As you read in Part I, The Duchess Fund has recently received medical records on two purebred potbellied pigs involving Porcine Stress Syndrome (PSS). PSS is also known as “Malignant Hyperthermia”.

CASE A – CONFIRMED (Case #000196 – Duchess Fund Medical Database) A pig expired on the table during a routine spay. PSS was suspected so a cardiac puncture was done to obtain fresh blood and it was sent off for DNA testing. The test result was homozygous HAL 1843 dm, which means she was a dimutant or had two copies of the mutant PSS gene and PSS was the cause of death. Attempts were made to locate the parents of this pig but all efforts have been unsuccessful. This is believed to be the first documented (confirmed) case of PSS in a potbellied pig.

CASE B – SUSPECT (Case #000197 – Duchess Fund Medical Database) This was a young piglet with a history of being stressed easily. She also had a difficult recovery from a routine spay. The owners reported what may have been seizure activity in the pig and she expired about 3 months after the spay. The pig was subsequently taken to a university for a necropsy. The liver was sent to a lab to rule out a selenium deficiency and white muscle disease. The pathology report indicated death was from suspected PSS. Since there was no fresh blood available for DNA testing, it could not be confirmed. Both parents of this pig were subsequently DNA tested for PSS and both returned as negative.

Due to ongoing questions from pet pig owners, we have continued with the following questions that are answered by Bruce Lawhorn, DVM, MS.

Bruce Lawhorn, DVM MS
Associate Professor/Extension Swine Veterinarian
Texas Agricultural Extension Service/Dept Large Animal Medicine & Surgery
College Veterinary Medicine
The Texas A&M University System
College Station, Texas 77843-2487

Duchess Fund: How did PSS originate?
Dr. Lawhorn: During the 1930’s through the 1950’s, the heavy muscled, low fat Pietrain swine breed was developed in Belgium (by crossing of the local Normand and Berkshire breeds) to meet the demand for high quality, extra lean fresh pork. Associated with the selection for heavy muscling and low fat was the tendency for Pietrain hogs to be easily stressed by ordinary management practices such as movement from pen to pen, loading into a trailer and transportation to market. Sudden death occurred in many of these animals after becoming stressed. It was also noticed that pale, soft, exudative (PSE) pork was common in hams and loin chops from this breed (compared to the uniform pink to pinkish-red color of normal pork). During this time period, the cause of this condition was unknown and no real diagnostic tests other than observation were available to identify what we now call PSS or malignant hyperthermia (MH).

Apparently this condition was spread by breeding Pietrain pigs with the PSS gene to swine in other European countries. It is speculated that PSS was introduced into the U.S. through Danish Landrace swine in 1934, and then became more common when this breed was released to the public in 1950, resulting in the creation of the American Landrace breed. However, the Poland China breed which was developed in Ohio, became well known for having PSS traits. Since the Berkshire breed was used in the development of both the Pietrain and Poland China breeds, the PSS mutant gene was probably introduced by this common ancestry. Poland China hogs were further selected for heavy muscling and low fat content as the demand for lard decreased and vegetable oils became more popular after WW II. This selection process for extremely lean animals unknowingly increased the occurrence of PSS . Subsequently the Poland China breed was noted for having a high prevalence of PSE pork (late 1950’s), became associated with a high frequency of susceptibility to stress (mid-to-late 1960’s), and was identified with having high prevalence of reactivity to halothane gas anesthesia (early 1970s).

It is noteworthy that anesthetizing young pigs with halothane gas was the first accurate test to identify PSS swine (those having 2 copies of mutant PSS gene). However, it had the drawback of not separating carriers (having one copy of the mutant PSS gene) from normal swine (having no copies of the mutant PSS gene) since halothane caused no increase in rectal temperature (MH) or stiffening of the limbs (uncontrolled muscle contraction) in carrier and normal swine. Nevertheless, it was a good testing method, because discontinuing halothane anesthesia in young swine (20 to 40 pounds) after they exhibited elevated temperature and stiffening of the limbs as signs of PSS, allowed complete recovery. Older, larger PSS swine such as sows would not recover from MH induced by halothane anesthesia; this indicated body muscle mass and the heat and metabolic disturbances caused by uncontrolled anaerobic muscle activity influenced the case mortality rate.

