC on the transition of independent older subjects into disability. Subjects were evaluated annually over a 3 year period with a comprehensive clinical and neuropsychological evaluation. Previous episodes of depression and current DS were assessed during each interview. Severity of DS was assessed using the self-rated 15 item Geriatric Depression Scale. A neuropsychological battery and clinical criteria for cognitive impairments were applied in all clinical visits, and cognitive compound measures were made based on neuropsychological results. MRI was performed at baseline and at year 3. RESULTS: 639 subjects were included (74.1 ± 5 years old, 55% women, 9.6 ± 3.8 years of schooling). Dementia was diagnosed in 90 patients and cognitive impairment not dementia in 147 patients at the last clinical evaluation. DS were an independent predictor of cognitive impairment (dementia and not dementia) during follow-up, independent of the effect of the severity of WMC, medial temporal lobe atrophy, age, education or global cognitive function at baseline. CONCLUSIONS: DS are associated with an increase risk of cognitive decline, independent of the effect of WMC, probably due to an additive or synergistic effect. In this context, DS probably represent a subtle ongoing organic dysfunction.

Deep hypothermic circulatory arrest during the arterial switch operation is associated with reduction in cerebral oxygen extraction but no increase in white matter injury.

OBJECTIVE: Deep hypothermic circulatory arrest may be associated with increased neural injury. We investigated whether short periods of deep hypothermic circulatory arrest are associated with altered neurophysiologic recovery or greater risk of injury. METHODS: Eighteen term infants with transposition of the great arteries undergoing the arterial switch operation were enrolled. Deep hypothermic circulatory arrest was used in 11, and bypass alone in 7. Near-infrared spectroscopy and amplitude-integrated electroencephalography were recorded with standard monitoring during and from 4 to 16 h after surgery. Fractional tissue oxygen extraction was determined from arterial oxygen saturation and venous weighted intracerebral oxygenation. Magnetic resonance imaging was performed before and 5 to 7 days after surgery. RESULTS: There were no significant differences between patients requiring deep hypothermic circulatory arrest (median, 5 min; range, 3-6 min) or cardiopulmonary bypass only at the beginning of surgery. At the end of surgery, amplitude-integrated electroencephalography minimum amplitude was significantly lower in the deep hypothermic circulatory arrest group (P < .05), and fractional tissue oxygen extraction tended to be lower (P = .068). After surgery, deep hypothermic circulatory arrest was associated with significantly higher tissue oxygenation index, lower fractional tissue oxygen extraction, and lower core temperature (P < .05). Magnetic resonance imaging-defined white matter injuries before and after surgery were similar between groups. CONCLUSIONS: In this prospective, observational study, brief deep hypothermic circulatory arrest during arterial switch was associated with reduced cerebral oxygen uptake during recovery, with transient electroencephalographic suppression but no increase in risk of white matter injury.

Evaluation of copper concentration in subclinical cases of white muscle disease and its relationship with cardiac troponin I.

The present study aims to evaluate the serum level of copper (Cu) in lambs suffering from subclinical forms of white muscle disease (WMD) and its relationship with cardiac troponin I (cTn-I) as a novel biomarker of cardiovascular disorders. Ten milliliters of jugular blood were taken from 200 lambs less than one year old to measure serum concentrations of Cu, selenium (Se), and cTn-I. The subjects were divided into 2 groups, namely, the deficient group which included 36 lambs, and the control group which included 164 lambs according to the reference serum Se concentration (50 ng/mL). Serum Se levels in the deficient group were lower than 50 ng/mL. By contrast, the control group showed Se levels higher than 50 ng/mL. Differences among the serum Cu and cTn-I levels were determined in both groups. The mean ±SD and median of serum Cu and cTn-I levels in the deficient group were lower and higher than those in the control group, respectively. A significant positive correlation was observed between serum Cu and Se levels, and also serum Cu and Se levels showed a negative correlation with serum cTn-I concentrations. Stepwise linear regression analysis showed that serum Cu levels were correlated positively with serum Se levels (p<0.05). Receiver operating characteristic (ROC) curve analysis indicated that the area under curve (AUC) of Cu was significantly higher than that of cTn-I based on the reference diagonal line. It is important to keep in mind that the value of AUC for the ROC curve is between 0.5 and 1.00, in which the lowest accuracy is related to the reference diagonal line with AUC of 0.5. A cut-off was determined to indicate which Cu level can discriminate between affected and healthy lambs. The cut-off level, sensitivity, and specificity of Cu in this study were 144.5 ng/mL, 74%, and 61%, respectively.

