Spontaneous primary myopathies in domestic mammals: A review

Abstract

SUMMARY By reviewing the literature concerning primary myopathies in man and animals, a classification of spontaneous primary myopathies in domestic mammals is made. This classification is based on aetiological factors. Primary myopathies are divided into metabolic, immunologic, toxic, nutritional, congenital, inherited, and inflammatory myopathies. Muscular dystrophies, in accordance with the definition in human cases, are considered as a separate entity. In the description of the different muscle disorders the emphasis is on the structural changes and the pathogenesis. Clinical signs and diagnostic criteria are considered only briefly.

Microstructure of skeletal muscles of growing calves fed silage-based vs hay-based diets. I. Fibre diameters

“…Again, mean fibre diameter of older animals, ie 10-month-old calves (feeding systems pooled) were smaller than those quoted by Wegner (1983) (Goedegebuure, 1987). According to Pellegrini et al (1982) …”

Epidemiological Aspects of Cerebrospinal Elaphostrongylosis in Small Ruminants in Northern Norway

“…signs restricted to posterior paresis were defined as cases of CSE. These criteria were chosen to minimize the risk of including other small ruminant diseases known to occur in northern Norway: caprine arthritis encephalomyelitis and ovine nutritional muscular dystrophy, which mainly affects animals less than 6 months old (CORK et al, 1974;GOEDEGEBUURE, 1987), and primary brain diseases such as encephalitic listeriosis and cerebrocortical necrosis.…”

Scientific, sustainability and regulatory challenges of cultured meat

“…For example, it has been suggested that acidosis caused by rapid glycolysis leads to degenerative changes in muscles, which are solitary and rich in type II fibres [55][56][57] . Affected muscles show undesired characteristics, such as being pale, soft and exudative 58 . In cell culture, highly proliferating cells can metabolize more than 70% of the glucose to lactate -with associated acidosis -leaving only 20%-30% of the glucose available for tricarboxylic acid (TCA) cycle 59 .…”

“…In cell culture, highly proliferating cells can metabolize more than 70% of the glucose to lactate -with associated acidosis -leaving only 20%-30% of the glucose available for tricarboxylic acid (TCA) cycle 59 . Nutritional deficiencies, such as lack of vitamins, cause degenerative changes in muscle, as indicated in the case of vitamin D 60 , vitamin E and selenium 58 .…”