Exertional myopathy results from overly strenuous muscular exercise and can be precipitated by preexisting conditions such as selenium deficiency. Inadequate energy metabolism and/or mechanical stresses occurring during contraction are thought to be the cause of myofiber degeneration.
Deep pectoral myopathy and capture myopathy are the main examples of exertional myopathy in birds. Leg muscle myopathy can occur after transport of poultry.
Exertional myopathy lesions can be monophasic (resulting from a single event—eg, transport, capture, or restraint myopathy) or polyphasic (resulting from repeated or ongoing events).
Early gross lesions of exertional myopathy include muscle pallor with edema or bloodstained transudate. There is swelling, degeneration, necrosis, and mineralization of muscle fibers, with edema, hemorrhage, and infiltration of heterophils and macrophages.
Deep Pectoral Myopathy in Poultry
Deep pectoral myopathy (also known as degenerative myopathy or green muscle disease) is characterized by degeneration, necrosis, and, later, fibrosis of the deep pectoral (supracoracoideus) muscle in heavy meat birds (chickens, turkeys); see deep pectoral myopathy images.
A: Courtesy of Dr. T. A. Abdul-Aziz. B: Courtesy of Dr. Jean Sander.
Deep pectoral myopathy develops secondary to excessive muscle activity. The function of the deep pectoral muscle is to elevate the wing. The pectoral muscles are well developed in modern meat birds, but the muscles are seldom used. Prolonged episodes of wing flapping (eg, during handling, when a lame bird uses its wings to assist ambulation, or when a bird is placed on its back) lead to deep pectoral muscle injury and swelling.
Because of the tight surrounding fascia, the swollen muscle cannot expand, and the blood vessels supplying the muscle collapse as a result. The decreased or absent blood perfusion leads to ischemia, tissue hypoxia, and muscle necrosis (ie, compartment syndrome).
The lesion can be produced artificially by stimulating the deep pectoral muscle to contract and, before exercise, can be prevented by surgically opening the fascial sheath covering the muscle.
Pectoral myopathy can be unilateral or bilateral, with the central one-third to two-thirds of the muscle most prominently affected.
Early after the injury, the involved muscle is pale, swollen, and edematous. Later, it becomes dry, green colored, and sharply demarcated from adjacent, viable muscle.
Eventually, the necrotic muscle becomes enclosed in a thick, fibrous capsule (see chronic deep pectoral myopathy image).
The defect can be identified by a palpable flattening or depression of the breast over affected muscles, or by transillumination of carcasses at slaughter.
Courtesy of Dr. H. J. Barnes.
Flock prevalence of deep pectoral myopathy is usually low (< 1%) (1); however, prevalence as high as 25% has been reported. Few birds develop the disease before 24 weeks of age. Deep pectoral myopathy occurs frequently in turkey breeder hens during artificial insemination.
Deep pectoral myopathy is usually subclinical, and major loss is from downgrading or condemnation at processing. When birds are marketed as whole carcasses, the disease is not easy to detect at processing.
Incidence of deep pectoral myopathy can be decreased by careful handling of susceptible birds to prevent excessive wing flapping and, as a long-term method, by selective breeding, because the condition has a genetic component.
Supplementing rations with selenium, vitamin E, or methionine has not been found to influence the incidence of deep pectoral myopathy.
Capture Myopathy in Poultry
Capture myopathy (exertional rhabdomyolysis) occurs mainly in zoo and wild birds and is rare in poultry. Long-legged wading birds are particularly susceptible.
Capture myopathy results from exertion, struggle, or stress occurring during capture, handling, immobilization, or transport. Hyperthermia and metabolic acidosis due to anaerobic glycolysis are important factors contributing to the pathogenesis of capture myopathy.
Affected birds are often unable or do not want to stand. Movements can be stiff, and muscles can be swollen or firm. Limb injuries due to trauma while struggling to move might be present. Sudden death from cardiac failure can also occur.
Pale skeletal muscle (especially muscle from the legs) or sometimes cardiac muscle can be observed grossly with capture myopathy. However, no gross lesions are present in peracute cases. Ischemic and myoglobinuric nephrosis can be present in birds that survive for a few days.
The prognosis of birds showing clinical signs of capture myopathy is usually poor.
Treatment of single, valuable birds can be attempted and might be successful. Such treatment can consist of a combination of corticosteroids, vitamin E, selenium, parenteral fluids, and forced feeding in conjunction with physiotherapy.
Pearls & Pitfalls
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Prevention of capture myopathy is paramount. Well-planned and well-executed capture and restraint methods that minimize pursuit time, struggling, noise, and visual stimulation are key. Sedation or anesthesia can be useful.
Transport Myopathy of Turkeys
Transport myopathy (leg edema syndrome) affects primarily heavy toms; however, it can also develop in hens. Transport myopathy is associated with the following factors:
increased body size and weight
increased transport time to processing plants
extremes in ambient temperature
valgus leg deformities
Clinical signs are often not reported, because this condition develops during transport to the slaughterhouse. Lameness might be apparent in some birds.
The pathogenesis of transport myopathy is unknown; however, it is presumed to be similar to that of other types of exertional myopathy. Often, only one leg is affected.
With transport myopathy, there is no evidence of external trauma. Skin over edematous subcutaneous tissue is pale, feather follicles are less visible, and the skin slips easily over underlying muscle when moved (see gross lesions image). Occasionally, there is crepitation due to the presence of edema and gas in the subcutis.
Images courtesy of Dr. H. J. Barnes.
Areas affected by transport myopathy are dark when the edematous areas contain blood. Typically, when lesions are cut, the edematous subcutis is a few to several millimeters thick and is amber, occasionally green, or, rarely, red.
Purulent exudate is absent, thus distinguishing transport myopathy from cellulitis.
If hemorrhage is present, the adductor muscles usually are torn.
Removal of affected legs at processing results in carcass downgrading.
On microscopic examination, acute multifocal muscle necrosis is evident (see photomicrograph), primarily in the adductor muscles.
Subacute or chronic lesions, if present, suggest earlier episodes of myopathy that occurred on the farm.
Serum creatinine kinase activity increases sharply between farm and processing.
Courtesy of Dr. H. J. Barnes.
Selection programs designed to improve leg strength and conformation in poultry, as well as improvements in handling and transportation conditions, have decreased the frequency of transport myopathy.
Key Points
Deep pectoral myopathy is caused by episodes of prolonged wing flapping in broilers and turkeys (eg, in reaction to mishandling or by a lame bird using its wings to assist ambulation).
Capture myopathy results from exertion or struggle during capture, handling, or transport.
Leg muscle myopathy occurs after transport of poultry, especially male turkeys. It is associated with increased body size and weight, as well as increased transport time to the processing plant.
Careful handling and transportation can decrease the incidence of exertional myopathies.
For More Information
Klasing KC, Korver DR. Nutritional diseases. In: Swayne DE, ed. Boulianne M, Logue CM, McDougald LR, Nair V, Suarez DL, associate eds. Diseases of Poultry. 14th ed. Wiley Blackwell; 2020:1255-1385.
References
Bianchi M, Petracci M, Franchini A, Cavani C. The occurrence of deep pectoral myopathy in roaster chickens. Poult Sci. 2006;85(10):1843-1846. doi:10.1093/ps/85.10.1843
