Nutritional muscular dystrophy in lambs reared on pasture in semiarid region of Brazil

This article presents important data on the diagnosis of nutritional muscular dystrophy (NMD) in sheep reared in the semiarid region of Northeast Brazil, with a focus on medical clinic data, nutritional management, anatomopathological aspects and quantification of serum selenium by highly sensitive analytical methodology. The semiarid region of Brazil is of great importance in the creation of small ruminants and many diseases that affect herds are related to failures in nutritional management, sanitary measures, periods of greater drought or low rainfall, little availability of native forage at certain times of the year and lack of supplementation with energy nutrients, proteins and minerals. The lack of publications on outbreaks of selenium deficiency demonstrates the importance of diagnosing in this area. The mean concentration of Se in the serum from the lambs was very low (2.52±1.02µg/L). The findings in the skeletal muscles are compatible with the characteristics observed in NMD, characterized by necrosis and calcification of myofibrils. In addition, necrotizing vasculitis in hepatic arterioles and hepatocellular coagulation necrosis in hepatocytes were observed, probably triggered by lipid peroxidation of cell membranes. The lambs from this outbreak, reared on pasture in the semiarid region, presented low serum Se concentration, with clinical and anatomopathological manifestation of NMD. Thus, supplementation with Se in the diet should be recommended regularly to avoid the appearance of new cases. Serum Se levels are useful indicators for the diagnosis of nutritional muscular dystrophy in lambs, associated with clinical and anatomopathological data.

Applicability of the protein-lipid profile and activity of lactate dehydrogenase isoenzymes for diagnosing nutritional muscular dystrophy in calves

Introduction: In calves, hyposelenosis degenerates skeletal muscles in different parts of the body. The extent of damage to muscle cells can be diagnosed by determining the activity of creatine kinase (CK), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH). The aim of this study was to analyse variations in the serum levels of LDH isoenzymes in calves with nutritional muscular dystrophy (NMD), to determine the applicability of this parameter for diagnosing NMD, and to describe the influence of hyposelenosis on total protein (TP), triglyceride (TG), and cholesterol (CHOL) levels.Material and Methods: Two groups of calves (n = six animals per group) were used. After birth, control group calves (SC) were intramuscularly administered 10 ml of a preparation containing selenium (Se) and vitamin E, and experimental group animals (SE) that were not injected. Blood was collected after 5, 15, and 25 days, and the concentrations of Se, vitamin E, TP, TG, and CHOL and the activity of glutathione peroxidase (GSH-Px), CK, and LDH fractions were determined.Results: Hypocholesterolaemia and elevated TG levels were found in SE group calves whose LDH fractions revealed a significant increase in LDH4 and LDH5 activity and a decrease in LDH1 activity when electrophoretically separated.Conclusions: Nutritional muscular dystrophy is accompanied by hypocholesterolaemia and elevated TG levels caused by muscle lipolysis. LDH4 and LDH5 activity parameters assist early diagnosis of NMD in calves.

Coagulology, biochemical profile and muscle pathology in calves diagnosed with nutritional muscular dystrophy

The aim of this study was to explain the correlations between selenium deficiency, hemostatic and biochemical disorders, and the progression of pathological changes in calves diagnosed with nutritional muscular dystrophy (NMD). The study was performed on 20 calves with supplementation of 8 ml selenium and vitamin E preparation and 20 calves with symptoms of NMD. Blood was sampled from calves aged 5, 12 and 19 days. On day 19, samples of the biceps femoris muscle were collected from 6 animals in each group for histopathological analysis. The following blood parameters were determined: PLT, PT, TT, APTT, fibrinogen and D-dimer concentrations, antithrombin III activity, glucose, selenium and vitamin E concentrations, activity of CK, LDH and GSH-Px. Muscle sections were stained with H&E and HBFP. Platelet counts were significantly lower in calves with symptoms of NMD. No significant differences in coagulation parameters were observed between the groups. Sick calves were diagnosed with hyperglycemia and elevation of CK and LDH activity. Selenium and vitamin E concentrations in the blood serum were significantly lower in the experimental group together with significant drop in GSH-Px activity. Changes characteristic of Zenker’s necrosis were observed in a muscle of the sick animals. To our best knowledge this is the first study in which the attempt was made to explain the relationship between selenium deficiency and changes in the coagulation system in ruminants.

Cardiac troponin I in healthy newborn goat kids and in goat kids with cardiac nutritional muscular dystrophy

This study was designed to establish serum cardiac troponin I (cTnI) concentrations in healthy newborn goat kids and in those with cardiac nutritional muscular dystrophy (NMD). Thirty-five single full-term newborn goat kids (20 males and 15 females; age: 6.1 ± 3.5 h; weight 3.4 ± 0.68 kg), together with their respective mothers (Group 1; G1) were enrolled consecutively. Thirty-one goat kids (age: 9.5 ± 4.3 days) with NMD, together with 20 control goat kids (age: 7.8 ± 4.3 days) were also included in this study (Group 2; G2). Blood samples were collected from G1 within 12 h of birth and from G2 on admission. Serum samples were collected and analysed for cTnI. In G1, the mean serum concentration of cTnI in goat kids was 0.290 ± 0.37 ng/mL, with no statistically significant difference between male and female kids (P = 0.61). The mean cTnI concentration in the does was 0.017 ± 0.04, ng/mL. Serum values of cTnI in the goat kids and in their respective mothers differed significantly (P = 0.0001). In G2, the mean cTnI concentration was 0.02 ± 0.05 ng/mL in the control and 11.18 ± 20.07 ng/mL in the diseased goat kids, with a statistically significant difference between diseased and control goat kids (P = 0.017). Serum concentrations of cTnI are higher in goat kids than in their respective mothers. In conclusion, the cTnI assay appears to be a sensitive and specific marker for myocardial injury in goat kids.