Difference between revisions of "Porcine Stress Syndrome"
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| − | Also Known As | + | Also Known As: '''''PSS — Malignant Hyperthermia — MH — Back Muscle Necrosis — Fulminant Hyperthermia Stress Syndrome — Pale Soft Exudative Pork/Musculature — PSE — Hyperthermia Syndrome — Transport Myopathy''''' |
==Introduction== | ==Introduction== | ||
Porcine stress syndrome (PSS) is a '''congenital, autosomal recessive pharmacogenetic disorder''' which affects pigs, dogs, cats, horses and humans. It is caused by a fundamental '''intolerance of stress''' due to a '''defective ryanodine receptor''' which affects '''closure of calcium channels in the sarcoplasmic reticulum''' and causing a sudden, sustained rise in '''intracellular calcium and consequent muscle contracture and upregulation of metabolism.''' | Porcine stress syndrome (PSS) is a '''congenital, autosomal recessive pharmacogenetic disorder''' which affects pigs, dogs, cats, horses and humans. It is caused by a fundamental '''intolerance of stress''' due to a '''defective ryanodine receptor''' which affects '''closure of calcium channels in the sarcoplasmic reticulum''' and causing a sudden, sustained rise in '''intracellular calcium and consequent muscle contracture and upregulation of metabolism.''' | ||
| − | It can also be induced by exposure to certain anaesthetics, most markedly '''halothane''' | + | It can also be induced by exposure to certain anaesthetics, most markedly '''halothane''' (which can also generate the disease in people), intense exercise, coitus, parturition and transport. |
| − | PSS leads to an increase in metabolism and intense production of '''heat, carbon dioxide and lactic acid and contraction of skeletal musculature'''.<ref> Gronert, G. A (1986) '''Malignant hyperthermia'''. In: Engle, B., Banker, B. eds. '''Myology'''. ''New York, USA: McGraw Hill'', 1763-1783</ref> The fall in muscle pH following slaughter causes '''denaturation of muscular proteins, myofibre shrinkage and the PSE appearance''' of the pork. PSS mainly affects the Type IIB muscle fibres. | + | PSS leads to an increase in metabolism and intense production of '''heat, carbon dioxide and lactic acid and contraction of skeletal musculature'''.<ref> Gronert, G. A (1986) '''Malignant hyperthermia'''. In: Engle, B., Banker, B. eds. '''Myology'''. ''New York, USA: McGraw Hill'', 1763-1783</ref> The fall in muscle pH following slaughter causes '''denaturation of muscular proteins, myofibre shrinkage and the pale, soft and exudative (PSE) appearance''' of the pork. PSS mainly affects the Type IIB muscle fibres. |
PSS is not zoonotic. Although PSS meat is of poor quality and poor aesthetic appeal, it is not a hazard on its own. | PSS is not zoonotic. Although PSS meat is of poor quality and poor aesthetic appeal, it is not a hazard on its own. | ||
==Distribution== | ==Distribution== | ||
| − | '''Worldwide'''. Prevalence is | + | '''Worldwide'''. Prevalence is dictated by emphasis on quality or quantity of meat produced and cultural/traditional differences in pig selection and production. |
==Signalment== | ==Signalment== | ||
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==Clinical Signs== | ==Clinical Signs== | ||
| − | Affected pigs undergoing an episode of PSS will be '''hyperthermic, panting, sweating excessively, markedly tachycardic with possible arrhythmias, trembling, hypertonic''', stiff or paretic, lame and sometimes '''cyanotic'''. Muscle atrophy may be evident, usually of large muscle groups around the back and hindlimbs. The skin often becomes '''blotchy, erythematous and cyanotic. Haemoglobinuria/myoglobinura''' is a common consequence of muscle damage/lysis. | + | Affected pigs undergoing an episode of PSS will be '''hyperthermic, panting, sweating excessively, markedly tachycardic with possible arrhythmias, trembling, hypertonic''', stiff or paretic, lame and sometimes '''cyanotic'''. Muscle atrophy may be evident, usually of large muscle groups around the back and hindlimbs. The skin often becomes '''blotchy, erythematous and cyanotic. |
| + | |||
| + | Haemoglobinuria/myoglobinura''' is a common consequence of muscle damage/lysis. | ||
| + | |||
Pigs may be '''found dead''', particularly after times of stress, e.g. transport. | Pigs may be '''found dead''', particularly after times of stress, e.g. transport. | ||
Early signs of disease may be '''tail tremors''' and fine fasciculations. | Early signs of disease may be '''tail tremors''' and fine fasciculations. | ||
