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Diseases
MAST CELL TUMORS IN PIGS by: Beth A. Valentine, DVM, PhD
PORCINE REPRODUCTIVE RESPIRATORY SYNDROME by: Bruce Lawhorn, DVM, MS    
PORCINE STRESS SYNDROME - PART I    
PORCINE STRESS SYNDROME - PART II    
INJECTABLE ANESTHETICS
by D. Bruce Lawhorn DVM, MS    
POTENTIALLY FATAL DISEASE DISCOVERED IN POTBELLIED PIGS
by: Christina Mehra, Staff Writer, VetCentric.com
A NEW PIG DISEASE by: Dr. John Carr, B.V.S.C., PhD, DPM, MRCVS
DIPPITY PIG SYNDROME by: Jenny Blaney
WHAT ABOUT MANGE? by: Jenny Blaney
MONITORING URINARY FUNCTION by: Jenny Blaney
MAST CELL TUMORS IN PIGS: by Beth A. Valentine, DVM, PhD
When Barbara Baker noticed that Lord had developed a lump on his right cheek, she didn't give it much thought. It was about the size of a cherry, and was not growing, bleeding, changing shape or color, or otherwise bothering the pig. It was only when Dr. Lawhorn, who was attending the potbellied pig symposium in Florida, visited her home and examined Lord's lump that she became concerned. Dr. Lawhorn advised Barbara to have the lump removed and sent for pathologic examination. A few weeks later the surgery was performed. It was easy for the veterinary pathologist to identify the characteristic features of a mast cell tumor, but it was almost impossible for the pathologist, or anyone else for that matter, to offer an idea of what might happen now that the tumor was removed. We just don't know enough about mast cell tumors in pigs to be able to predict their behavior.

When Barbara asked if I would be willing to write an article on mast cell tumors in pigs, I went to my files to see what I could find. There is precious little written about mast cell tumors in pigs, so at least I didn't have to wade through a lot of material! In this article I will try to summarize what we do know about mast cell tumors in pigs and in other species.

First off, let me explain what a mast cell is. Mast cells are normal residents of the areas of the body that are exposed to what can be considered an "external" environment. This includes the skin, sinuses, the lining of the airways from the nose to the lungs, and the lining of the stomach and intestines. Mast cells are identified by their characteristic granules. The purpose of mast cells is to release the contents of their granules during infections. The granules of mast cells contain a variety of substances, many of which make blood vessels "leaky," which helps other inflammatory cells to get to the site of an infection to try to clear it up. This normal role is often overlooked in discussions of mast cells, because mast cells are so often involved in allergic responses. Allergies can be considered a form of "healthy" inflammation gone awry. One of the substances that mast cells produce and release is histamine, which is the basis for the use of antihistamines in allergic conditions. Histamines cause vessels to be leaky, which leads to fluid accumulation and tissue swelling, and often cause an itching sensation in the area.

Tumors of mast cells, called either mast cell tumors or mastocytomas, are common in dogs, cats, and ferrets, and are much less common in horses, cattle, pigs and people. We know a lot about the behavior of mast cell tumors in dogs, cats, ferrets, and horses, but very little about their behavior in cattle and pigs. Such tumors are very uncommon in people, usually occurring in children, where they often regress on their own. In dogs, mast cell tumors are graded 1, 2 and 3, with grades 1 and 2 being relatively benign and generally cured by wide surgical excision, and grade 3 being malignant and likely to recur and/or spread. Mast cell tumors in cats are most often benign, although there is a less common malignant variant. Mast cell tumors in ferrets and horses are considered benign tumors. In cats, the most common mast cell neoplastic processes are skin tumors (that can be multiple), and an internal mastocytosis syndrome in which neoplastic mast cells infiltrate multiple internal organs. In the cat, these appear to be two distinct disorders.

Adding to the confusion is that there is a condition called mastocytosis, in which mast cells are increased throughout the body, creating havoc by producing their inflammation-promoting substances. In some cases the mast cells themselves are not thought to be neoplastic, but in others they are. I should define the term neoplastic here. Neo means new, and plastic means growth, so a neoplasm is a growth of new tissue. Neoplasia can be benign, meaning that the tumor does not invade or spread. Malignant tumors invade and/or spread through the body, causing what is often called cancer. The term cancer comes from the Latin word for crab, because the spread of cancer can resemble the spreading legs of a crab. And, to make matters worse, there is also a condition in which neoplastic mast cells circulate in the blood, known as mast cell leukemia.

The literature regarding mast cell disorders in pigs includes mast cell tumors, mastocytosis, and mast cell leukemia. Mast cell tumors of the skin or of internal organs are the most common mast cell problems in pigs, and have even been reported in young meat pigs examined at slaughterhouses. These tumors are not common in young pigs, though, with one study citing only 5 cases of mast cell tumors of the skin in 664 million pigs examined.

Barbara was able to find me pathology reports from three other potbellied pigs with mast cell tumors. Two were single tumors, similar to Lord's, and another pig had multiple mast cell tumors in the skin. The ages recorded were around 7 years of age. The pig with multiple tumors had re-growth of three of the tumors following removal. So far, I have not seen any reports of internal mast cell tumors in potbellied pigs. But, given findings in other breeds of pigs, I suspect that this is a possibility. The behavior of mast cells tumors is often described as unpredictable, usually because we simply don't know enough to be able to predict it. This is certainly the case with mast cell tumors in pigs. From what I can gather from the literature to date, mast cell tumors in pigs appear to be more similar to cats than to other species. That is, tumors that form in the skin may be multiple and can recur following incomplete excision, but they tend to stay in the skin. Tumors that form internally are not often associated with skin tumors. I hasten to add that this is still speculation, based on a very small number of reported cases of mast cell neoplasia in pigs. We still have a lot to learn about mast cell tumors in pet pigs.

So, what should you do if your pig develops a skin lump? My best advice is to have it examined by a veterinarian and removed as soon as possible. A mast cell tumor that is completely removed early on is far less likely to recur or to spread than is one that has been there for awhile. The veterinary surgeon will aim to remove the tumor as widely as possible, and removing a small tumor is much preferred to waiting for it to grow to a really worrisome size. Always insist on sending the sample for pathologic evaluation.

It is only by removing tumors and having them identified as mast cell tumors, and then following up on the pigs to see what happens, that we will be able to learn about the behavior of mast cell tumors in potbellied pigs. The efforts of people like Barbara Baker and of organizations like the Duchess Fund are to be lauded. Only by continuing to gather and examine data on disorders of potbellied pigs will we be able to learn more about these vexing tumors, as well as other problems that plague potbellied pigs.