By the 1970’s, the Pietrain, Landrace and Poland China breeds were known for their high prevalence of PSS. Other domestic swine breeds have been affected by PSS since that time. Understanding how widespread PSS had become, it is remarkable that modern DNA testing throughout the world has established that the PSS mutation was introduced by a single breeding founder pig!

Duchess Fund: What is a spontaneous mutation?
Dr. Lawhorn: A mutation is defined as an error or errors in copying of nucleic acid such as DNA during cell division. For example, every time the cells of a mammal divide, an exact copy of DNA code for the new cell is made. Cell division in mammals occurs billions and billions of times every day. Mutations or errors in DNA copying may have no consequences or be the cause of major problems such as cancer. “Spontaneous” mutation implies that there is no apparent cause. It is well known that there are specific causes for cell mutations such as ultraviolet light. Sunscreen is applied to minimize the mutating effects of ultraviolet light that can cause skin cell cancer. Scientists use ultraviolet light in the laboratory as a disinfectant because it causes errors in DNA replication during bacterial cell division; bacteria are killed as a result. Spontaneous mutations may actually have a cause, but the cause may not be currently known. The immune system of mammals kills mutated cells if they can be recognized as “different”. For example, the immune system kills “changed” cells that could become cancer and the mammalian host is totally unaware this is happening. Some mutations do not alter the cell enough to signal the immune system to kill it. These undetected mutations are likely to be passed on during subsequent cell divisions; this is the case for the PSS mutation.

Duchess Fund: What are the chances of a potbellied pig having a spontaneous mutation?
Dr. Lawhorn: Any living organism can experience a spontaneous mutation or mutations from known causes. As previously discussed, such mutations may have no consequences or be life threatening. Inbreeding probably increases the chances for mutations.

Duchess Fund: In Part I of PSS, Case A pig test results returned as HAL1843dm. How does this affect the relatives of the Case A pig? Also, what is the difference between a carrier and a positive?
Dr. Lawhorn: The results ‘HAL1843dm’ refer to the original halothane anesthesia test ‘HAL’ and ‘dm’ means dimutant. The HAL1843dm result for Case A pig means it had 2 copies of the PSS gene (One copy from each parent). Inheriting 2 copies of the PSS gene is what makes a pig a PSS positive animal. Inheriting one copy of the PSS gene makes a pig a carrier. Inheriting no copies of the PSS gene means a pig is normal. It takes two carrier parents that have one copy of the PSS gene to produce 25% offspring with 2 copies (PSS pigs), 50% offspring with one copy (carriers), and 25% with no copies of the PSS gene (normal). So this means the parents and carrier littermates of Case A pig should not be used for breeding and should be altered to prevent reproduction. Also, grandparent stock that may still be reproductively active should be tested and any carriers found should not be used for breeding. Any littermates of Case A pig with 2 PSS genes are likely to die after almost any stress including anesthesia, so PSS is then a fatal or self-limiting mutation. However, if PSS pigs survive, the owner will have to avoid almost all stressors on the pig for it to survive. Of course the only way to know the PSS gene status of any littermates to a pig that died of lab-confirmed PSS is to also lab test them for PSS. Part I of the PSS Case A pig article discussed lab testing. The parents of a PSS pig that dies may also be lab tested, but it is already known that both had to be carriers to produce offspring with 2 copies of the PSS gene.

Duchess Fund: If both parents test negative for PSS by a DNA test, can we assume that all babies are PSS free?
Dr. Lawhorn: Yes!

