Porcine Stress Syndrome Gene and Pork Production
Agdex#: 440/11
Publication Date: 06/04
Order#: 04-053
Last Reviewed: 06/04
History:
Written by: Wayne Du - Pork Quality Assurance Program Lead/OMAFRA
Introduction
The porcine stress syndrome (PSS) gene is found to cause malignant hyperthermia (heat shock) when pigs are exposed to environmental stressors. This gene is commonly referred to as the halothane gene, because the PSS condition can be triggered by exposing pigs to the anesthetic, halothane gas. Researchers established the presence of the PSS condition in 1968 when they observed that physically stressed, susceptible pigs would collapse in a shock-like state and die. Pigs carrying the PSS gene are more prone to producing pale, soft and exudative (PSE) pork, which is not only unattractive to consumers because of its unappealing greyish, soft and watery appearance, but is also less suitable for further processing because of its low water-holding capacity.
Inheritance
The PSS condition is an inherited disorder in swine. Inheritance of the PSS gene is at a single locus and there are two alleles, one dominant (N) and one recessive (n). There are three possible genotypes: homozygous recessive (nn), heterozygous or carriers (Nn) and homozygous normal (NN). Swine inheriting the n allele are more sensitive to stress. Pigs that are homozygous recessive (nn) are called PSS homozygous. PSS homozygous pigs are more prone to developing PSE pork after slaughter than PSS carriers (Nn), which are more prone than normal pigs (NN).
Each parent provides one allele to his or her progeny. Possible mating combinations and resulting genotypes are listed in Table 1.
Understanding the impact of carriers (Nn pigs) in breeding is key to reducing the incidence of PSE pork. For example, if a nn boar is mated to a NN sow, 100% of the offspring will be PSS carriers. The mating of a Nn boar with a NN sow will result in 50% of the piglets being carriers. Testing of breeding pigs can assist in identifying carriers so informed breeding decisions can be made.
Table 1. Possible Mating Combinations and Resulting Porcine Stress Syndrome Genotypes
Parent A Parent B Progeny Genotypes
NN NN 100% NN
NN Nn 50% NN, 50% Nn
NN nn 100% Nn
Nn Nn 50% Nn, 25% NN, 25% nn
Nn nn 50% Nn, 50% nn
nn nn 100% nn
Effects of PSS Gene on Animal Well-Being, Meat Quality and Pork Production
Effects of PSS gene on animal well-being
The PSS gene causes animal suffering from the stress syndrome. Animals carrying the PSS gene lack the ability to adapt to stresses and once the PSS condition is triggered, they exhibit symptoms quickly. Table 2 summarizes some of the physical stressors that trigger the PSS condition and the symptoms that are typical in affected pigs.
Table 2. Physical Stressors Triggering Porcine Stress Syndrome and Typical Symptoms Exhibited by Affected Pigs
Physical Stressors
Rough or unfamiliar handling
Rough loading and unloading
Transportation
Mixing and fighting
Mating, estrus, parturition
Hot weather
Typical Symptoms
Rapid respiration (short and heavy breaths)
Increase in body temperature >41 C (106 F)
Marked muscle tremors
Twitching of the face
The skin becomes red and blotched
Sudden collapse or death
Effects of PSS gene on pork quality
Since the discovery of the PSS gene, much attention has been given to how it affects meat quality. To date, the impact of the gene on pork quality has been well researched and documented. The typical effect of the PSS gene on pork quality is that it causes PSE pork, which is unattractive to consumers due to its unappealing greyish, soft and watery appearance. PSE pork is also less suitable for further processing because of its low water-holding capacity.
Although any severely stressed pig can develop PSE pork, animals that carry the PSS gene are much more likely to develop PSE pork than PSS gene-free animals. The key factors causing PSE pork are the prolonged high carcass temperature after slaughter, accompanied by a rapid decline in muscle pH during the first 45 minutes post-slaughter. This rapid decline in muscle pH results from excessive muscle energy depletion and a build-up of lactic acid in the muscle. Figure 1 illustrates the relationship between post-mortem (post-slaughter) changes in muscle pH and pork quality.