Beth A. Valentine, DVM, PhD, is a board-certified veterinary pathologist on the faculty of the College of Veterinary Medicine at Oregon State University, Corvallis, OR.

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PORCINE REPRODUCTIVE RESPIRATORY SYNDROME by: Bruce Lawhorn, DVM, MS

Porcine Reproductive Respiratory Syndrome (PRRS) is one of the most important diseases in the domestic swine industry. As the name implies, PRRS causes reproductive and respiratory disease. PRRS actually is a new worldwide swine disease that was not even recognized before the late 1980s. The disease pattern in domestic swine herds caused by PRRS virus infection was actually called "mystery swine disease" for several years until the cause was discovered and proven to be a virus in 1991. It was named the Lelystad virus because the location of its discovery at the Central Veterinary Research Institute in Lelystad, Netherlands. Since that time, many strains of PRRS virus have been recognized. With the exception of mallard ducks, other animals and humans are not known to be hosts for the PRRS virus of swine.

It is still unknown where PRRS virus originated or how it was introduced into domestic swine. Free-roaming feral swine in the US and wild boar in other countries were thought to be likely sources. Obviously feral and wild swine were in existence a long time before PRRS emerged, but they could have been infected with PRRS virus from some unknown source and then made contact with domestic swine and infected them. In a joint Texas Agricultural Extension Service/Texas Parks & Wildlife 1996 - 1999 survey in the Texas Rolling Plains, only 1/135 samples tested positive by the PRRS ELISA antibody test. This PRRS positive animal was a twenty-month-old, 155 pound boar. 1 In a US survey of feral swine, all sera collected and tested between 1976 and 1993 were negative and only 2 positives were found in 1994.2 Only 2/1250 wild boar samples collected in Europe from 1991 through 1996 were PRRS positive.2 From these US and European surveys it was speculated that domestic swine probably transmitted PRRS virus to feral and wild swine, and not vice versa. 1, 2

Another wild species, the mallard duck, has been proven to be susceptible to PRRS virus infection and has extended virus shedding (39 days after exposure in some).3 It is interesting that PRRS virus is very fragile and is inactivated in an unprotected environment at room temperature, but can survive in room temperature well water and city water for 8 and 11 days, respectively. Mallard ducks can be infected through PRRS-contaminated water and shed virus into feces to infect other mallard ducks. PRRS virus isolated from mallard duck feces has been shown to be infectious for pigs when challenged intranasally; these infected pigs were then able to infect susceptible contact pigs. Scientists discount the idea that mallard ducks have spread PRRS virus to and between swine herds probably because duck to pig contact is very infrequent in modern swine production. However, many swine farms around the world with less intensive production practices have frequent duck to pig contact. Although it is unknown where PRRS virus originated, scientist do agree that mallard ducks could be a possible host for introduction of different strains of PRRS virus into swine in the future.3

It was not likely that PRRS virus infection in US domestic swine originated from PBPs since there was already a low PRRS prevalence in domestic swine in Iowa by 1985 (shown by retrospective studies)2, and PBPs did not become popular as US pets until the late 1980's (the time of emergence of "mystery swine disease"). However, it would be interesting to know if there is currently any evidence of PRRS virus infection in the PBP population of the US.

Recently, 29 sera from normal PBPs of various ages, sex and weights from a Florida location were blood sampled and tested for PRRS antibody by the ELISA test. All 29 sera were negative. When infection to PRRS virus in swine does occur, antibody to the PRRS virus detectable by ELISA persists for about 4 to10 months. Since the average age for these 29 PBPs was 2.6 years (9 month - 6 years range), it is possible that PRRS virus infection in some animals could have occurred previously but antibody was no longer detectable at the time of sampling. Although this is a very small survey and has the aforementioned limitation, it may indicate that, like feral swine, PRRS virus infection is probably not important as a cause of disease in PBPs. Testing other populations of PBPs could substantiate this hypothesis.

References

1. Lawhorn B. Texas Rolling Plains Feral Swine Survey, Proceedings of the 1999 National Feral Swine Conference, Ft. Worth, Texas, 124-127.

2. PRRS Compendium. National Pork Producers Council, Des Moines, Iowa, 1998, 61, 78.

3. Benefield DA, Collins JE, Dee SA, et al. Porcine Reproductive and Respiratory Syndrome. In:Straw BE, D'Allaire S, Mengeling WL, et al, eds. Diseases of Swine, Eighth edition, Ames: Iowa State University Press, 1998; 201-232.

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PORCINE STRESS SYNDROME - PART I 

The Duchess Fund recently has received medical reports on two purebred potbellied pigs from registered stock involving Porcine Stress Syndrome (PSS). PSS is also known as "Malignant Hyperthermia".

CASE A - CONFIRMED (Case #000196 - Duchess Fund Medical Database) The first case was in July, 2000 when a pig expired on the table at a university during a routine spay. PSS was suspected so a cardiac puncture was done and blood sent off for DNA testing. The result of the DNA test was homozygous, HAL 1843 dm, which means she was a dimutant or had two copies of the mutant PSS gene and malignant hyperthermia (same as PSS) was the cause of death. A complete summary will be in Part II.

CASE B - SUSPECT (Case #000197 - Duchess Fund Medical Database) The second case was on a young piglet with a history of being easily stressed. It was reported that she had a difficult recovery following her spay. The pig expired approximately 3 months after the spay. The owners took the pig to a university for a necropsy. We have the pathology report as well as the liver tissue analysis. There was no selenium deficiency. Fresh blood was not available for DNA testing because the pig had expired hours before reaching the university. However, based on the history of the pig, microscopic change in muscle tissue and the selenium tissue analysis of the liver, the parents are being DNA tested for PSS. Test results will be in Part II as well as a complete summary.

Naturally, this has raised many questions from concerned pet pig owners. In an effort to better explain this genetic syndrome, we asked Barbara Straw, DVM, PhD, to share her expertise on the subject for the benefit of potbellied pig owners. Dr. Straw is the Editor-In-Chief of "Diseases of Swine" 8th edition. 

The following is an interview on 9/21/00 conducted by The Duchess Fund:

Duchess Fund:
Dr. Straw, could you explain in layman's language what Porcine Stress Syndrome is (also known as malignant hyperthermia) ?
Dr. Straw: Porcine Stress Syndrome (PSS for short) is an inherited defect in muscle metabolism that can be life-threatening to the pig under certain triggering situations. Pigs with PSS have a defect in the transport channel that moves calcium into their muscle cells. Normally for a muscle to contract, calcium must be moved from outside the cell to inside. In certain situations, this defect in which the muscle is trying to function without the right level of calcium results in abnormal muscle metabolism in which lactic acid builds up. Accompanying the acidosis is a build-up of heat due to a wasteful process of utilizing muscle glycogen for energy. The acidosis and hyperthermia can be severe enough to cause death. PSS is caused by a recessive gene. When animals carry two copies of the gene they are prone to showing clinical signs when certain stresses are applied.