| − | PSS pigs will '''develop rigor mortis very rapidly''' after slaughter and significant economic losses from rejected meat. | + | PSS pigs will '''develop rigor mortis very rapidly''' after slaughter and there will be significant economic losses from rejected meat. |
==Diagnosis== | ==Diagnosis== | ||
The traditional method of diagnosis is the '''halothane challenge'''. Susceptible pigs become rigid within 5 minutes of exposure to the agent. It will however only detect homozygous animals. | The traditional method of diagnosis is the '''halothane challenge'''. Susceptible pigs become rigid within 5 minutes of exposure to the agent. It will however only detect homozygous animals. | ||
| − | A '''DNA PCR''' is available to accurately detect '''heterozygous''' (carrier) pigs.<ref> Rempel, W. E., Lu, M. Y., El-Kandelgy, S., Kennedy, C. F. H., Irvin, L. R., Mickelson, J. R., Louis, C. F (1993) '''Relative accuracy of the halothane challenge test and a molecular genetic test in detecting the gene for porcine stress syndrome.''' J Animal Science, 71(6):1395-1399; 16</ref> This can be performed on any material containing DNA including hairs. A complete elimination of the recessive gene is thus possible, but there remains an interest in breeding heterozygous animals for the production of pigs with superior carcasses. | + | A '''DNA PCR''' is available to accurately detect '''heterozygous''' (carrier) pigs.<ref> Rempel, W. E., Lu, M. Y., El-Kandelgy, S., Kennedy, C. F. H., Irvin, L. R., Mickelson, J. R., Louis, C. F (1993) '''Relative accuracy of the halothane challenge test and a molecular genetic test in detecting the gene for porcine stress syndrome.''' ''J Animal Science'', 71(6):1395-1399; 16</ref> This can be performed on any material containing DNA including hairs. A complete elimination of the recessive gene is thus possible, but there remains an interest in breeding heterozygous animals for the production of pigs with superior carcasses. |
A pig that has died of PSS may have '''congested viscera on post-mortem''' and have frothy bronchiolar contents due to terminal pulmonary oedema. The most striking feature is the '''rapid onset of rigor mortis''', as mentioned above. Most pigs develop pale, watery musculature within '''15-30 minutes''' of death. No microscopic lesions or abnormalities are present. | A pig that has died of PSS may have '''congested viscera on post-mortem''' and have frothy bronchiolar contents due to terminal pulmonary oedema. The most striking feature is the '''rapid onset of rigor mortis''', as mentioned above. Most pigs develop pale, watery musculature within '''15-30 minutes''' of death. No microscopic lesions or abnormalities are present. | ||
==Treatment== | ==Treatment== | ||
| − | If only early signs are present, '''removal of the animal | + | If only early signs are present, '''removal of the animal from the impending stress''' and allowing rest may prevent the episode without further intervention. |
If rigidity and blotchiness has begun, the pig should be '''sedated with a fast acting agent, and given hydrocortisone and bicarbonate''' to alleviate the lactic acidosis. | If rigidity and blotchiness has begun, the pig should be '''sedated with a fast acting agent, and given hydrocortisone and bicarbonate''' to alleviate the lactic acidosis. | ||
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Animal Health & Production Compendium, '''Porcine Stress Syndrome datasheet''', accessed 03/07/2011 @ http://www.cabi.org/ahpc/ | Animal Health & Production Compendium, '''Porcine Stress Syndrome datasheet''', accessed 03/07/2011 @ http://www.cabi.org/ahpc/ | ||
| − | [[Category: | + | |
| + | {{review}} | ||
| + | [[Category:CABI Expert Review]] [[Category:Musculoskeletal Diseases - Pig]] | ||
[[Category:Muscles - Developmental Pathology]] | [[Category:Muscles - Developmental Pathology]] | ||
Revision as of 22:25, 6 July 2011
Also Known As: PSS — Malignant Hyperthermia — MH — Back Muscle Necrosis — Fulminant Hyperthermia Stress Syndrome — Pale Soft Exudative Pork/Musculature — PSE — Hyperthermia Syndrome — Transport Myopathy
Introduction
Porcine stress syndrome (PSS) is a congenital, autosomal recessive pharmacogenetic disorder which affects pigs, dogs, cats, horses and humans. It is caused by a fundamental intolerance of stress due to a defective ryanodine receptor which affects closure of calcium channels in the sarcoplasmic reticulum and causing a sudden, sustained rise in intracellular calcium and consequent muscle contracture and upregulation of metabolism.
