Difference between revisions of "Porcine Stress Syndrome"

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(Created page with "*'''Malignant hyperthermia''' *Pigs, dogs, humans *Possibly a cellular defect resulting in high intacellular calcium ion concentration **-> Activates myofibrillar ATPase -> rapid...")
 
 
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*'''Malignant hyperthermia'''
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{{OpenPagesTop}}
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*Pigs, dogs, humans
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{{Podcasts
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*Possibly a cellular defect resulting in high intacellular calcium ion concentration
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|link = http://media.bloomsburymediacloud.org/podcasts/wikivet-english/porcine-stress-syndrome
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**-> Activates myofibrillar ATPase -> rapid intracellular glycolysis -> increase in body heat -> denature protein -> cell death -> leakage of cellular content -> oedema
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}}
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*Grossly:
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Also Known As: '''''PSS — Malignant Hyperthermia — MH — Back Muscle Necrosis — Fulminant Hyperthermia Stress Syndrome — Pale Soft Exudative Pork/Musculature — PSE — Hyperthermia Syndrome — Transport Myopathy'''''
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**Muscles are pale, soft and exudative
 
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*Histologically:
 
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**Segmental hypercontraction
 
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**Monophasic, multifocal [[Muscles Degenerative - Pathology#Necrosis|segmental necrosis]]
 
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*Inherited
 
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*Triggered by halothane anaesthesia, stress of handling, transportation or slaughter
 
  
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==Introduction==
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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.'''
  
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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.
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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>
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PSS appears as three different syndromes:
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:'''Sudden death''', usually during transport
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:'''Pale, soft and exudative (PSE) meat''' in which the fall in muscle pH following slaughter causes denaturation of muscular proteins and myofibre shrinkage. PSS mainly affects the Type IIB muscle fibres. The meat is of poor quality and is rejected in the abattoir.
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:'''Halothane sensitivity''': manifested as malignant hyperthermia during anaesthesia
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PSS is not zoonotic.
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==Distribution==
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'''Worldwide'''. Prevalence is dictated by emphasis on quality or quantity of meat produced and cultural/traditional differences in pig selection and production.
 +
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It is '''very rare in the developed world''' due to selective breeding.
 +
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==Signalment==
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The genetic trait is most commonly manifested in '''Landrace, Poland-China, Pietrain''' and associated crossbreeds. Historically, because affected pigs often had more developed musculature and therefore larger carcass weights, the genes translating PSS were often favoured when selecting breeding stock. This is now not standard practice in the developed world.
 +
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==Clinical Signs==
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Pigs may be '''found dead''', particularly after times of stress, e.g. transport.
 +
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Before death, affected pigs will have been '''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.
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'''Haemoglobinuria/myoglobinura''' is a common consequence of muscle damage/lysis.
 +
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Early signs of disease may be '''tail tremors''' and fine fasciculations.
 +
 +
'''PSE''' will appear as inadequate setting of the carcass after slaughter and significant economic losses from rejected meat.
 +
 +
'''Malignant hyperthermia''' will occur during anaesthesia under halothane, and will appear as significant muscle contractions, pyrexia and muscle rigidity.
 +
 +
==Diagnosis==
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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.
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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.
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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.
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==Treatment==
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If only early signs are present, '''removal of the animal from the impending stress''' and allowing rest may prevent the episode without further intervention.
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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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'''Dantrolene sodium''' is the most effective method of preventing symptoms from halothane exposure and also reversing them if they occur.
 +
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==Control==
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'''Stress at slaughter''' is critical as PSS prone pigs will be very vulnerable during transport and progress through the slaughterhouse.
 +
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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.
 +
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Genetic breeding has largely eliminated the condition from pigs in developed countries.
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{{Learning
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|flashcards = [[Porcine Stress Syndrome Flashcards]]
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}}
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==References==
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<references/>
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{{CABI source
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|datasheet = [http://www.cabi.org/ahpc/?compid=3&dsid=68600&loadmodule=datasheet&page=2144&site=160 porcine stress syndrome]
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|date =3 July 2011
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}}
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<br><br>
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{{Mandy Nevel
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|date = 09 September 2011
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}}
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{{OpenPages}}
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[[Category:CABI Expert Review Completed]][[Category:CABI AHPC Pages]] [[Category:Musculoskeletal Diseases - Pig]]
 
[[Category:Muscles - Developmental Pathology]]
 
[[Category:Muscles - Developmental Pathology]]

Latest revision as of 14:45, 17 August 2012


WVpodcasts.png
Listen to Page Podcast or download via iTunes

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]

PSS appears as three different syndromes:

Sudden death, usually during transport
Pale, soft and exudative (PSE) meat in which the fall in muscle pH following slaughter causes denaturation of muscular proteins and myofibre shrinkage. PSS mainly affects the Type IIB muscle fibres. The meat is of poor quality and is rejected in the abattoir.
Halothane sensitivity: manifested as malignant hyperthermia during anaesthesia

PSS is not zoonotic.

Distribution

Worldwide. Prevalence is dictated by emphasis on quality or quantity of meat produced and cultural/traditional differences in pig selection and production.

It is very rare in the developed world due to selective breeding.

Signalment

The genetic trait is most commonly manifested in Landrace, Poland-China, Pietrain and associated crossbreeds. Historically, because affected pigs often had more developed musculature and therefore larger carcass weights, the genes translating PSS were often favoured when selecting breeding stock. This is now not standard practice in the developed world.

Clinical Signs

Pigs may be found dead, particularly after times of stress, e.g. transport.

Before death, affected pigs will have been 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.

Early signs of disease may be tail tremors and fine fasciculations.

PSE will appear as inadequate setting of the carcass after slaughter and significant economic losses from rejected meat.

Malignant hyperthermia will occur during anaesthesia under halothane, and will appear as significant muscle contractions, pyrexia and muscle rigidity.

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.

Genetic breeding has largely eliminated the condition from pigs in developed countries.


Porcine Stress Syndrome Learning Resources
FlashcardsFlashcards logo.png
Flashcards
Test your knowledge using flashcard type questions 		Porcine Stress Syndrome Flashcards


References

  1. ↑ Gronert, G. A (1986) Malignant hyperthermia. In: Engle, B., Banker, B. eds. Myology. New York, USA: McGraw Hill, 1763-1783
  2. ↑ 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


CABIlogo

This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project.

The datasheet was accessed on 3 July 2011.

This article has been expert reviewed by Dr Mandy Nevel

Date reviewed: 09 September 2011



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