Duchess Fund: What is the difference between PSS and White Muscle Disease?
Dr. Straw: White Muscle disease occurs because of a deficiency of an essential nutrient, selenium. Selenium is part of an enzyme that removes peroxidase waste products from liver, muscle and many other cells in the body When peroxidases accumulate in muscle they damage the tissue and it blanches out producing a "white muscle". While both PSS and selenium deficiency produce damage to muscle, they have completely different causes.

Duchess Fund: Since PSS is a genetic disease, could a supplement of Vitamin E and/or Selenium or any other vitamin/mineral supplement prevent symptoms or prevent death from PSS?
Dr. Straw: No. PSS is a genetic disorder not a nutritional deficiency and the nutritional status of a pig has not been shown to affect the expression of PSS. Supplementation with selenium or Vitamin E would not influence the expression of PSS since they are caused by two separate mechanisms. Calcium supplementation would not help either since there is plenty of calcium outside the muscle cell, but the cellular transport channel isn't working properly.

Duchess Fund: Under what conditions are pigs with PSS likely to show symptoms and possibly die?
Dr. Straw: Transportation, high environmental temperatures, exercise, mating and fighting can trigger muscle damage. Also certain compounds such as halothane anesthetic, succinylcholine and caffeine directly act on the calcium transport channel.

Duchess Fund: What is Dantrolene, how and when is it used and how effective is it?
Dr. Straw: Dantrolene is a drug given by injection that acts to stabilize the calcium transport channel. It has moderate to high effectiveness in treating an episode of PSS if given immediately after signs are noticed. However, because PSS is not a common condition, few veterinary clinics stock this drug.

Duchess Fund: Can a pig have a non-fatal PSS episode without spiking a high temperature?
Dr. Straw: An elevation in temperature is a consistent finding with PSS. The abnormal muscle metabolism generates excess heat that raises the rectal temperature. Events such as exercise or fighting that trigger an episode of PSS may also raise the pig's temperature. While an elevation in temperature by itself is not diagnostic, a pig with a normal temperature subjected to such events, is not likely to be experiencing a PSS episode.

Duchess Fund: If a veterinarian treats a pig that subsequently dies, what should that veterinarian do to confirm PSS if it was suspected?
Dr. Straw: When a pig dies after stressful physical activity or anesthesia, the first thing to do is take its temperature. PSS produces extreme elevations in body temperature, typically as high as 106 degrees F at the time of death. Even some time after death the muscle temperature will still be elevated. Next check for extreme rigidity of the legs. The abnormal events in the muscle produce immediate rigor mortis. The definitive test is to directly check for the defective gene, called HAL-1843. This test requires a sample of blood or tissue to be sent to a lab that performs DNA analysis. The laboratory will report whether the pig has two, one, or no copies of the HAL-1843 gene.

Dr. Barbara Straw, DVM, PhD
Professor Swine Medicine
Michigan State University

END OF INTERVIEW

We appreciate Dr. Straw taking the time to address this issue and thank her
for her assistance!

As you can see, PSS is an inherited defect in muscle metabolism. Dr. Straw has outlined the causes and symptoms of this syndrome as well as the steps that should be taken to diagnose and confirm it.

At this time it is unknown if Case A is an isolated case or if there are more potbellied pigs carrying the gene. As for Case B, the DNA test results on the pigs' parents will determine whether or not PSS was involved in the cause of death. Many swine experts believe that PSS is a minimal problem in potbellied pigs. We need more information and monitoring to confirm this.

If you are interested in having your pig tested for PSS, the following needs to be done:

  1. Contact: Ed Kenney at Swinetics, phone 877-440-0894 who will register you free of charge.
  2. 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. 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 it.

In Part II of PSS, we will be covering stress reducing management practices, alternative methods of medical management of pigs as well as the summaries of these cases.

If you have questions, please email them to or fax to 813-645-1625. Answers to your questions will also be covered in Part II.

The Duchess Fund is a non-profit 50l(c)(3) corporation whose purpose is to enlarge the amount and enhance the quality of data available to the individual practitioner relative to the care and needs of potbellied pigs as long term companion animals. Your donations make it possible for us to continue our important work and obtain our goals and accomplish our objectives.

The Duchess Fund
408 - 14th Street S.W.
Ruskin, FL 33570
813-641-3013
FAX: 813-645-1625

Copyright September, 2000 The Duchess Fund All Rights Reserved

A COPY OF THE OFFICIAL REGISTRATION AND FINANCIAL INFORMATION MAY BE OBTAINED FROM THE DIVISION OF CONSUMER SERVICES BY CALLING TOLL FREE WITHIN THE STATE. REGISTRATION DOES NOT IMPLY ENDORSEMENT, APPROVAL, OR RECOMMENDATION BY THE STATE. THE NUMBER FOR THE DIVISION OF CONSUMER SERVICES IN FLORIDA IS 1-800-435-7352. Registration #SC-11271 The Duchess Fund does not utilize any professional solicitors. 100% of contributions go directly to The Duchess Fund.

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PORCINE STRESS SYNDROME - PART II 

NOVEMBER, 2000

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.

References:

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
GeneScreen
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.

  1. Contact Ed Kenney at Swinetics, phone 877-440-0894 who will register you free of charge.
  2. 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.

Due to additional questions raised concerning Porcine Stress Syndrome, we
are now working on Part III. If you have any question(s), please submit to
us so we can include yours as well. Remember, there are no dumb questions
except the ones not asked!

If you need additional information, please contact us (below).

The Duchess Fund is a non-profit 50l(c)(3) corporation whose purpose is to enlarge the amount and enhance the quality of data available to the individual practitioner relative to the care and needs of potbellied pigs as long term companion animals. Your donations make it possible for us to continue our important work and obtain our goals and accomplish our objectives.

The Duchess Fund
408 - 14th St. S.W.
Ruskin, FL 33570
813-641-3013
FAX 813-645-1625

Copyright, November, 2000 The Duchess Fund All Rights Reserved

A COPY OF THE OFFICIAL REGISTRATION AND FINANCIAL INFORMATION MAY BE OBTAINED FROM THE DIVISION OF CONSUMER SERVICES BY CALLING TOLL FREE WITHIN THE STATE. REGISTRATION DOES NOT IMPLY ENDORSEMENT, APPROVAL, OR RECOMMENDATION BY THE STATE. THE NUMBER FOR THE DIVISION OF CONSUMER SERVICES IN FLORIDA IS 800-435-7352. Registration #SC-11271 The Duchess Fund does not utilize any professional solicitors. 100% of contributions go directly to The Duchess Fund.

