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Congressional Report Criticizes Risks at Proposed Kansas Labco

A new National Research Council report requested by Congress finds “several major shortcomings” in a U.S. Department of Homeland Security (DHS) assessment of risks associated with operating the proposed National Bio- and Agro-Defense facility (NBAF) in Manhattan, KS.

The laboratory, to be built at Kansas State University, would study exotic foreign animal diseases, including the highly contagious foot-and-mouth disease (FMD), which affects cattle, pigs, deer and other cloven-hoofed animals, and diseases deadly to humans that can be transmitted between animals and people.

Based on the DHS risk assessment reviewed by the Research Council committee, there is nearly a 70% chance over the 50-year lifetime of the facility that a release of FMD could result in an infection outside the laboratory. This release could have a $9-50 billion impact on the economy.

The Research Council report says the risks and costs of a pathogen being accidentally released from the facility could be significantly higher than that indicated by the DHS assessment.

Although the committee that wrote the report recognizes the need for a bio-containment facility to be built in the United States similar to the one proposed in Kansas, it was not required to provide judgment regarding whether the location is appropriate for the proposed facility.

The full 146-page report can be purchased at National Academies Press: http://www.nap.edu/catalog.php?record_id=13031.

Mexican Trucking Dispute Takes Heavy Toll on U.S. Pork

U.S. pork exports to Mexico have plummeted by a whopping 20% since the Mexican government added pork to its list of U.S. products it is retaliating against for the failure of the U.S. government to live up to its trade obligations.

Mexico imposed a 5% tariff on most U.S. pork imports in August, along with other U.S. products, in reprisal for the United States not complying with a provision of the 1994 North American Free Trade Agreement (NAFTA) that allows Mexican trucks to transport goods into this country. The provision was intended to become effective in December 1995.

The National Pork Producers Council (NPPC) has urged the Obama administration to expedite resolution of the trucking dispute, which first surfaced in March 2009, when Mexico imposed higher tariffs on an estimated $2.4 billion of U.S. products after the U.S. Congress failed to renew a pilot program that permitted a limited number of Mexican trucking companies to haul freight beyond a 25-mile U.S. commercial zone.

Recent data from the U.S. Department of Commerce and the Canadian government indicates that U.S. pork exports to Mexico dropped by nearly 5,500 tons from August to September, a loss of about $9 million, while Canadian pork exports climbed by almost 2,200 tons.

“The trucking issue needs to be resolved now, before the U.S. pork industry loses even more of its market share in Mexico,” says NPPC President Sam Carney, a pork producer from Adair, IA. “We’re talking about the livelihoods of American hog farmers; we’re talking about lost U.S. jobs. And it isn’t just the pork industry. This is happening to the producers of the other 98 products on the retaliation list.”

Mexico is the second-largest market for the U.S. pork industry, shipping $762 million of pork products to our southern neighbor in 2009. Since 1993, the year before NAFTA was passed, U.S. pork exports to Mexico have increased by 580%.

Bar GIPSA Leader From Work on Marketing Rule

An ethics group is raising questions about whether a former trial lawyer turned government official is making policy decisions at the U.S. Department of Agriculture (USDA) that will serve his future financial interests.

Citizens for Responsibility and Ethics in Washington (CREW) is asking the USDA general counsel to investigate after learning J. Dudley Butler, the administrator of USDA’s Grain Inspection, Packers and Stockyards Administration (GIPSA), has boasted about putting in place regulations that make it easier to sue meat and poultry companies. Before joining USDA, Butler’s legal practice involved suing the companies he now regulates.

“When he took office, President Obama issued an order closing the revolving door that allowed departing executive branch officials to cash in on their government service. While the new policy was aimed at those who lobby after leaving office, the same rationale applies here. Mr. Butler stands to benefit financially once he leaves the government by exploiting a loophole he helped create,” says Melanie Sloan, CREW executive director.

“Whether or not this meets the legal standard of a conflict of interest, it seems wrong. The Department of Agriculture should bar Mr. Butler from continued work on these regulations and the department should consider reissuing them for further public comment,” she says.

Learn more at http://www.citizensforethics.org.

When Good Pigs Die Young

A recurrence of mulberry heart disease (MHD) is likely due to a whole new set of factors. Linked to oxidative imbalance, changes in sow diets may be responsible for the damage to heart muscle that leads to sudden death in weaned pigs.

