Splay leg

Occurrence: Worldwide.
Age affected: Newborn.
Causes: Genetic; mycotoxins.
Effects: Muscle weakness and difficulty standing.

Causes

This important (up to 1.5 percent) congenital condition can have a genetic, nutritional, toxic or infectious cause. The commonest genetic mechanism is an additive polygenic trait with no clear evidence of dominance, especially in Piétrain, Landrace and Welsh pigs. It appears to occur twice as frequently in males and a maternal effect has been identified, apparently mediated through larger litters which have more affected piglets and a shorter ( by 0.9 day) gestation period.

Weakness of the legs causing the splaying is due to the presence of too few Type 1 myofibrils in the fibres of muscles of the foreleg, lumbar group and, most importantly, the hind leg. The condition appears to represent a failure of muscle fibres to mature in sufficient numbers to provide adequate support at birth. The semitendinosus muscle is most severely affected in the hind limb.

The myofibrillar changes are associated with poor myelin (sheathing) development of the nerves supplying the affected muscles. Splay leg is more common in pigs born before 113 days of gestation, and infection, nutrition and early induction of farrowing using prostaglandins may all increase the numbers with splay leg. Zearalenone ingestion by the sow can cause splay leg in the litter. The condition usually resolves within 1-2 weeks of birth.

Mode of transmission

Where there is a genetic component to the condition, heredity affects its transmission. Where infection with viruses such as PRRS are involved, the mode of transmission is that of the virus. Nutritional and management factors (including mycotoxicosis) are dependent to a large extent on the management system and will tend to recur when these factors continue.

Clinical signs

Affected piglets are unable to stand, and are often found with a hind limb extended forward along the axis of the body with the opposite leg abducted (at right angles to the body). They can move slowly by dragging themselves along by the front legs. If not killed by crushing and if able to feed, affected piglets become normal within 10 days of birth. Affected piglets may develop sores on the perineum (hind quarters) and erosion of the base of the tail. Up to 50% of affected piglets may die if not assisted. They are particularly prone to chilling. The condition becomes apparent 2-3 hours after birth and 2-3 piglets may be affected in each litter and are often the smaller members of the litter.

The identification of splay leg is normally a matter of inspection of the litter when affected animals can be seen. The identification of the condition post-mortem is important as splay leg is a major contributor to pre-weaning mortality and must be identified. Affected piglets usually have sores on the hind quarters and erosion of the base of the tail and are in poor condition with empty stomachs if unable to feed. The actual cause of death may be hypoglycaemia or crushing.

The cause of the splay leg is often genetic, but the possibility that it is associated with zearalenone toxicity should be investigated. If this is the case, it is likely that there will be vulval enlargement and a prominent udder in newborn piglets. Confirmation is by analysis of the feed. Where PRRS infection during pregnancy has increased the numbers of piglets with splay leg, antibody is often present in sow sera and in stillborn piglets. Injudicious induction of farrowing with prostaglandin can be identified from the service, treatment and farrowing records.

Postmortem lesions

Affected piglets are often undersize and have external evidence for having been sliding on a hard surface. This includes erosion of the skin at the base of the tail, exposing the muscle and wear to the skin around the anus. The stomach is usually empty and the carcass is thin if death has been from hypoglycaemia alone. Injuries from crushing are often present, and splayleg is a major predisposing factor in this cause of death. Microscopical examination of the affected muscles may reveal low numbers of myofibrils and poor insulation of the supplying nerves. 

Treatment and prevention

Affected piglets should be kept warm and helped to take colostrum. They may be reared artificially for 2-3 days and returned to the sow. The use of physostigmine has been suggested as an aid to recovery in piglets 12 hours or more of age. Repeated massage of the hind limbs improves survival dramatically, but the commonest aid to survival is probably the practice of taping the hind limbs together or the use of elastic bands.

This improves piglets’ ability to stand and move around until the legs strengthen. Non-slip floors may also improve footing and improve viability. The effects of zearalenone toxicity can be reduced by removing he contaminated sow feed, but this takes up to 14 days to reduce the levels of zearalenone in milk and thus fostering or artificial feeding may be required to reduce mortality and air recovery.

Crossing Landrace or Welsh sows with Large White boars reduces the incidence. Farrowing before day 113 should be avoided and management of PRRS helps ensure that intrauterine infection does not occur.