(Spraddleleg, Myofibrillar hypoplasia)
In splayleg, a condition of neonatal pigs, the hindlegs are spread apart or extended forward because of weakness of the adductor muscles relative to the abductors. The condition is seen at or soon after birth and can present in a number of forms. 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 most common form of the condition is hindleg splays; the back legs 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 backsides. This can lead to considerable skin trauma and secondary infection. Front leg splays also occur. The hindlimbs work normally, but the front legs splay out sideways such that the pig moves around with its chin on the ground. Such pigs have great difficulty sucking, and mortality levels are high. The incidence of splayleg is greater in the Landrace than in other breeds.
Histologically, there is a continuous gradation in myofibrillar content between normal and severely affected muscles. Myofibrils in affected fibers are scanty and small in cross section. No other morphologic or histochemical abnormalities have been detected. The cause of the condition remains obscure. Newborn piglets of hybrid stock tested for defects of neuromuscular transmission by stimulation electromyography reveal that congenital myofibrillar hypoplasia is not primarily a myasthenia-like syndrome, but that either excitation-contraction coupling or the contractile mechanism itself is primarily affected.
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 and should be treated as a trait of the sow, rather than of the individual pig. Affected pigs are susceptible to overlaying, starvation, and chilling because of poor mobility. Mortality may reach 50%. Genetic influence has been demonstrated. There are significant differences in the incidence among litters of different sires and breeds. It is seen 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 it appears possible that stress-sensitivity of the heavily muscled parent(s) may be a contributing factor. However, any cause of stretching of the adductor muscles increases the 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 the incidence, but benefits from feeding supplements to sows is questionable.
The clinical signs are distinctive. In utero infections with hemagglutinating encephalitis virus, enteroviruses, other viruses, and postpartum bacterial meningeal infection and trauma should be considered. The affected muscles are generally hypoplastic, and the 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.
Dry, nonslippery floors should be provided, with no cracks in which the legs can become trapped, 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 hindlegs should be secured together above the hocks with a loose “figure 8” of adhesive tape for 2–4 days. Appropriately treated pigs usually recover within a week, although few recover if the front legs are also affected. Glucocorticoids should not be administered late in gestation. Highly susceptible blood lines should be eliminated.
Last full review/revision December 2013 by Russell R. Hanson, DVM, DACVS, DACVECC