Veterinary consultant Roy Schultz of Avoca, IA, believes the mulberry heart that’s dropping pigs may be related to distiller’s dried grains with solubles (DDGS) in sow diets. And there’s good theory behind the relationship, he says.

High levels of oxidative fatty acids and sulfur in some distiller’s grains “tie up” fat-soluble vitamin E and selenium in sows, Schultz points out, leading to deficiencies in the colostrum. Without the vitamin E and selenium transfer in the sow’s milk, pigs become more susceptible to oxidative imbalance and reduced performance.

Research led by University of Minnesota swine nutritionist Jerry Shurson is measuring the level of lipid oxidation in a variety of fat sources, including DDGS.

“We’re looking at the connection,” Shurson says. “If we’re feeding diets high in oxidative fats to sows or growing pigs, we may not be providing enough vitamin E and perhaps selenium to counteract compounds like free radicals, peroxides and other things that cause cell damage and lead to increased mulberry heart disease.”

DDGS contain 10% corn oil, which in turn contains a high amount of linoleic acid, a long-chain poly unsaturate that is susceptible to oxidation and a likely contributor to oxidative imbalance. DDGS are going into sow diets at levels as high as 50% in Minnesota studies. That’s a heavy dose of corn oil for animals that never received such high-fat diets before, Shurson notes. The amount of oxidative fats depends on the source of DDGS, he adds.

Shurson’s preliminary research found that of the 32 ethanol plants tested, the highest oxidative sample was five times greater than the lowest.

“It gives an idea of the range in oxidation levels,” Shurson says. “Feeding high levels of DDGS for a continuous period with marginal vitamin E could theoretically contribute to some of these mulberry heart problems.”

Vitamin E is a natural antioxidant, but is expensive to use at high levels. Shurson is seeking funding to compare synthetic antioxidants to alpha tocopheral, the preferred and most active form of vitamin E.

Schultz suggests his clients feed synthetic antioxidants to offset any oxidation imbalance. He uses a product from Novus International called Agrado Plus. Used at a half pound per ton of feed, the product costs $1.65 to $1.70/ton of finished feed and claims to enhance oxidative balance by neutralizing free radicals.

Sensitive Hearts

Heart muscle is particularly sensitive to oxidizing agents, notes Chad Hagen, swine nutritionist and vice president of Value-Added Science and Technologies (VAST), a Mason City, IA, company he co-founded in 2007.

“It’s possible the increased incidence of mulberry heart could be due to high levels of DDGS being used in sow diets,” Hagen says. “Some sources have elevated levels of oxidized fatty acids. That said, we work with many producers who add high levels of DDGS in sow diets and are not experiencing problems with mulberry heart, which indicates there are other factors involved.”

Sulfur levels are another factor, and it is antagonistic to selenium absorption, Hagen says. VAST offers a trademarked tool called Illuminate Services that shows wide variation in sulfur levels in DDGS sources.

Illuminate is a DDGS analysis service that uses a proprietary technique to determine accurate nutrient profiles. Those profiles are added to a growing VAST database that contains thousands of samples from over 70 ethanol plants. Rations are formulated using the nutrient compositions at least cost (see http://nationalhogfarmer.
com/mag/swine-feed-value-ethanol
0515/index.html).

Hagen offers the following advice to counter sudden death from MHD:
• Select a high-value source of DDGS.
• Use organic selenium in diets.
• Make sure vitamin E and selenium levels are optimum in both sow and nursery diets. Injectable vitamin E is not necessary.
• Consider using an antioxidant product like Agrado Plus in diets containing high levels of DDGS.

With or without mulberry heart, colostrum management is critical.

“We believe it is more critical in herds with mulberry heart,” Hagen says. “Split suckling and hot boxing are important tools to ensure adequate colostrum management. We also believe that farrowing induction can reduce colostrum quality and are in favor of minimizing its use. There are also tools available to improve colostrum quality.”

If MHD is suspected, Schultz says it’s important to differentiate the malady from diseases like Strep suis, Hemophilus parasuis and gut edema. A good pathologist will see the gross lesions on the heart.

Debra Neutkens is a freelance writer from White Bear Lake, MN.

Assessing Supplementation for Mulberry Heart

While it is true vitamin E and selenium supplementation are involved with mulberry heart disease (MHD), new research at Iowa State University (ISU) points to other risk factors.

Steve Ensley, DVM, a toxicologist at ISU’s Veterinary Diagnostic Lab, says increased incidence of MHD prompted a study in 2008 that just now is being published. The investigation was triggered by the fact that MHD was not responding to vitamin E/selenium supplementation as in the past. “We had a lot of questions, including whether it was due to DDGS in sow diets or infectious agents,” Ensley says.