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More Precision in Control of Intramuscular Injectable Anesthetics in Swine by D. Bruce Lawhorn

In swine destined for human consumption, veterinarians correctly stress that the ham muscles are not to be used for injection because any lesions in this area will reduce the value of a major portion of the pork carcass. The neck muscles and subcutaneous areas behind the ears and the lose skin in the axillary spaces of the front or hind limbs are excellent sites for antibiotic and deworming injections and vaccinations (always follow product label instructions for injection site). However, intramuscular injection of tranquilizers such as xylazine and anesthetics such as TelazolR and ketamine have the most predictable onset of action, duration of anesthesia and recovery time when injected into the ham muscles. Tranquilizer and/or anesthetic injection using the neck muscles in obese potbellied pigs or even lean show swine seem to be more poorly absorbed and often necessitate repeat administration to achieve an acceptable plane of anesthesia or restraint, and makes the recovery time prolonged. The worst scenario is lack of anesthetic control when previously injected drugs suddenly exert their action and cause the plane of anesthesia to become too deep. At this point, resuscitation may be required.

In addition, every possible advantage should be sought before anesthetizing Sus scrofa. Fast the animal for 12 to 24 hours and withhold water 4 hours prior to the procedure. Aspiration pneumonia in non-intubated pigs (intubation is difficult in pigs) is a real risk Preanesthetic injection of atropine (0.05 mg/kg IM) has been recommended to reduce salivation induced by inhalant anesthetics such as halothane. It has been reported that xylazine prevents salivation induced by TelazolR or ketamine. Clinical experience with xylazine and TelazolR anesthesia in swine substantiates this reported claim.

Perform a physical exam to rule out obvious problems such as pneumonia, that significantly increase the odds for anesthetic death. Also obtain a history that includes tolerance to exercise and on the pig's arrival to the clinic walk it around to observe for signs of respiratory distress or muscle tremoring. Pigs with pneumonia will usually cough after light exercise. Heavily muscled show pigs may display signs of Porcine Stress Syndrome (PSS) such as stiffness, muscle tremors, extremely rapid elevation of body temperature (PSS also called malignant hyperthermia), vasodilation and red blotching of entire skin surface (seen in white pigs), and mouth breathing when exercise stressed. The smaller the size of the pig, the better the chance for recovery from a PSS episode. This is why the history is so important. Smaller pigs may have had non-fatal episodes of PSS that can be described or "hinted at" by the owner in a thorough history. One probable nonfatal case of PSS in a potbellied pig (PBP) under isoflurane gas anesthesia has been documented, and another PBP case with a fatal outcome during a routine spay was recently diagnosed PSS positive and confirmed by a DNA blood test at Marshfield Laboratory. PSS genes are inherited in association with heavy muscling, therefore light muscled breeds, such as the PBP, are expected to have a low prevalence of this genetic defect. However, if PSS cases continue to be reported in PBPs, extensive inbreeding could be the cause.

Care must be exercised in blood sampling a suspected PSS pig since any stress such as restraint may trigger the syndrome and cause death. Alternatively, the sire and dam may be blood sampled and tested. If both parents are carriers (have one PSS gene [heterozygous] ), 25 percent of a litter will carry two mutant genes and be PSS animals (homozygous recessive), likely to express PSS signs after stress and die; 50 percent will be carriers and 25 percent will be normal. If one parent is a carrier and one is normal, 50 percent of offspring will be carriers and 50 percent will be normal. Carrier swine do not express malignant hyperthermia of PSS when stressed.

Two labs currently offering the PSS test are Marshfield Laboratory, 1000 North Oak Avenue, Marshfield Wisconsin, 54449 (800-222-5835) and GeneScreen, 2600 Stemmons Freeway, Suite 133, Dallas, Texas 75207 (800-752-2774). Marshfield requires at least a 2 ml EDTA blood sample that is refrigerated and sent overnight with coolent, but Genescreen uses a testing procedure requiring only several drops of blood on a card that may be sent unrefrigerated in an envelope (also will accept whole blood EDTA samples). Obviously it is much easier and less stressful to obtain several drops of blood from a needle prick of ear vein or other area than to collect larger quantities. However, remember that any amount of stress on a PSS pig may cause expression of the syndrome and possible death. Both test are expensive but registration (registration instructions available from either lab) slightly decreases the cost.

Swine recovering from anesthesia seem to take at least 6 hours to regain adequate thermoregulatory ability. This means they are susceptible to hypo- or hyperthermia depending on their recovery environment. Show swine are commonly anesthetized in a trailer and transported before completely recovering from anesthesia. PBPs may be anesthetized at the client's home with recovery observation assigned to the owner. On days with temperature extremes, swine recovering from anesthesia are at risk for complications and death. Animals recovering from anesthesia should be observed, temperatured and turned at least once an hour until they are walking around and alert. This usually takes 2 to 6 hours with IM anesthetics. Monitoring recovery is best performed by veterinarians or professional staff that can recognize hypo- or hyperthermia and other complications and take appropriate actions.

Injectable anesthetics in swine can be safely and effectively utilized if the previously discussed practices are considered and implemented to fit into each practitioners routine of swine practice..

From Bruce Lawhorn, DVM, MS, Associate Professor and Extension Veterinarian, Texas Agricultural Extension Service and Dept. of Large Animal Medicine and Surgery, College of Veterinary Medicine, The Texas A&M University System; Swindle MM. "Anesthetic and Perioperative Techniques in Swine: An Update," Charles River Laboratories http://www.criver.com/techdocs/anesth.html , Spring 1994; Ko JCH, Thurmon JC, Benson GJ, et al. "Using Telazol-ketamine-xylazine anesthesia for castration of cryptorchid pigs," Veterinary Medicine, October 1994, 999-1002; Claxton-Gill MS, Cornick-Seahorn JL, Gamboa JC, et al. "Suspected Malignant Hyperthermia Syndrome in a Miniature Pot-Bellied Pig Anesthetized with Isoflurane," Journal American Veterinary Medical Association, Vol. 203, No. 10, November 15, 1993, 1434-1436; and personal communications with Barbara Baker and Jenny Blaney, The Duchess Fund, Inc. www.Duchessfund.org, Ruskin, Florida, Sept 2000.