Intoxicação espontânea de bovinos por Senna obtusifolia no Estado do Paraná / Spontaneous Senna obtusifolia poisoning in cattle in the state of Parana, Brazil

Plantas do gênero Senna causam miopatia degenerativa em bovinos e o maior número de relatos envolve Senna occidentalis. O objetivo desse trabalho é relatar, pela segunda vez no Brasil, um surto de intoxicação natural por Senna obtusifolia. É descrito um surto de intoxicação por Senna obtusifolia, na região noroeste do estado do Paraná, que aconteceu em um lote de 200 vacas, com idade entre 45 e 152 meses, introduzidas em um confinamento para melhorar a condição corporal antes do parto. A área do confinamento estava invadida pela planta e as vacas permaneceram no local durante oito dias. Entre quatro e nove dias após a entrada no confinamento 20 vacas adoeceram e somente uma se recuperou. Os sinais consistiram em mioglobinúria, incoordenação e decúbito esternal permanente. As vacas doentes apresentaram aumento das atividades das enzimas creatina quinase, aspartato aminotransferase, gamaglutamiltransferase e fosfatase alcalina. Lesões na musculatura esquelética dos membros posteriores caracterizadas por áreas pálidas representaram as principais alterações observadas à necropsia de quatro bovinos. Necrose segmentar multifocal da musculatura esquelética e necrose paracentral multifocal no fígado foram as alterações histopatológicas mais relevantes. As evidências epidemiológicas, clínicas e patológicas indicam o diagnóstico de intoxicação por Senna obtusifolia. A planta demonstrou ter efeito miotóxico e hepatotóxico nos animais intoxicados e a doença foi quase sempre fatal.

Plants of the genus Senna cause a degenerative myopathy in cattle and most of the reports refer to Senna occidentalis. The aim of this paper is to report, for the second time in Brazil, an outbreak of natural poisoning by Senna obtusifolia. It happened in the northwestern Paraná in a herd of 200 cows, 45 to 152 months of age, which had been placed into a feedlot to improve their nutritional status before the calving period. The cows stayed for eight days in this feedlot infested by the plant. Four to nine days after they got into the feedlot, 20 cows became ill and only one recovered. The clinical signs consisted of myoglobinuria, incoordination and permanent sternal recumbency. The affected cows showed increased activity of creatine phosphokinase, aspartate aminotransferase, gama-glutamyltransferase, and alkaline phosphatase. The main postmortem changes were in skeletal muscles of the hind limbs characterized by pale areas. The histological alterations were multifocal segmental necrosis of skeletal muscles and hepatic multifocal paracentral necrosis. Epidemiological, clinical and pathological data led to the diagnosis of Senna obtusifolia poisoning. The plant showed miotoxic and hepatotoxic effects on the poisoned animals and the disease was almost always lethal.

Detection of myocardial degeneration with point-of-care cardiac troponin assays and histopathology in lambs with white muscle disease.

The aim of this study was to evaluate the use of human cardiac troponin-I (cTn-I) and cardiac troponin-T (cTn-T) kits for the determination of myocardial degeneration in lambs suffering from white muscle disease (WMD). Cardiac troponin (cTn) analyses and necropsy were performed on 12 lambs with acute WMD. Only cTn analyses were tested in six healthy lambs. cTn-I and cTn-T tests were positive for all lambs with WMD, but negative in healthy lambs. Necropsy revealed that the cardiac and skeletal muscles of lambs with WMD had chalky white lesions, which appeared as necrosis and calcification in histopathology. The histopathological findings of the heart muscle and increased cTn in lambs with WMD suggested that marked myocardial degeneration may be detected by point-of-care cTn assays in lambs.