Incidences of myopathies such as white striping (WS), woody breast (WB) and spaghetti meat (SP) in breast meat from young broilers have been observed globally over the past decade. Some industry reports suggest up to 20% WB occurrence in fast growing heavy broilers (~4.0 kg) with an estimated cost of more than US$500 million/year to the US industry alone, but may actually be far higher. The proportions and severity of the anomaly appear to be flock-dependent and are related to factors such as genetics, nutrition (e.g. protein level during the fast-growing phase), growth rate, activity of the birds at young age, sudden bursts of activity, number of embryonic stem cells and litter management. These three myopathies can appear together or individually, but it appears that they are all related. When meat is processed, these myopathies represent quality issues (firmer meat and/or lower water binding, aesthetics) but do not present a food safety issue. The poultry industry is now focusing on ways to reduce or eliminate the occurrence of these myopathies. Recently some improvements have been made as more is learned about the interactions between environmental and management (e.g., nutrition) factors, and some producers are already implementing new procedures. Breeding programmes are starting to show some promise and are expected to help reduce WB (estimated at 10% of birds per year) and deliver more solutions in the future.

Objectives: Differentiating genetic myopathies from inflammatory myopathies can be challenging because of multiple overlapping clinical features. Examples are presented to highlight important clinical features that assist in the differentiation between the two. Methods: Clinical features including age at onset, history, pattern of weakness, serum creatine kinase activity, electromyography findings, and muscle biopsies are reported in six patients initially thought to have an inflammatory myopathy in whom the final diagnosis was a genetic myopathy. Results: All six patients met Bohan and Peter criteria for at least probable idiopathic polymyositis and were subsequently found to have a genetic myopathy (4 DYSF, RYR1, and GNE). The key distinguishing clinical were minimal to no response to immunosuppression and atypical involvement of distal muscles in the majority of cases. Conclusions: Patients diagnosed with inflammatory myopathies should be reevaluated for the possibility of a genetic myopathy if they fail to respond to a course of disease-modifying agents and/or there is atypical distal muscle involvement.

Deep pectoral myopathy (DPM) of musculus pectoralis minor is an anomaly observed in gallinaceous poultry. To date its cases have been reported in adult pedigree turkeys and hens and in recent years also in broiler chickens. This degeneration is manifested in an abnormal appearance of breast muscles, with changes in colour from pink to green, as well as changes in the texture of the muscle tissue. The anomaly is found most frequently in genetic lines of chickens characterised by dynamic weight increment in the rearing period as well as a considerable increase in the proportion of pectoral muscles. The mechanism for the development of myopathy is already well known. It is related with ischemic necrosis initiated by rapid physical activity of birds, which mobilises pectoral muscles, normally relatively inactive in modern intensive animal management systems. Absence of symptoms manifested in vivo results in a situation when muscles affected by myopathy are identified only during carcass dissection. An increasing number of cases of this anomaly, as well as the fact that necrotic lesions affect valuable carcass elements make this problem one of great importance for chicken growers and abattoirs and poultry processing plants. In recent years DPM cases have been reported with increasing frequency in the USA, Italy, Greece and Bulgaria in commercial genetic lines. In Poland, a number of DPM cases have been recorded in large populations in flocks of five to seven week old chickens from 0.02% up to 1.9%. Risk factors for the occurrence of DPM on farms have been analysed, and are considered mainly due to intensive wing flapping. Identification of these factors may result in better farm management and constitute the basis for the DPM prevention system. A solution to this problem is not available currently.

With better survival of critically ill patients, ‘de novo’ arising neuromuscular complications like critical illness myopathy or polyneuropathy have been increasingly observed. Prolonged hospitalization not only imposes risks like pneumonia or thrombosis on patients but also represents a real budget threat to modern intensive-care medicine. Clinical symptoms like muscle weakness and weaning failure are common to critical illness myopathy and critical illness polyneuropathy and do not allow for distinction. Specific therapies are not yet available, and the quest for the pathomechanisms has proved more complicated than anticipated. Especially for critical illness myopathy, multiple sites of disturbances to the excitation–contraction coupling cascade are possible causes of muscle weakness. The present review summarizes the epidemiological, clinical and diagnostic features of critical illness myopathy and then focuses on current concepts of the presumed pathomechanisms of critical illness myopathy. Sepsis was shown to be a major cause of critical illness myopathy and special emphasis will be placed on how sepsis and inflammatory mediators influence (i) the membrane excitability at the level of voltage-gated ion channels and (ii) the intracellular protein signalling that results in selective loss of myosin protein content and muscle wasting. For (i), critical illness myopathy represents a new type of acquired channelopathy affecting the inactivation properties of Na+ channels. For (ii), both protein proteolysis and protein build up at the transcriptional level seem to be involved. Findings from different studies are put into a common context to propose a model for cytokine-mediated failure of muscle in severe sepsis. This can open a series of new possible trials to test specific therapeutic strategies in the future.

A Case Is reported of a 59-year-old Caucasian male with oculopharyngeal myopathy and sensorineural hearing loss. He presented with progressive ptosis, sensorineural hearing loss over several years and symptoms of mild dysphagia. Further enquiry into his family history revealed that every male member in his family that lived beyond the age of 60 exhibited identical symptoms. Symptoms of ptosis and dysphagia are consistent with the rare autosomal dominant condition of oculopharyngeal myopathy, believed to be due to mitochondrial disease. The combination of ptosis, dysphagia and sensorineural hearing loss with normal distant muscle group biopsy has not been described before.