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POTENTIALLY FATAL DISEASE DISCOVERED IN POTBELLIED PIGS by: Christina Mehra, Staff Writer, VetCentric.com

Potbellied pig owners may have cause for concern. Porcine stress syndrome (PSS), a potentially life-threatening genetic disease, thought only to affect commercial swine, has recently been found in the genes of at least one potbellied pig.

PSS is a syndrome of acute death, and signs may include progressive breathing problems, tremors and stiffness, and high body temperature. The disease causes incorrect calcium transport to muscles, which creates an excess of lactic acid as well as a high temperature. Both symptoms can be fatal. In livestock pigs, the disease usually is onset after transportation, and due to fighting, exercise, and even a hot climate.

One potbellied pig has already died from the disease and another pig, suspected of dying from PSS as well, is being tested. According to the Duchess Fund, an organization that provides medical information about potbellied pigs to the public, the first pig, known as "Case A," died during a spay procedure and a DNA test revealed the pig had PSS. "Case B" also died during a spay, but no fresh blood was available so the parents are being tested. The mother was negative for PSS, or malignant hyperthermia as it is also called, and the test results of the father pig are pending, said Barbara Baker of the Duchess Fund.

PSS has long been known as a genetic disease in commercial swine that is promoted by overgrown muscles and stress. As of yet, there is no way of knowing if Case A was an isolated incident or if the PSS gene is widespread in potbellied pigs.

"They’ve bred it out of commercial swine," Ms. Baker said. In fact, commercial breeders were able to breed the gene out of the pigs fairly easily, added Barbara Straw, DVM, Ph.D.

"It’s controlled at a single gene," Dr. Straw explained. "This gene is associated with heavy muscling."

Potbellied pigs are often kept as companion animals and how the disease got into their gene pool so far is a mystery. The pigs are not bred for food and so their muscles are not overly developed. PSS can be brought on, however, by anesthesia, which is what happened in Case A. Potbellied pig owners may be concerned because if their pig has the PSS gene, it might die from a simple procedure requiring the use of anesthesia, such as a spay or tusk trimming, Ms. Baker said.

If a pig was known to have PSS, Ms. Baker said, "you would certainly want to limit the procedures down." For example, a pig with PSS might not have its tusks trimmed as often as a pig without the gene.

A drug called Dantrolene can be used to stop a PSS attack, Ms. Baker, said but few veterinarians carry it since PSS had never been known to affect potbellied pigs.

Dr. Straw said she doesn’t think the disease is widespread among potbellied pigs; if it were, more pets would have died during spays.

It should be just as easy to breed the gene out of potbellied pigs as it was to remove the gene from the commercial pigs’ pool, but since only one case of PSS has been confirmed, this may not even be necessary, Dr. Straw said.

"It may be that very few carry this trait," she said. Even the pigs that do have the gene do not always get PSS. "Most of them get along without having an episode."

For more information:
To find out if your potbellied pig has the PSS gene, you can order a special test kit from GeneScreen, a genetic testing laboratory. The kit costs $33 (or $25 if you pre-register with Swinetics at (877)-440-0894) and contains instructions and a blood absorbent card. Once the card containing a drop of the pig’s blood is mailed back, it takes five days to get the results.
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A NEW PIG DISEASE by: Dr. John Carr, B.V.S.C., PhD, DPM, MRCVS Garth Veterinary Group. Many of you may have heard rumors of a new disease which has been seen in the UK particularly since the summer. The full name for this disease is Post-weaning Multisystemic Wasting Syndrome. The problem currently is mainly confined in Anglia and the Midlands, however, as the disease has no specific causal agent, its precise means of spread can not be determined. In general this disease should pose little risk to the pet pig population however, it is better to be advised of its existence.

Clinical Signs

As its name suggests the disease's principle sign is severe rapid weight loss in young pigs of 6-15 weeks of age. Pigs also show respiratory distress, pale skin and occasionally scour. The disease is a syndrome and this means that we do not know exactly what causes it. There is some evidence from Europe e.g. France and Spain where it has been causing problems since 1997 that a Porcine Circovirus type 2 (PCV-2) is at least partly involved.

The disease appears to infect piglets before 4 weeks of age, and then at least 5 weeks later starts to cause the wasting symptoms. The disease can also spread from the wasting pigs to other in contact pigs, with an incubation period of some 4 weeks before symptoms are seen.

Post Mortem Findings

If you are unlucky enough to have a case please contact your vet. If the pig dies, and mortality can be quite high, for your vets information, the post mortem findings suggestive of the syndrome are rubbery lungs with interlobular oedema giving a mosaic pattern to the external surface of the lung. Lymph nodes are massively enlarged indicating that at least part of the disease is due to a dysfunctional immune system. Gastric ulcers are often identified. There are tests on tissues which will confirm the PCV-2 presence.

Treatment

To date we have not come across any really effective treatment. In cases the best thing to do is to keep the pigs well bedded down to keep them warm without restricting ventilation. Soluble antibiotics seem most effective rather than using injectables as this only causes more stress so making it more difficult for the pig to fight the primary viral disease. Routine vitamins in the drinking water help the pigs to fight off the viral challenge and broad spectrum in feed antibiotics help prevent secondary infections.

Control and Prevention

PMWS is spread predominantly by pig movements therefore the risks to pet pigs are minimal assuming basic health precautions are adhered to. In particular it would be wise to isolate all incoming stock for at least 3 weeks off farm if possible and contact the supplier to see there have been no further disease problems before moving them onto your unit. Use different clothing and boots when feeding and cleaning out the new arrivals. Discuss with the breeder that there are no PMWS problems. Report any suspicious problems to your veterinarian.

URL: http://www.garth.demon.co.uk. Used With Permission From The Potbellied Pig Club, England

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DIPPITY PIG SYNDROME by: Jenny Blaney

It's spring. I can tell because the calls about Dippity Pig are coming in. The medical term for Dippity is Erythema Multiforme. Literally translated it means: a superficial reddening of the skin, usually in patches, that takes many forms. Personally, I like "Dippity Pig" better!

Symptoms

While Dippity can vary in character and severity from pig to pig, there are certain definite symptoms. These include, but not necessarily all at once:

  • A sensitivity to being touched around the back end of the pig sometimes to the point that the pig squeals when touched
  • A "hunkered-down" stance with the tail tucked between the back legs and clamped to the body
  • Weakness of and/or inability to use the back legs to the point of falling down
  • Pain, restlessness, distress

The above symptoms may or may not be accompanied by moist, red areas appearing over the rump region and extending halfway up the back toward the head. These moist areas sometimes turn into actual lesions that can ooze serum or blood. They usually run from side to side, not head to tail.