Production sites involved in the ’08 study were high-health herds that did everything right, he explains. Tissue samples from 83 pigs from 38 farms were analyzed for vitamin E, selenium and 13 other minerals. The farms had a history of increased MHD cases with 1 to 10% affected by sudden death.

Results of the study, “Assessment of vitamin E levels, selenium levels and presence of viral pathogens as the etiology of mulberry heart disease,” were presented at the 2010 American Association of Swine Veterinarians annual meeting. Ensley and his co-authors reported no new infectious agents were found in MHD, nor did they see a vitamin E/selenium deficiency associated with MHD.

“Mulberry heart is responsive to vitamin E and selenium, but it’s not related to a deficiency in the pig. That is pretty new information,” Ensley notes. Experimental diets had adequate selenium and sometimes levels double and triple the legal limit of 0.3 parts per million.

“We think it’s more of an antioxidant condition in rapidly growing animals,” he continues. “The reason selenium and vitamin E worked in the past was they were natural antioxidants that protected pigs from oxidative intermediates present during rapid growth.

“Now the biggest risk factor to non-responsive MHD is high-health herds — herds that did not have porcine reproductive and respiratory syndrome (PRRS), were on a good circovirus vaccination program and did not have disease pressure. When infectious agents that could potentially slow growth are removed, those were herds with high incidence that we couldn’t control, he says.”

Ensley says the window is narrow after weaning, with MHD hitting pigs at 5 to 21 days of age. Once pigs have adjusted to feed and their growth rate has stabilized, the risk is much lower.

Iron dextran injections, too, can be a risk factor, Ensley adds. Iron is an oxidant and uses some of the antioxidant capabilities of the pig.

“We don’t want to discourage anyone from increasing vitamin E levels,” he continues. “We still think it’s an antioxidant condition. But boost only vitamin E. Selenium has a narrow safety margin, so we have to be very careful. We saw selenium concentrations in the liver that approached toxicosis in this study.”

Ironically, the highest risk producer for MHD is the one doing the best job, Ensley points out. “Genetics are so high, disease control and nutrition are so good, and then boom, the animal can’t compensate for rapid growth, and we’ve got a pig that has outgrown our ability to provide nutrition.”

Circovirus Vaccines Are Modern Marvel

The disease complex called PCVAD or porcine circovirus-associated disease includes many disease syndromes involving type 2 porcine circovirus (PCV2). These other viral and bacterial pathogens manifest themselves differently in each pig affected. All North American swine herds are believed infected, but this doesn’t mean all pigs become sick.

A diagnosis of PCVAD requires an increase in mortality, demonstration of PCV2 in affected tissues and microscopic confirmation of specific cellular changes.

For most veterinarians and producers, the circovirus vaccines have been a marvel of modern swine veterinary medicine necessary to maintaining a healthy herd.

However, PCV2 vaccines are expensive and compel some producers to experiment with dosage(s). Vaccine timing is critical to pig protection, and may be complicated by vaccine strategies used for other diseases, like mycoplasma, swine influenza and PRRS (porcine reproductive and respiratory syndrome).

Case Study No. 1

The owner of a two-barn, wean-to-finish site purchased weaner pigs from a sow farm that was PRRS-virus positive but stable for the last two years. Last winter, the sow farm became exposed to another strain of PRRS virus that caused significant losses. Testing illustrated most pigs were not viremic with PRRS virus but 10% were positive. All buyers were advised to protect incoming weaner pigs upon arrival against PRRS virus, using modified-live-virus vaccine. The owner of the finishing barns followed those recommendations, but to reduce stress on the pigs, delayed PCV2 vaccination until 3-4 weeks later.

Mortality was 8% in the first barn filled with the PRRS-vaccinated pigs at 8-10 weeks post-placement, which the producer attributed to the PRRS virus brought in with the pigs. After the second barn was filled, the pigs started to experience similar problems as the first barn. At this point, the producer became frustrated with pig health and called me out to walk through both barns and collect tissues for diagnostics. A few unthrifty pigs from each barn were selected for euthanasia and sampling.

The results indicated pigs in both barns were positive for PCVAD and PRRS virus in serum. We concluded death loss was due to PCVAD from poor PCV2 vaccine timing. I recommended PCV2 vaccine be given to the pigs upon arrival, and the PRRS vaccine be delayed one week after arrival. This new vaccine schedule improved performance.

