Myofibrillar Hypoplasia (Splayleg) in Pigs
In splayleg, a condition of neonatal pigs, the hindlimbs are spread apart or extended forward because of weakness of the adductor muscles relative to the abductors. The condition is observed at or soon after birth and can develop in a number of forms:
The most common form of the condition is hindlimb splays; the back limbs splay out sideways and forward, causing the pig great difficulty in standing on its hind end. Many will "dog sit" and shuffle around on their hindquarters, which can lead to considerable skin trauma and secondary infection.
Front limb splays also occur. The hindlimbs work normally; however, the front limbs splay out sideways such that the pig moves around with its chin on the ground. Such pigs have great difficulty nursing, and mortality levels are high.
In the "stars" form, both sets of limbs are splayed out sideways, such that the pig cannot stand and can move about only by crawling or shuffling.
The incidence of splayleg is greater in the Landrace than in other breeds.
Selection for increased litter size indirectly increases the genetic potential for sows to create a uterine environment more likely to produce litters with splayleg pigs.Splayleg in a neonate should be regarded as a trait of the sow, rather than of the individual pig. If a sow repeatedly produces high numbers of piglets with splayleg despite optimal management, removing her from the breeding program may be considered to reduce the genetic contribution to the issue.
Affected pigs are susceptible to overlaying, starvation, and chilling because of poor mobility. Mortality rate may reach 50%.
Genetic influence has been demonstrated. There are notable differences in incidence among litters of different sires and breeds.
Histologically, there is a continuous gradation in myofibrillar content between normal and severely affected muscles. Myofibrils in affected fibers are scant and small in cross-section. No other morphological or histochemical abnormalities have been detected.
Splayleg's etiology remains obscure. Newborn piglets of hybrid stock have been tested for defects of neuromuscular transmission by stimulation electromyography; testing reveals that congenital myofibrillar hypoplasia is not primarily a myasthenia-like syndrome but rather that either excitation-contraction coupling or the contractile mechanism itself is primarily affected.
Splayleg is observed more frequently in males than females and in pigs of lower birth weight. The syndrome also may be produced if glucocorticoids are administered during pregnancy, and stress-sensitivity of heavily muscled parents may be a contributing factor. Glucocorticoids should not be administered late in gestation. However, any cause of stretching of the adductor muscles increases incidence. Stretching can result from slippery or sloping floors, struggling while legs are caught in cracks in the floor, or as the result of damage to nerve pathways from intrauterine viral infections.
Mycotoxins have been suggested to play a role in some cases. The general nutrition of the sow (choline, methionine, and vitamin E levels) may influence incidence; however, benefits of feeding supplements to sows are questionable.
Clinical signs are distinctive. Trauma to the neonate or in utero infections with hemagglutinating encephalitis virus, enteroviruses, other viruses, and postpartum bacterial meningeal infection should be considered as contributing factors. Affected muscles are generally hypoplastic, and small muscle fibers contain few myofibrils, as would be found in muscles of normal fetuses nearing parturition. Frequently affected muscles include the semitendinosus, longissimus dorsi, and triceps.
For affected neonates, dry, nonslippery floors without cracks in which the legs can become trapped, should be provided, especially for the first 2 days. Pigs should be protected from injury by the sow, and adequate suckling should be ensured. In affected piglets, the hindlimbs should be secured together above the hocks with adhesive tape in a loose “figure 8” for 2–4 days. Appropriately treated pigs usually recover within a week, although few recover if the forelimbs are also affected.
Highly susceptible bloodlines should be eliminated.
Malignant Hyperthermia (Porcine Stress Syndrome)
Malignant hyperthermia is an inherited disorder, characterized by a stressful event causing a sudden increase in myoplasmic calcium concentrations, leading to progressive, sustained myofibrillar contraction, muscle rigidity, hypermetabolism, tachycardia, metabolic acidosis, and a gradual increase in body temperature. Hyperthermia is often so severe that the smell of cooked porcine flesh can be detected externally.
On necropsy, muscles are soft, pale, and exudative, particularly the muscles of the back, loin, thigh, and shoulder. Heavily muscled pigs seem to be most susceptible, and triggering events can include transport, fighting, handling, or anesthetic episodes.
A single point mutation in the skeletal muscle ryanodine receptor (ryr1) at locus HAL-1843 has been identified as the cause of malignant hyperthermia in most domestic pig breeds. A DNA test of peripheral blood has been developed to aid detection; however, increasing evidence suggests that multiple gene defects are involved.