Lisle George, D.V.M. from the University of California at Davis, describes Dippity as:

"The clinical signs include squealing and inability to walk without falling down in the rear limbs. Affected pigs suddenly howl painfully, and fall with the rear limbs extended backward, and the back arched. They may pull themselves forward with the fore limbs while keeping the rear limbs extended behind them. The skin over the lumbar area is extremely painful, and the pig resists vigorously whenever the back is touched lightly. Severe responses can be evoked by blowing on the back. The skin thickens over twelve hours, and begins weeping. This forms an oval wet patch over the lumbar area measuring 5 by 10 cm."

The onset of symptoms of Dippity is often quite sudden. The weakness and sensitivity in the back legs can occur in a matter of hours. A perfectly normal pig can be incapacitated three hours later. Any skin eruptions or lesions can occur in a matter of minutes. Depending on the pain threshold of the pig and the severity of the case, the animal ends up anywhere from uncomfortable to screaming with pain.

Causes

The primary cause of Dippity appears to be stress. It is not clear whether the stress is external or internal in nature, or whether it can be self-induced. External stress could include a pig show, a trip to the vet, the introduction of a new pig or owner, a violent thunderstorm or a sudden deviation in normal routine.

There also appears to be some correlation between Dippity and exposure to the sun. A friend of mine acquired ten, white, commercial pigs who were about ten weeks old. They had been in a total confinement system, therefore, had never been out in the sun. Upon their release into the great outdoors, these white pigs all developed the "dipping" and "squealing" symptoms of Dippity, without the lesions. Was this just a case of severe sunburn or Dippity Pig?

Internal stress could mean an inappropriate diet or a change in diet, inadequate water supply, a sudden drastic change in body temperature due either to illness or climate, even the onset of a particularly hard heat cycle for the female pig. Often the triggering of a Dippity episode can be traced back to an unusual, recent event in the pig's life.

Treatment

There is no treatment for Dippity, nor is there any preventive medication available at this time since the exact causes have not been determined. Topical creams or sprays can encourage healing of the sores and lesions. Injectable drugs can be used to alleviate discomfort or pain. However, once Dippity occurs, no drugs will prevent it from running its course. The onset of Dippity is quite spontaneous. Duration of symptoms can be anywhere from 24-72 hours. Complete recovery is just as spontaneous and mysterious. Spring and summer seem to be the most common times of year for Dippity to occur. More often than not it is younger pigs who are affected - that is pigs under two years of age.

The most important thing you can do for your piggies if Dippity strikes, is to immediately reduce stress, both internal and external. Confine your pig in a suitable temperature for the time of year. A quiet, dark place does a lot to calm your pig. Low music helps to soothe also. Keep your pig well hydrated during the episode. Reassure and comfort your pig often, but complete rest is a must. Prevention of sunburn can be accomplished by using a sun screen on your pig. If lesions are present, liquid vitamin E or aloe vera gel are soothing and healing. Some vets prescribe topical 1% hydrocortisone cream. Consult your veterinarian as to the appropriateness of drugs to alleviate discomfort or pain.

Dippity can occur as a single, one-time event, or a pig can suffer multiple attacks. Seldom does it occur in older pigs, even though they may have been affected as younger kids. Perhaps they outgrow it. In seven years, I have never heard of any lasting ill effects from this mysterious condition.

For pigs who have had Dippity more than once, there is a check list available to help determine the causes and possibly provide preventive measure. For further information, contact Jenny Blaney.

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WHAT ABOUT MANGE? by: Jenny Blaney

What is mange?

Mange is a skin disease that is caused by mites, small insect-like parasites, almost invisible to the naked eye. Each species of domesticated animal has it's own species of mange mites; and, with the exception of the sarcoptic mites, the mites from one species of animals cannot live normally on a different species. However, the sarcoptic mites are transmissible from one class of animals to another. The spread of mange is most often through physical contact, such as a pig touching another pig. Bedding that holds moisture (such as straw) and cold temperatures makes it easier for the mite to survive off the pig. The sarcoptic form of mange is the most damaging, causing severe skin irritation including itching, lesions, and crusting, as well as unthriftiness. The female mite attacks her host laying eggs for about two weeks. The eggs are hatched and the mites reach maturity in another two weeks. Therefore, a new generation of mites can be produced every fifteen days. This high rate of proliferation makes the eradication of mange difficult.

Diagnosing Mange

Mange was first identified as a pest in pigs 140 years ago. It continues to this day to be a challenge to veterinarians and remains a costly proposition in commercial pig operations. Don't assume that because your potbelly is a pet in the house that the following information does not apply to your situation. The sarcoptes scabies var. suis is just as content to munch on your potbelly as a commercial pig.

Symptoms

Symptoms of mange can be anywhere from sub clinical to very subtle to obvious. Potbellies with sub clinical mange could be regarded as "carriers" with no visible signs of the parasite. These are the most difficult cases to spot. They do not rub or scratch nor do they have any discoloration of the skin. There are no "flakes" or dandruff. There are no lesions. However, when sub clinical potbellies are subjected to stress such as traveling to the vet or a show, a sudden cold or hot change in the weather, a new member added to (or subtracted from) a household, mange can spontaneously erupt. A gilt coming into their first heat can suddenly break out with mange. Symptoms of mange can be very subtle, but left untreated will develop into more obvious signs. Symptoms characteristic of mange infestation are as follows:

  • The pigs's skin is dry and scaly, like "dandruff" (potbellies are known for their dry skin making it even more difficult to differentiate between mange and a normal dry skin condition.)
  • The pig begins to rub against objects - a black pig will leave white "tracks" on the body where it has rubbed against furniture, etc.
  • Tiny bumps and/or scabs appear just under the surface of the skin most often found behind the ears, under the front legs and on the chest, between the back legs and on the ankles just about the hard hoof. These bumps become more prevalent anywhere the skin is thin or moist or both.
  • These same moist areas take on an orange cast in color, more easily seen on pigs with white skin, but present on black pigs as well. The orange color will wash off only to reappear in two or three days.
  • Ears begin to exude excessive amounts of reddish-brown debris. Ears sometimes have a bad smell.
  • Eyes have the same reddish-brown, crusty matter in the corners and sometimes on the eyelashes.
  • Eyes begin to tear, sometimes to the point of leaving tear "tracks" down the face. The pig looks like he is crying.

A pig may have all of the above symptoms without having started to scratch or rub. A pig may rub or scratch a lot with only one or two of the above symptoms. Some pigs just have filthy ears and eyes that "cry" but no other symptoms. As with most syndromes, some pigs seem to have a higher resistance threshold while other pigs are super sensitive to mange infestation.