PSE pork is often characterized by a low muscle pH at 45 minutes post-slaughter, with lighter colour muscle and greater drip losses (water losses) during chilling, processing and cooking than normal pork. The light or pale colour occurs due to the denaturation (breakdown) of the pigmented protein (myoglobin) under the conditions of low pH and high temperature, as well as accumulation of water on the cut muscle surface. Results from the Ontario Pork Carcass Appraisal Project (OPCAP) conducted from 1990 to 1994 showed that the loins from the PSS carriers had a 10% lower marbling score, 6%-8% lower meat colour score, and 5% higher drip loss than loins from the normal animals. Table 3 compares muscle pH, colour and drip loss between normal pigs and PSS gene carriers.
Figure 1. The relationship between post-mortem changes in muscle pH and pork quality. (Source: Austin Murray, Lacombe Research Centre, Agriculture and Agri-Food Canada)
Text version of graphic
Pigs carrying two copies of the PSS gene (nn) tend to have a much higher chance of producing PSE pork than carriers (Nn) and normal animals (NN). It was suggested that 30%-50% of the carrier market hogs would produce carcasses with inferior pork quality. The negative effects of this gene on pork quality seem to be further increased by the trend to select for lean hogs in recent years.
Effects of PSS gene on production
During the 1980s and 90s, the use of nn sires to produce PSS carriers in market hogs was a popular practice in the hog industry. This was due to the perception that carriers would not be susceptible to stress and PSE, but would produce more desirable, lean pork with higher lean yield. However, numerous studies have shown that this belief was not actually correct. For example, the OPCAP project demonstrated that carriers had no significant effects on growth (average daily gain), back fat thickness (live animal and carcass), estimated lean yield or carcass index, although there were slight improvements in lean content, loin eye area, feed conversion (feed to gain ratio) and dressing percentage observed. Table 4 compares production performances between PSS carriers and normal pigs.
Table 3. Effect of the Porcine Stress Syndrome Gene on Loin Quality
Parameter PSS gene Carrier (Nn) Normal (NN) Significance*
Muscle pH at 45 min. post-slaughter 5.91 6.28 Yes
Muscle pH at 24 hr. post-slaughter 5.41 5.42 No
Reflectance L** 46.80 44.50 Yes
Drip loss (%) 5.02 3.06 Yes
Source: Pommier et al., 1998
* Yes means that the PSS gene had a significant effect on the measurement. No means that the PSS gene had no effect on the measurement.
** The greater the L values, the lighter the meat colour (consumers don't like meat that is too pale or too dark in colour).
Table 4. Effects of Porcine Stress Syndrome Gene on Pig Production Performance
Trait PSS gene Carrier(Nn) Normal (NN)
Weight on test (kg) 31.4 31.6
Weight at slaughter (kg) 106.2 106.5
Days to 100 kg (days) 160.0 160.4
Average daily gain (kg/day) 0.867 0.866
Back fat at 100 kg (mm) 13.4 13.6
Feed conversion (feed:gain ratio) 2.63 2.66
Hot carcass weight (kg) 84.5 84.1
Source: Proceedings of the Ontario Pork Carcass Appraisal Project (OPCAP) Symposium (1996)
Results from the U.S. National Genetic Evaluation Program published in 1995 showed that there were no significant differences between carriers and normal pigs for growth rate, leg soundness and back fat over the tenth rib and the last lumbar vertebra. Results from all these studies showed that PSS gene carriers (Nn) had no significant production-performance benefits.
Effect of the PSS gene on economic returns
The presence of the PSS gene in pigs tends to cause development of PSE pork, higher mortalities and loss of meat yield, which directly translate into economic losses for the entire pork production chain. The PSS gene is one of the major swine genes that cost the pork industry profits. In 1994, U.S. researchers reported that the total loss from colour and PSE-related problems was $1.05 per hog in the U.S. They also estimated that of this amount, losses of $0.79 per pig were directly controllable by hog producers and pre-slaughter handling. It was also reported in 2001 that on average, a total of $0.34 lost on every hog marketed in the U.S. was due to PSE, which was mainly because of the yield losses from shrinkage. As well, death losses due to PSS cost an additional $0.06-$0.07 per hog marketed. Based on these estimations, PSE-related direct costs could reach approximately $2.5 million per year for a pork industry with an annual production of 5-6 million hogs such as Ontario. Furthermore, loss of market share in the world exports causes additional economic losses.