Duchess Fund: Do carriers demonstrate PSS signs after stress?
Dr. Lawhorn: No. Even PSS swine may not demonstrate signs of malignant hyperthermia after mild stress. For example, many domestic swine that are known to have PSS have been successfully transported to slaughter and not shown outward signs of PSS. However, both PSS and carrier swine are predisposed to exhibit the undesirable meat quality of PSE pork. It is noteworthy that PSE can occur in pork from normal pigs that have been overly fatigued during an extended transit time to slaughter. This means that the PSS mutant gene is not the only cause of PSE pork and shows how a stress, such as muscle fatigue, can affect even normal pigs.

Duchess Fund: Are there outward signs or characteristics that might indicate a pig is a carrier or has PSS?
Dr. Lawhorn: There are no outward signs for a carrier but a PSS pig may show signs of becoming stiff-gaited after exercise or other stress followed by muscle tremors, mouth breathing and rapid over heating. If the pig dies, rigor mortis will already be present to some degree. Young pigs may exhibit mild signs of PSS that worsen as the pig ages and gains muscle mass.

Duchess Fund: Is a PSS pig at less risk as he/she ages?
Dr. Lawhorn: As previously discussed, as the weight and age of the pig increases, the risk of MH and death after stress increase because there is more muscle mass to uncontrollably contract and generate excessive body heat and metabolic disturbances not compatible with life. As a PSS pig reaches a mature body weight, the risk of stressing out and dying should remain constant since the genetics of the pig never changes.

Duchess Fund: If a pig has been under anesthesia for a medical procedure and recovered without incident, can it be assumed that pig is PSS free?
Dr. Lawhorn: It was discussed previously that younger and smaller body weight PSS pigs (2 PSS gene copies) easily survived brief anesthesia with halothane gas even though they did show increased temperature and muscle stiffening before being taken off anesthesia. Also remember that the halothane anesthesia test could not differentiate between normal and carriers (1 PSS gene copy). Therefore, successfully undergoing any type of anesthesia (gas, injectable or combinations) does not mean the PBP is not a carrier. It is even possible that a young PBP with PSS might successfully undergo anesthesia once but demonstrate PSS signs and die under anesthesia when older and heavier. Therefore, successfully undergoing anesthesia, especially at a young age, is no guarantee that the PBP is not a carrier or PSS animal.

Duchess Fund: If a pet pig tests PSS positive and subsequently needs veterinary care (which may be stressful), can any technique or drug be used to prevent a PSS episode?
Dr. Lawhorn: To date the need for such intervention has been extremely uncommon since PSS is extremely rare in pet pigs like PBPs. However, if a pet pig has been acclimated to going to the veterinarian’s office even by mock health visits, there should be less stress on the animal. It must be emphasized that any stress on a PSS pig of any breed may result in an acute PSS episode and sudden death. For this reason pretreatment at home with a drug such as dantrolene sodium could prevent a PSS episode. Dantrolene sodium is muscle relaxant used to prevent MH in humans. It is available to physicians under the trade names Dantrium(r), Dantrolen(r), Dantamacrin(r) and Danlene(r). Dantrolene sodium is an expensive drug only available by a veterinary prescription. The client’s veterinarian would have to make a PSS diagnosis before it would be practical for the veterinarian to prescribe such a drug (dantrolene is not normally kept by most veterinarians since it is expensive and rarely needed).

Duchess Fund: Can PSS skip a generation or more?
Dr. Lawhorn: To answer this question it is important to understand that normal sire and normal dam matings produce only normal pigs and no PSS carriers (1 PSS gene copy) or PSS pigs (2 copies of PSS gene) . A normal sire mating to a PSS carrier dam (or vice versa) produces 50% PSS carrier offspring and 50 % normal offspring. As long as PSS carrier offspring kept as breeders are never mated to another PSS carrier, no PSS offspring will ever occur; so many generations could be “skipped” before PSS pigs were produced. However, the only thing that determines whether PSS pigs are produced is strictly genetics, not number of generations.