Chronic Mange

Left untreated, a pig with some or all of the symptoms above will develop a "chronic" condition that is classic and easy to recognize. Aside form the stated indicators of mange, there are some additional signs to look for:

  • scaly, scabby, thickened skin
  • coat thin and/or actual hair loss
  • black skin becomes dark gray
  • orange cast is more prevalent
  • on top of the back between the shoulder blades will be a greasy patch due to constant localized irritation.

Since chronic and/or obvious cases of mange are more prone to being treated, I would like to focus further on the less obvious sub clinical "carriers."

Often, potbellies are vaccinated and wormed twice a year as part of their normal medical management routine. In addition many owners worm in-between those visits to the veterinarian. A pre-existing case of mange is probably kept somewhat under control in these cases, although it is never really eradicated. Therefore, lingering subtle symptoms are present but not always recognized. Skin and hair coat damage from mange mites is gradual and may be misinterpreted as due to inadequate diet and/or vitamins.

Many times I have been told of a change in temperament of the pig. The pig may become a little more lethargic, less "sweet," cranky and less tolerant of being handled. Since worming is being done at least twice a year and there are no obvious symptoms, mange is seldom considered the culprit. In almost all cases the dirty ears are the big tip-off. Proper treatments for mange, even without a confirmed diagnosis almost always results in improvement in general condition, appearance and temperament of the pig.

Treating Mange

Understanding the life cycle of the mange mite helps to tailor treatments accordingly in order to kill the mites continuously as more eggs hatch, thereby effectively breaking up the cycle. Since mites eventually find their way to the pig's head, especially the ears, I have found it necessary to treat the ears specifically and in conjunction with the rest of the pig's body. The canals in the ears are dark and moist and serve as a perfect protected environment for the mange mite. The ear tissue is very thin which makes it easy to penetrate. Often the ears will exude excessive amounts of dark red-brown debris. Similar debris is often found in the corners of the eyes and in any wrinkles about the face. Alex Hogg, DVM, University of Nebraska, shared a diagnostic approach with me:

  1. Scrape deeply in the ear of the pig with a curette or small melon baller. Get some skin and debris - sometimes you need to see a little blood to be sure you are deep enough.
  2. Put all the debris in a small, clear, plastic petri dish.
  3. Cover debris with one teaspoon baby oil.
  4. Incubate petri dish at 37°c (body temperature) overnight.
  5. The mites will come out of the debris, skin, etc. and can be observed swimming in the baby oil the next day.
  6. Place under a 10 X dissecting microscope to examine.

Ears:

My personal feeling is that mites are able to survive for a time in the debris in the ears, rather than in the ear tissue itself. The ear is the only place where debris can build up significantly without dropping off the body. By the time the mites have exhausted the debris and need to tunnel back into the skin, any mange treatment given the pig has worn off. If the ears are treated separately and simultaneously with the rest of the protocol, the whole pig clears up faster. I have had very good results with the following:

  1. Prepare a mix of ˝ hydrogen peroxide and ˝ isopropyl alcohol and put in a small plastic bottle with a tapered snout on the end. Warm solution before each use - the pig will object less.
  2. Squirt warmed solution directly into each ear. Try to rub and massage the ears to work the solution down deep into the ears.
  3. The solution will help loosen any large pieces of debris that may be lodged where you can't see. The pig will shake its head which will also help free up chunks of gunk.
  4. Try to clean as much discolored debris out of each ear. Never go deeper into the ear than you can see.
  5. Place recommended number of drops of Tresaderm® into each ear and massage. This is a dog/cat ear preparation for ear mites. It also contains an antibiotic that reduces inflammation of the sensitive ear tissue.

Note: I didn't say any of this would be easy....I'm just saying it works!

Repeat this procedure every other day for five treatments. Always clean the ears first so that the medication can get down deep enough to work. After five treatments, check ears weekly for signs of re-infestation. If needed repeat above steps for five more treatments.

There are various treatment protocols for mange on the body, depending on the severity of infestation. Injectables remain the drugs of choice since they can reach all parts of the pig, except perhaps the ears for reasons previously stated. The following, as well as the earlier described ear treatment, is based on my personal experience. As with any health issue concerning your potbelly, always consult with your veterinarian and follow his/her recommendations.

Before administering any medication to your potbelly you need an accurate weight. That doesn't mean a "guesstimate". That means actually weigh your pig. For any drug to be successful, the dosage must be accurate.

PREVENTION AND MAINTENANCE

A preventive maintenance regimen can be achieved by using a pour-on topical, an oral, or an injectable preparation designed to kill both internal and external parasites. Pour-ons work best on pigs with a fairly heavy hair coat since the medication needs the hair shaft to penetrate into the body. Frequent close examination of the pig's skin and ears should inform you of the presence or absence of mange. If no signs of mange are evident, periodic treatment according to your veterinarians' recommendations, can keep your pig mange free.

Spring and Fall seem to be the two most common times of year when manage mites are prevalent. However, depending on climate and immediate environment, infestation can occur any times of the year.

I have found the following to be effective:

Ivomec® Pour-On for Cattle and Ivomec® Injection for Cattle and Swine are ivermectin-based drugs. Ivomec® is the Merial Ltd. registered trademark for ivermectin. Another injectable drug option is Dectomax®. This is the registered trademark of Pfizer Animal Health for the drug called doramectin. Dectomax® lasts eighteen days in the pig's system. It is virtually pain free. Dectomax® may prove to be a good alternative to Ivomec® for this reason. Seek the advise of your veterinarian as to which product will produce the best result and recommenced treatment regimen.

THE OCCASIONAL OUT-BREAK

For the occasional out-break brought on by exposure to another pig or simply environmental conditions, topical or injectable preparations can be quite effective in stopping the mite in its tracks provided treatment commences early on. Use product and protocol recommended by your vet but increase the number of treatments to at least three and possibly four. Treatments must be given at proper intervals. In addition, the ears should be treated at the same time following the procedure outlined. If these protocols seem like "overkill", bear in mind that it is worth the expense and time spent, rather than dealing with re-infestation.

CHRONIC MANGE

In my experience, when mange becomes a chronic condition in pig, the luxury of a topical preparation is no longer an option. A more aggressive approach will be needed. The most effective treatment is going to be the injection and it will ultimately be the least stressful for the pig. Coupled with the Tresaderm® in the ears, the injections will need to be timed to interrupt the life cycle of the mite. The whole treatment protocol should be structured around the level of infestation, the possible exposure to re-infestation (as in multi-pig situation), and the pig's general environment such as bedding, housing, etc.

