A myopathy affecting the pectoralis major muscle of the commercial broiler has emerged creating remarkable economic losses as well as a potential welfare problem of the birds. We here describe the macroscopic and histologic lesions of this myopathy within 10 pectoralis major muscles of 5- to 6-week-old broilers in Finland. Following macroscopic evaluation and palpation of the muscles, a tissue sample of each was fixed in formalin, processed for histology, and histologically evaluated. The muscles that were macroscopically hard, outbulging, pale, and often accompanied with white striping histologically exhibited moderate to severe polyphasic myodegeneration with regeneration as well as a variable amount of interstitial connective tissue accumulation or fibrosis. All affected cases also exhibited perivenular lymphocyte accumulation. The etiology of this myodegenerative lesion remains yet open. Polyphasic myodegeneration is associated with several previously known etiologies, but palpatory hardness focusing on the pectoralis major, together with perivenular lymphocytes, has not been described in relation to them. The results of this study provide the pathological basis for further studies concerning the etiology of the currently described myopathy.

Wooden breast (WB) myopathy of broiler chickens is a myodegenerative disease of an unknown etiology and is macroscopically characterized by a hardened consistency of the pectoralis major muscle. Our aim was to describe the development and morphology of WB over the growth period in broilers. Additionally, the effect of restricted dietary selenium on the occurrence of WB was examined by allocating the birds in 2 dietary groups: restricted and conventional level of selenium. The experiment included 240 male broilers that were euthanized at ages of 10, 18, 24, 35, 38, or 42 days and evaluated for WB based on abnormal hardness of the pectoralis major muscle. The severity and the distribution of the lesion and presence of white striping were recorded. The first WB cases were seen at 18 days; 13/47 birds (28%) were affected and the majority exhibited a mild focal lesion. In subsequent age groups the WB prevalence varied between 48% and 73% and the lesion was usually diffuse and markedly firm. White striping often coexisted with WB. Histological evaluation performed on 111 cases revealed a significant association of myodegeneration and lymphocytic vasculitis with WB. Vasculitis and perivascular cell infiltration were restricted to the veins. Restricted dietary selenium did not affect the occurrence of WB ( P = .44). Our results indicate that WB starts focally and spreads to form a diffuse and more severe lesion.

In wooden breast myopathy (WBM) of broiler chickens, the pectoralis major muscles show abnormally hard consistency and microscopical myodegeneration of unknown aetiology. To date, previous studies have focused primarily on chronic WBM and ultrastructural descriptions of early WBM are lacking. The aim of this study was to elucidate the pathogenesis of WBM by light microscopical morphometry of vessel density and the ultrastructural description of early WBM changes with transmission electron microscopy. The pectoral vessel density was compared between unaffected chickens (n = 14) and two areas of focal WBM in affected chickens (n = 14). The transverse myofibre area per vessel was highest in the unaffected area of muscle from cases of focal WBM, significantly higher (P = 0.01) than in macroscopically unaffected tissue, indicating that relatively decreased blood supply may trigger the development of WBM. The ultrastructural study included unaffected chickens (n = 3), two areas of focal WBM from affected chickens (n = 3) and areas of diffuse WBM from affected chickens (n = 3). The morphologically least affected myofibres within the WBM lesion areas in light microscopy exhibited ultrastructural changes of increased sarcoplasmic reticulum diameter and mitochondrial hyperplasia. Such changes originate typically from osmotic imbalance, for which the most likely aetiologies in WBM include tissue hypoxia or myodegeneration of the surrounding myofibres. The findings suggest that a relative reduction of blood supply in the major pectoral muscle occurs in the early phase of WBM, which may be linked to the ultrastructural changes of osmotic imbalance.

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Summary A case of a neonatal foal with acute colic and respiratory distress is described. The foal presented with signs of acute colic and was treated medically. The foal did not respond to treatment and 2 h after admission the foal began to demonstrate signs of respiratory distress. Thoracic and abdominal radiographs were obtained and a diagnosis of a diaphragmatic hernia was made. Surgical repair of the hernia was recommended but the owner declined and the foal was subjected to euthanasia. Post mortem findings confirmed the diagnosis and revealed that the defect was of congenital origin. Congenital diaphragmatic hernia is an unusual cause of colic in a neonatal foal.

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