Case Study No. 2

An 1,800-sow, farrow-to-finish farm schedules quarterly visits to the sow unit and walk-throughs of all finishers. This farm is PRRS-virus negative and vaccinates the weaned pigs with a two-dose program for circovirus and mycoplasma. In reviewing a finisher closeout report, the producer expressed concerns about the gains and feed conversion of all finishing sites. All of the finishing spaces were contract finishers fed by his feedmill. Recently, he had pulled the distiller’s dried grains with solubles (DDGS) from the diets, thinking this was impacting the performance.

After visiting all of the finishing barns, we observed that finishing pigs in the 10- to 16-week age groups were stalling out. An analysis of tissue samples from the diagnostic lab indicated a mixed bacterial infection found in the lungs with PCV2 virus also present. Histopathology (tissue) exam did not confirm PCVAD, but only that PCV2 virus was present. The current vaccine schedule and procedures were reviewed. The farm was giving a half dose of a commercial PCV2 vaccine at weaning and again three weeks later. I suggested that he try using a full dose of the vaccine instead. This program has always worked well to stop the high mortality in the finishers.

We reviewed some finisher closeout reports for pigs vaccinated with the new dosing schedule. The average daily gain had improved by 8% and the feed conversion decreased by 5%. The producer was particularly stunned that a subtle change in vaccine protocols would have such a significant impact on performance.

Summary

The impact of PCV2 vaccines on the U.S. pork industry has been profound. Initially, when the vaccines were released, the availability was limited and producers tried to stretch the vaccine by cutting dosage rates so that more pigs could be vaccinated. Also, the industry has discovered that timing of PCV2 vaccines are fundamental for a successful response by the pig.

Other disease pressures are important to consider when developing a vaccination program. Consult with your veterinarian to establish an effective vaccination program for improving performance on your farm.

Nursery Pigs’ Failure to Thrive Syndrome Befuddles Producers and Veterinarians

Not all pig maladies fall neatly into a category of diseases, syndromes or conditions. Lacking notoriety, they become an “orphan topic,” which no one wants to talk about; nonetheless, they’re still there, notes veteran swine practitioner Steve Henry from the Abilene (KS) Veterinary Clinic.

One such topic is the newly weaned pig that inexplicably loses its appetite, fails to eat, then descends into a series of catabolic events that depletes its body reserves. In the end, the pig dies or is humanely euthanized because of its serious debility. In less scientific terms, Henry says these pigs simply “fail to thrive.”

As stakeholders in the pork industry are wont to do, a campaign was launched to come up with a proper name for this condition and, as often as not, a universal acronym that would be widely accepted among producers and veterinarians. A group of those stakeholders — predominantly veterinarians, diagnosticians and researchers — met during the International Pig Veterinary Society Congress in Vancouver, BC in July. By consensus, they christened the baffling disease “periweaning failure to thrive syndrome” (PFTS), which in everyday vernacular has become “P-fits.”

In a special presentation during the Leman Swine Conference in mid-September, two members of the Swine Health Management section of the American Board of Veterinary Practitioners (ABVP), Henry and John Harding, DVM, with the University of Saskatchewan, provided an update on PFTS that included a clinical definition, and explained the course of the catabolic disease in newly weaned pigs.

Clinical Diagnosis

The clinical definition of PFTS is: “A pig on a farm with no obvious clinical diseases in suckling pigs, being representative of a larger group of clinically normal pigs that are afibrile, with normal behavior and body condition at weaning and initially lacking evidence of respiratory, systemic and enteric diseases, and within seven days of weaning is not eating, is depressed, may show signs of chewing or chomping behavior and becomes progressively debilitated within 2-3 weeks of weaning,” Henry explains.

Stepping to the microphone, Harding explains how PFTS was established as the working description of the syndrome.

“The new name — periweaning failure to thrive syndrome — initially describes failure to thrive. We’re trying to leave the impression that most pigs in the nursery get on to feed and eat and grow well,” Harding explains. “The part of the definition that is more likely to be controversial is our choice of ‘peri’ (meaning around, about or through) weaning as opposed to postweaning.

“Periweaning suggests there may be some preweaning factors, or maybe even some gestational factors, that increase the pig’s risk of developing this clinical entity,” he adds. “It leaves the door open to define more clearly the preweaning factors, some related to sows, which may be involved in this syndrome.”