It can also be induced by exposure to certain anaesthetics, most markedly halothane (which can also generate the disease in people), intense exercise, coitus, parturition and transport.
PSS leads to an increase in metabolism and intense production of heat, carbon dioxide and lactic acid and contraction of skeletal musculature.[1] The fall in muscle pH following slaughter causes denaturation of muscular proteins, myofibre shrinkage and the pale, soft and exudative (PSE) appearance of the pork. PSS mainly affects the Type IIB muscle fibres.
PSS is not zoonotic. Although PSS meat is of poor quality and poor aesthetic appeal, it is not a hazard on its own.
Distribution
Worldwide. Prevalence is dictated by emphasis on quality or quantity of meat produced and cultural/traditional differences in pig selection and production.
Signalment
The genetic trait is most commonly manifested in Landrace, Poland-China, Pietrain and associated crossbreeds. Because affected pigs often have more developed musculature and therefore larger carcass weights, the genes translating PSS are often favoured when selecting breeding stock.
Clinical Signs
Affected pigs undergoing an episode of PSS will be hyperthermic, panting, sweating excessively, markedly tachycardic with possible arrhythmias, trembling, hypertonic, stiff or paretic, lame and sometimes cyanotic. Muscle atrophy may be evident, usually of large muscle groups around the back and hindlimbs. The skin often becomes blotchy, erythematous and cyanotic.
Haemoglobinuria/myoglobinura is a common consequence of muscle damage/lysis.
Pigs may be found dead, particularly after times of stress, e.g. transport.
Early signs of disease may be tail tremors and fine fasciculations.
PSS pigs will develop rigor mortis very rapidly after slaughter and there will be significant economic losses from rejected meat.
Diagnosis
The traditional method of diagnosis is the halothane challenge. Susceptible pigs become rigid within 5 minutes of exposure to the agent. It will however only detect homozygous animals.
A DNA PCR is available to accurately detect heterozygous (carrier) pigs.[2] This can be performed on any material containing DNA including hairs. A complete elimination of the recessive gene is thus possible, but there remains an interest in breeding heterozygous animals for the production of pigs with superior carcasses.
A pig that has died of PSS may have congested viscera on post-mortem and have frothy bronchiolar contents due to terminal pulmonary oedema. The most striking feature is the rapid onset of rigor mortis, as mentioned above. Most pigs develop pale, watery musculature within 15-30 minutes of death. No microscopic lesions or abnormalities are present.
Treatment
If only early signs are present, removal of the animal from the impending stress and allowing rest may prevent the episode without further intervention.
If rigidity and blotchiness has begun, the pig should be sedated with a fast acting agent, and given hydrocortisone and bicarbonate to alleviate the lactic acidosis.
Dantrolene sodium is the most effective method of preventing symptoms from halothane exposure and also reversing them if they occur.
Control
Stress at slaughter is critical as PSS prone pigs will be very vulnerable during transport and progress through the slaughterhouse.
Testing breeding stock or suspect animals and eliminating them from breeding stock is ideal, but often poorly accepted due to the favourable characteristics of PSS animals.
| Porcine Stress Syndrome Learning Resources | |
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Porcine Stress Syndrome Flashcards |
References
- ↑ Gronert, G. A (1986) Malignant hyperthermia. In: Engle, B., Banker, B. eds. Myology. New York, USA: McGraw Hill, 1763-1783
- ↑ Rempel, W. E., Lu, M. Y., El-Kandelgy, S., Kennedy, C. F. H., Irvin, L. R., Mickelson, J. R., Louis, C. F (1993) Relative accuracy of the halothane challenge test and a molecular genetic test in detecting the gene for porcine stress syndrome. J Animal Science, 71(6):1395-1399; 16
Animal Health & Production Compendium, Porcine Stress Syndrome datasheet, accessed 03/07/2011 @ http://www.cabi.org/ahpc/
 |
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