Duchess Fund: What impact does inbreeding have on PSS and potbellied pigs?
Dr. Lawhorn: To put this question into perspective, consider that only one lab-confirmed fatal PSS Case A (2000) and one possible nonfatal case of PSS (Journal American Veterinary Medical Association, 1993) have been reported since potbellied pigs (PBPs) have been introduced into the U.S. Case A (fatal PSS PBP) means the its parents are PSS carriers and one or both of the grandparents were PSS carriers and so on. Since not many PBPs were originally introduced into the U.S., the gene pool that established PBPs as U.S. pets is very small. When breeding within a very small gene pool, inbreeding cannot be avoided unless new genetics is introduced. Since this original gene pool has probably not been expanded, the PSS mutation must have been passed down from generation to generation until PSS carrier parents were finally mated and produced offspring that were PSS PBPs. Therefore it could be argued that the breeding within the narrow gene pool has already been the cause of PSS in PBPs. Since DNA testing to distinguish normal, carrier and PSS swine has only been readily available since about 1993, cases of sudden death in PBPs from PSS may have gone undiagnosed until recently. If PSS cases or carriers in PBPs continue to be lab-confirmed by DNA testing, it seems that breeding for years within a narrow gene pool has contributed to the problem.


O’Brien PJ and Ball RO. Porcine Stress Syndrome. In: Straw BE, D’Allaire S, Mengeling WL, et al, eds, Diseases of Swine. Eighth edition, Ames: Iowa State University Press, 1998; 757-775.

Viral Genetics and Evolution. In: Fenner F, Buchanan PA, Gibbs, EPJ, et al, eds, Veterinary Virology. Orlando: Academic Press, 1987; 89-116.

Micromedex (R) Health Care Series Integrated Index, Vol. 106, expires 11/2000, Micromedex, Inc.

We thank Dr. Lawhorn for his time and effort in helping our readers understand this better.

A new diagnostic technique has just become available and is being offered by GeneScreen. In the past, fresh blood or fresh tissue from a live pig had to be sent to a lab for DNA testing in order to confirm PSS. Now, however, tissue and/or bones from a deceased pig can be sent to GeneScreen for DNA testing. We asked DNA Technologist, Jarrod Waton with GeneScreen to elaborate on this new technique for our readers, which follows:

Jarrod Watson, DNA Technologist
2600 Stemmons Fwy. #133
Dallas, TX 75207
(214) 631-8152 or toll free (800) 752-2774

The test that GeneScreen, Inc. uses to detect the presence of the Porcine Stress Syndrome (PSS) gene requires DNA from the pig. DNA is in every cell of the body. Generally this test is performed using DNA isolated from the pig’s blood. GeneScreen, Inc. utilizes blood stain cards requiring significantly less blood, primarily to decrease cost for the pig owner. In addition, the same test can be run using various postmortem body tissue samples. Some of these tissue samples include skin, internal organs, and
hair (including the follicle), given proper quantities of the particular tissue. However, many of the methods used for the extraction of DNA from these tissues do incur additional costs. If you are wishing to have a test performed using these tissues, be sure to call and ask about feasibility and increased cost.

We thank Mr. Watson for his time and effort to provide us with information on this advancement.

As we outlined in Part I, here are the instructions if you would like to have your pig tested for PSS.

Contact Ed Kenney at Swinetics, phone 877-440-0894 who will register you free of charge.
After registration with Swinetics, contact Jarrod Watson at GeneScreen, phone 800-752-2774 and he will send you the material for the card test which consists of a few drops of your pigs’ blood placed on a card and mailed to their lab. Directions will be given for tissue and/or bone samples also as well as any cost differences.

Registration with Swinetics first will reduce the cost of this test. Please
furnish a copy of the test results to your veterinarian and The Duchess Fund
so we can document them.