Age affected: All ages.
Causes: Genetic; stress and transport; heat stress.
Effects: tremor, rigidity, sudden death, PSE meat, malignant hyperthermia, back muscle wasting.
A complex of conditions associated with an autosomal recessive gene of variable penetrance, the commonest cause of the condition is the substitution of cytosine C (-) for thymidine (T) at position 1843 on the ryr 1 gene on chromosome 6 P11 921. The gene codes for ryanodine, responsible for gating (controlling) the calcium (Ca++) channel in skeletal muscle.
The altered protein stimulates contraction of the muscle and sets in train all the features of the condition. The mutation appears to have arisen once and to have spread to all affected breeds. The ryr 1 gene was previously designated for halothene sensitivity with n for sensitive i.e., affected pigs were Hal nn and normals Hal NN. The homozygote (pure bred) Hal NN and the heterozygote (cross bred) Hal Nn are both resistant to the effects of simple halothane anaesthesia.
Possession of the gene is associated with heavily muscled or lean breeds. A switch of energy utilisation in the muscles of susceptible pigs occurs from aerobic to anaerobic metabolism and prolonged activity follows. An enormous increase in lactate production and an increased production of body heat result. Triggering of the mechanisms can result from stress of movement, some anaesthetic agents and slaughter when anaerobic glycolysis (breakdown of muscle carbohydrate) also develops.
Genetic, the stress phenotype is recessive. The clinical effects depend upon environmental factors.
The underlying muscular reaction causes animals or well-muscled strains to die suddenly form the porcine stress syndrome (PSS), to develop back muscle necrosis, malignant hyperthermia (MH) when exposed to halothane anaesthesia and pale soft, exudative muscle (PSE) at slaughter.
The condition occurs in pigs aged 9 weeks or more and especially in heavy hogs or adults. Early signs of the porcine stress syndrome include muscle and tail tremor which progress to breathing difficulties, blotched red and pale skin, an increase in body temperature to more than 41.5°C followed by collapse, muscle rigidity and death. These changes may occur following anaesthesia with halothane. The condition is more common when the environmental temperature rises about 22°C and especially 28°C and occurs during transport, moving or stressful management procedures, such as weighing.
The time taken between onset and death can be as little as 10 minutes. The halothane susceptible gene is associated with an increase of carcase lean, a slower growth rate and, in sows, 1.16 fewer births and 1.76 fewer weaned pigs per litter than in resistant litters. Heterozygotes are economically superior to either homozygote and the gene has been perpetuated and spread to produce them.
Clinical signs of blanching of the skin, difficulty in breathing and rigidity prior to death suggest PSS in heavily muscled breeds, finishers or adults, in high environmental temperatures and following management stress such as transport. Back muscle necrosis causes pain, difficulty in moving, fever and swollen back muscles on one or both sides. PSS-susceptible pigs can be identified by the polymerase chain reaction (PCR) for the normal and altered genes in blood or tissue. Negative pigs are given an ear tag ‘N 1843’. The halothane test can be used in pigs 9 weeks of age. Affected pigs become rigid, sometimes develop raised rectal temperatures and may die if anaesthesia is continued.
Pigs which have died from PSS are usually in good condition and develop rigor mortis rapidly. There is some oedema and collapse of the lung. Pale, soft exudative muscle (PSE) develops in 60-70% of affected pigs within 15 minutes of death and appears as pale areas contrasting with the deeper red unaffected muscle when the longissiimus dorsi (back) or ham muscles are cut. Muscle pH falls to pH 6.0 or less within 45 minutes of death.
PCR techniques developed for meat use may be used on tissue at post-mortem to confirm the presence of genetic susceptibility. The muscle changes of PSE are seen at slaughter in pigs which have not shown clinical signs in life and may lead to downgrading of affected portions of the carcase.
Pigs which develop malignant hyperthermia under anaesthesia may be treated successfully if the condition is recognised early (for instance, by a rise in end expiratory pCO2) by hyperventilating with oxygen, use of metamizol beta-blockers, bicarbonate and cooling or with Dantrolene at 7 mg/kg. Some muscle damage may occur. In farm animals, treatment is not possible.
Clinically affected animals or those prone to stress should be given adequate ventilation, cooled with water drips or sprayed in hot weather, starved for 12 hours before transport and not transported at environmental temperatures exceeding 22°C (72°F). Tail lifts help reduce transport stress. Any mixing likely to result in fighting should be avoided. Access to sugar solutions in the lairage may prevent PSE. Pentobarbitone anaesthesia should be used in stress-susceptible pigs. Stress can be reduced by the use of azaperone or carazalol prior to movement where allowed. Selection for lean carcases and large hams tends to increase the prevalence of PSS.
Screening for the gene by PCR has allowed its elimination from the some breeds or lines and homozygous stress susceptible sire lines can be used on resistant dam lines to combine the economic advantages, carcase quality and prolificacy of the heterozygote and the occurrence of clinical PSS is now unnecessary.