Murrellen Pork

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 Porcine Stress Syndrome

The mutated gene responsible for Porcine Stress Syndrome (PSS) has been maintained in some breeding stocks for the slight benefits it yields over normal pigs. These benefits include leaner and bulkier pigs and an increase in development. Some believe that the increase in lean meat content is approximately 1 to 2 % for heterozygous carriers and 4 to 5 % for homozygotes.

On the other hand, the PSS gene also has negative effects which can lead to premature death or more commonly Pale, Soft Exudative (PSE) pork. PSE pork begins to lose its water content shortly after slaughter and its appearance and smell are not appealing to the consumer. In fact, one half of poor quality pork is attributed to the PSS gene. In addition to these obvious sources of economic loss, sows that have the PSS gene have reduced reproductive performance.

 

 

Many large overseas breeders have opted to develop new PSS-free breeds which offer improved leanness and muscle bulk without the ill effects or economic loss caused by PSS. When all things are considered, one comes to realize that it is in one's best interest to eliminate or at least control the PSS gene in their breeding stocks.

 

PSS is a hereditary disorder in swine of all ages. Pigs affected with this disorder display the following characteristics when subjected to stress:

·          dyspnoea (rapid heavy breathing)

·          premature death

·          muscle rigidity

·          hyperthermia

PSS is caused by a mutation in the halothane gene. It was called the halothane gene because PSS positive pigs exposed to halothane gas show typical PSS symptoms. Since all animals carry two copies of every gene, the status of the halothane gene can be classified by one of three designations:

·                "NN" (normal or negative) - This indicates that both copies of the PSS gene are normal and the pig is negative for PSS.

·                "Nn" (heterozygous or carrier) - This indicates that one copy of the PSS gene is normal and the other is mutated. These pigs are often called carriers because they do not always show typical PSS symptoms but can still pass on the mutant PSS gene.

·                "nn" (homozygous or positive) - This indicates that both copies of the PSS gene are mutated and the pig is referred to as being positive for PSS.

 

Malignant hyperthermia leads to a rapid pH fall (pH 45 minutes post-mortem <6.1), which results in a pale, soft and exudative meat (PSE meat). In pigs the Hal gene is located on chromosome 6 and is comprised of 2 alleles: a normal allele (HalN ) and a recessive mutant allele (Haln ). In 1991, Canadian researchers demonstrated that malignant hyperthermia in pigs was caused by a mutation at position 1843 of the gene encoding for the ryanodine receptor (locus ryr-1) (Fujii et al., 1991). It was also demonstrated that the Haln allele was present among Canadian populations of Duroc, Landrace, Yorkshire and Hampshire (Houde et al., 1993).

 

The 3 possible genotypes (NN, Nn and nn) can now be specifically identified using a molecular test. Heterozygote pigs with the Hal gene generally produce lower quality meat than pigs free of this gene (Table 1). Meat properties are also strongly influenced by slaughtering conditions. Generally, the advantages brought about by the Haln allele in terms of body composition do not offset its adverse effects on meat quality. This may explain why the Hal n allele has been gradually removed over recent years from most pig populations.

 

Table 4. Effect of Hal gene on quality of loin.

 

Parameter

Heterozygotes (Nn)

Homozygotes (NN)

Significance

pH45 minutes1

5.91

6.28

0.001

Reflectance L*1

46.8

44.5

0.05

pH 48 hours1

5.41

5.42

NS

Drip loss %

5.02

3.62

0.001

 

1 LD, Longissimus dorsi                                                                   Source: Pommier et al., 1998.

 

What this table is telling us is that:

·                 The pH falls faster immediately after slaughter in those pigs with the mutant gene that it does for normal pigs. The chances that these results could be achieved by chance is 1:1000.

·                 The reflectance values (optical probe such as a Hennessey GP4) show changes at the same time and the chances that these results could be achieved by chance is 1:20.

·                 The ultimate ph in both types of animal ends up about the same after 48 hours.

·                 The drip loss from the pigs containing the mutant gene is 36%greater than normal pigs and the chances that these results could be achieved by chance is 1:1000.

 

So the strategies available to the producer are two-fold:

 

1.    Eliminate the Halothane gene from the breeding herd (Switzerland did this as a national exercise).

 

2.    Live with the gene (or its possible presence) but maximise the systems between production and slaughter so that pigs are not subjected to stress.

 

Murrellen Pork has no breeding stock in its operation and has no means to determine whether the gene is present in the incoming stock. However the second alternative seemed to make a lot of sense and that is the key distinguishing feature of the Murrellen System – the elimination or minimisation of stress on the animal.