PSS Gene Test
In the 1980's, researchers developed the halothane gas-screening test to detect mutant genotype pigs. However, this testing method was unable to distinguish between normal pigs (NN) and PSS carriers (Nn). In the 1990s, researchers in Canada developed a quick, simple and accurate DNA test for PSS gene detection, which makes it possible to identify all three PSS genotypes and to evaluate the effect of the PSS gene on production performance and meat quality traits. The University of Toronto's Innovation Foundation patented the DNA test. The accuracy of the test is approaching 100%. The DNA test provides the pork industry with a powerful tool to detect the PSS gene in live pigs and eradicate it from the entire pig population. Table 5 lists several labs in Ontario and Quebec that currently provide this genetic testing service to the pork industry.
Table 5. Laboratories Providing the DNA Test for Porcine Stress Syndrome Gene in Ontario and Quebec
Lab Service Division
University of Guelph P.O. Box 3650
95 Stone Road West,
Guelph, Ontario, N1H 8J7 (519) 823-1268
Contact: Dr. Chen
schen@lsd.uoguelph.ca
Vita-Tech Laboratories
1345 Denison Street
Markham, Ontario,
L3R 5V2 (416) 798-4988
(800) 667-3411
Contact: info@vita-tech.com
CDPQ
2795, boul. Laurier bureau 340
Sainte-Foy Québec G1V 4M7 (418) 650-2440
Contact: Pierre Falardeau
cdpq@cdpqinc.qc.ca
Table 6. Porcine Stress Syndrome Genotypes across Breeds Tested in Ontario (1990-1994)
Breed Total of Number of Pigs Tested Homozygous Normal (NN) Heterozygotes
(Nn) Homozygous PSS (nn)
Duroc 533 489 43 1
Hampshire 279 262 17 0
Landrace 745 628 115 2
Yorkshire 1320 1180 136 4
Total 2877 2559 311 7
Source: Proceedings of the Ontario Pork Carcass Appraisal Project (OPCAP) Symposium (1996)
PSS Gene Frequency in the Ontario Swine Population
The frequency of the PSS gene in pig populations varies according to genetic breeds and country of origin. Results from the same OPCAP study referred to earlier show that this stress gene exists with variable frequencies in all of the major breeds tested in Ontario. Table 6 summarizes PSS gene incidence in four Ontario breeds tested in the OPCAP study.
The general belief within the Ontario pork industry is that the PSS gene is not commonly found in Ontario pigs and may have been completely eradicated from the Ontario swine population since the OPCAP study was completed in 1994. However, results from recent (2002-2003) routine tests carried out at the University of Guelph indicate that the PSS gene still exists with a higher than expected frequency, indicating that more work is needed to eliminate the gene from Ontario pigs.
Recommendations
Numerous studies support the conclusion that the PSS gene, even in the carrier state, contributes to poor meat quality. The positive effects brought by the PSS gene in terms of body composition do not offset its adverse effects on meat quality and financial returns. Therefore, it should be eradicated from the entire Ontario commercial pig population. This can be achieved by taking the following measures:
All market hog producers should adopt a PSS gene-free policy.
When purchasing new breeding materials (animals, semen and embryos), producers should require that all purchases be certified PSS gene-free.
On-farm selected breeding stock replacements should be tested for the PSS gene if their PSS gene status is not clear.
Genetics suppliers must ensure that no PSS gene exists in herds that are marketed as PSS gene-free.
The eradication of the PSS gene from the Ontario commercial pig population requires commitments and coordinated efforts from all parties involved in the pork chain. With such clear evidence of the detrimental effect of the PSS gene on pork quality and industry profitability, this is the time for the Ontario pork industry to completely remove the PSS gene from Ontario pigs and breeding stocks.
References
Gibson, J. P., R. O. Ball, B. E. Uttario and P. J. O'Brien. 1996. The Effects of PSS Genotype on Growth and Carcass Characteristics. Proceedings of the Ontario Pork Carcass Appraisal Project Symposium. P. 35-38.
Goodwin, G. G. 1994. Genetic Parameters of Pork Quality Traits. Ph.D. Thesis. Iowa State University, Ames, U.S.
Pommier, S. Al, C. Pomar and D. Godbout. 1998. Effect of the Halothane Genotype and Stress on Animal Performance, Carcass Composition and Meat Quality of Crossbred Pigs. Can. J. Anim. Sci. 78:257-264.
Related Links
Lab Service Division, University of Guelph
Vita-Tech Laboratories
CDPQ