Diseases: Porcine stress syndrome

Porcine stress syndrome occurs worldwide in pigs (swine) of all ages. The effects of porcine stress syndrome are tremors, rigidity, sudden death, PSE meat, malignant hyperthermia, back muscle wasting.

Causes of Porcine stress syndrome

A complex of conditions associated with an autosomal recessive gene of variable penetrance the 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 once physicians and to have spread to all affected breeds.
 
The ryr 1 gene was previously designated for halothane sensitivity with 'n' for sensitive ie, affected pigs were normals Hal NN and Hal nn. The homozygous (pure bred) Hal NN and the heterozygous (cross bred) Hal Nn are both resistant to the effects of simple halothane anesthesia.
 
Possession of the gene is associated with heavily muscled or lean breeds. A switch of energy utilization 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 results. Triggering of the mechanisms can result from stress or movement, some anesthetic agents and slaughter when anaerobic glycolysis (breakdown of muscle carbohydrate) also develops.

Effects of Porcine stress syndrome

The underlying causes muscular reaction well muscled animals or strains to which suddenly from the porcine stress syndrome (PSS), to develop back muscle necrosis, malignant hyperthermia (MH) when exposed to halothane anesthesia 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 tremors and tail 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 anesthesia with halothane. The more common when environmental conditions if the temperature rises above 22 ° C and 28 ° C and occurs especially during transportation, moving or stressful management procedures, such as weighing. The time between onset and death duties can be as little as 10 minutes.
 
The halothane susceptible gene is associated with an increase of carcass lean, a slower growth rate and, in sows, 1.16 and 1.76 fewer births fewer pigs weaned per litter than in resistant litters. Heterozygotes are superior to either homozygous Economically and the gene has been perpetuated and spread to produce them.

Diagnosis of Porcine stress syndrome

  • Clinical signs of blanching of the skin, difficulty in breathing and rigidity suggest PSS prior to death in heavily muscled breeds, finishers or adults, in high temperatures and following environmental stress such as transportation management.
  • 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 raised rectal temperatures and may develop if the anesthesia was continued.
  • Pigs which have died from PSS rapidly develop rigor mortis. There is some edema 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 unaffected red 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 use meat may be used on tissue at post-mortem to confirm the presence of genetic susceptibility.

Treatment & Control of Porcine stress syndrome

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).
 
Reduce transport stress
  • 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.
  • 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.