For chronic mange, my protocol is:

  1. Isolate pig(s) in question providing a clean, dry space either indoors or outdoors with fresh bedding.
  2. Begin with first injection of an appropriate dose level based on accurate weight.
  3. Begin ear treatment as previously described simultaneously with the injection.
  4. Administer second dose 10 days later.
  5. Continue ear treatments with Tresaderm®.
  6. While it is not necessary to treat the bedding, it is advisable to change the bedding at the same time each injection is given.
  7. Administer third injection 10 days later.
  8. Discontinue treating ears.
  9. Depending upon each pig's response, a fourth injection may be needed.
  10. Continue to check ears frequently for any signs of re-infestation.

Occasionally, in severe and/or long-standing cases of mange, I have encountered an additional problem. Due to self-mutilation by constantly scratching and rubbing, some pigs can break open the skin enough to set off a positive gram staph infection which further complicates their condition. This infection impedes healing, promotes further hair loss, and while mites may no longer be present, the over-all condition of the pig does not improve. In these cases antibiotic therapy has been necessary. Continue to examine the pig even after mange treatments are complete. Appreciable improvement in skin, hair coat, eyes, ears and even temperament can take as long as thirty days.

SUMMARY

Remember that mange is highly contagious from pig-to-pig through pig-to-pig physical contact. If one animal in your group of pigs is showing signs of mite infestation, the chances are others can or will be plagued as well. In multiple pig situations, a preventive mange control program should be followed. Treat all pigs on premise simultaneously at least biannually. When considering any mange prevention or control program, check with your veterinarian as to appropriate drug, dosage, and administration based on your individual needs.

Again, the mange mite can be a tough critter to irradiate. The best ammunition against infestation is as follows:

  1. Do frequent skin and ear checks.
  2. Get a timely diagnosis by your veterinarian of the presence of mites.
  3. Have a good understanding of the life cycle of the mite.
  4. Obtain an accurate weight of your pig.
  5. Consult with your veterinarian on appropriate medication.
  6. There is no short cut - all medication directions must be followed. Subsequent treatments must be given at proper intervals in order to break the life cycle of the mite.
  7. Treat ears simultaneously with Tresaderm®.

Maybe we can conquer the mange mite dilemma before another 140 years go by! After all, we humans are WAY more mighty than that pesky, microscopic mite!

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MONITORING URINARY FUNCTION by: Jenny Blaney

You, the owner, know your potbellied pig better than anyone. You, the owner, are in a unique position to observe your pig on a daily basis. It follows that maintaining your pig in a healthy state is going to be up to you. Consistent management practices will help you to quickly pick up on any deviation from your pig's normal affect and behavior. Your ability to notice changes will ultimately be proportionate to the depth of your relationship with your pet. This ability in turn will help ensure that your pig lives as long and happy a life as possible. There are some guidelines to be aware of, as well as tools available to you to help accomplish this goal.

Your veterinarian can tell much about the overall health of your piggy by examining a sample of urine. This is a relatively inexpensive diagnostic tool that can be used to monitor health over the life of your pig. Among other tings your veterinarian can check the urine for: Ph level, triple phosphate crystals, calcium phosphate crystals, protein, blood, pus and sugar. Bi-annual urine examinations over the life of your pig will provide valuable information on overall condition, nutrition, assimilation, metabolic capabilities and aging. Your veterinarian will be better able to head off a potential problem before it becomes a serious medical condition.

Collecting a urine sample from your pig is not as difficult as it may sound. As with any new activity you try with your pig, it takes some preparation for forethought. You know your pig's voiding routine better than anyone. There are sterile packaged kits (for people) you can obtain from your local pharmacy that are appropriate and convenient. Follow the directions included in the package to avoid contamination of the sample. (Any other container used for collection should be clean and dry and preferably sterile.) Collection needs to be done at the same time of day and in the same manner each time in order to provide consistent results. The best time for collection is probably first thing in the morning with a "mid-stream" catch, avoiding the very beginning of the urine stream. Discuss the "art" of collection with your veterinarian before you start, as to method, amount and delivery to his/her office. Generally, if the sample sits after collection for more than one hour, it needs to be refrigerated. The fresher the sample is when it reaches the veterinarian the better. Always collect and deliver in a consistent manner. Label, date and enter time of day on the sample.

To aid in the consistency of findings of each urine sample submitted, avoid any major diet changes for a few weeks prior to collection. If you make a diet change, wait for thirty days after the change before you collect. This applies to any medications given along the way as well. Always follow your veterinarians guidelines concerning the above.

Water consumption as well as diet affect your pig's voiding routine. The first urine sample you submit to your veterinarian should be based on what your pig is eating and drinking at present with no new changes introduced. This will provide a base for information gathered. Not all pigs are good water drinkers. If you make any changes to diet. or fluid consumption, such as adding juices to drinking water to encourage fluid intake, check with your veterinarian to see how long you should wait before taking another sample. Any changes in diet and fluid intake should be made one change at a time, with a period of time in between changes to allow for the body's adaption to that change. Again, follow your veterinarian's guidelines.

Collecting urine for examination twice yearly will make you more aware of your pig's voiding routine. You will begin to notice your pig's normal behavior before, during and after voiding. You will be better prepared to spot changes in behavior associated with voiding. Pay attention to the duration of the voiding process, whether it is a steady stream with some force behind it or just a trickle. Watch for straining or discomfort associated while voiding.

If the results of the first urine sample submitted are found to be within normal ranges, this is still valuable information. Those results will provide a basis for comparing subsequent samples taken every six months. This continued monitoring of urine will provide important diagnostic information on the overall condition of your pig as the aging process progresses. Again, consistency in collecting and submitting the sample is vital to obtaining accurate results.

There is one simple exercise that you the owner can do between urine collections. Periodically, while your pig is voiding, lay a section of white paper towel down to fully absorb the urine as it is voided. (Place the paper towel on the ground, in the litter box, wherever the pig is urinating.) Then take that piece of paper towel and lay it on any non-porous surface to dry naturally. After it has dried thoroughly, check that surface to see if the dried urine has left any cloudy, shinny, or white residue. Also examine the paper towel itself for any discoloration of the urine. If anything unusual is noted, collect a urine sample as previously described and submit to your veterinarian for examination.

You, the owner, can play a vital role in monitoring and maintaining the health of your potbellied pig. Three of the most important things you an do to make your potbellied pig experience a success are:

  • Develop and cultivate an in-depth relationship with your pig.
  • Keep your management practices as consistent as possible.
  • Develop and cultivate a mutually satisfying working relationship with your veterinarian.
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