Course of PFTS

Before describing the clinical signs and progression of the disease, Henry was compelled to point out what PFTS is not. “It is not the scourge of 2011 for pigdom. It is not a ‘new’ disease that should concern the (retail) industry and the markets. We do not even have a new pathogen for it at this point. It is not something that we understand, even though we can recognize it. Yes, it is real; yes, it’s OK to say ‘we don’t know’ when we are asked,” he says.

Although the causes of the syndrome are not understood, an infective agent(s) is/are suspected and various research groups are investigating cases. Henry feels it is important to recognize that PFTS occurs even when standards of postweaning care are high. This clearly is not a problem of neglected care. To better understand the key clinical and pathological features of PFTS, he offers these checkpoints:

  • Clinically normal, thrifty and robust pigs are weaned at about 21 days of age and placed in nursery or wean-to-finish facilities.
  • Common industry practices assist newly weaned pigs in the transition to solid feed at weaning (e.g. small amounts of highly palatable feed offered several times a day in feeders and/or on floor mats). Free-flowing water is provided for the first few hours after weaning to ensure pigs locate it. Heat zones are provided as needed.
  • Most pigs weaned in the group readily start on feed and rapidly increase feed intake and gain with no indications of health concerns.
  • In contrast, PFTS-affected pigs are easy to visually identify within 60-72 hours after weaning. While active, alert and without fever, their flat sides and empty abdomens are a clear indication that these pigs are not eating. At this point, affected pigs often appear confused and move less.
  • Incidence is quite variable. In low-incidence situations (less than 3% of pigs), the critical early stages of PFTS may not be recognized or fully appreciated, he continues. The lack of apparent indicators of disease — diarrhea, respiratory distress, lethargy, depression — results in the pigs being overlooked. Typically, at about 96 hours after weaning, caretakers begin to recognize the symptoms in the pigs — heads down, muscles slack, some not moving for hours. Incidence is usually less than 6%, but exceptional cases may be as high as 15-20% of the group.
  • It is recommended that the gaunt, anorectic pigs be moved to a special care pen with added heat, electrolyte solution in pans, special high-milk feed supplements, moistened feed, and individual pig feeding be undertaken to entice consumption. “Unfortunately, very few affected pigs respond to this special care. They have this one-way path,” Henry says.

The Witching Hour

There appears to be a critical point in time when, if the pigs are not eating, the syndrome is irreversible, Henry says. That point in time appears to be 96 hours postweaning, and the indicators include:

  • Behavior begins to change and activity declines. Affected pigs startle, but move only short distances; do not stay with the group; and appear “confused.”

“Abnormal oral behavior includes chewing motions and, in some pigs, display of a ‘chomping’ behavior with the pig resting its head on the back of a penmate while chewing,” he adds.

“The chewing/chomping mastication behavior, which occurs after 120 hours, may be an effort to dislodge the viscous purulent material (ropey snot) in the nasal cavity, but that’s just a guess,” Henry explains.

  •  Growth of affected pigs appears to stop, while unaffected penmates continue a normal growth pattern. If an observer doesn’t see the pigs and the daily progression, it is easy to mistakenly conclude these were just the smallest pigs at weaning. In their field experiences, Harding and Henry have observed that the affected pigs were actually in good body condition at weaning, and the smaller weaned pigs tended to be at less risk of contracting PFTS.

As the disease progresses, affected pigs often stand side-by-side with their heads lowered, essentially immobile at 6-8 days after weaning. “By this time, body condition has severely declined with prominent skeletal features seen, and dehydration and the impression of pallor are obvious,” Harding relates.

The terminal phase is surprisingly long without intervention/euthanasia. Affected pigs survive without eating for 17-20 days postweaning, but they do consume sufficient water to stay alive. Mortality charts show a pattern of high death loss in the third and fourth week after weaning, followed by minimal losses. “It’s a sporadically occurring situation that comes and goes within a system or a farm,” Henry adds.

Why PFTS Persists

Henry feels the reason it has been so difficult to tease out the true causes of PFTS is “we’ve obscured it in a blame game of nutrition, genetics, mycotoxins, diseases, PRRS, poor stockmanship, bad environment, or the farrowing house people must be terrible.”

And he adds: “Part of this is a veterinarian problem. When you land on farms intermittently, like every few weeks or months, you don’t see the progression of these pigs. Unless you’re with the pigs every day in that same nursery, you can really miss them.”

Henry says this is not a new pig disease, having seen the symptoms and outcomes in more than 20 years in practice. “We use excuses like mortality is only 4%; we had PRRS, and yada, yada. Mortality associated with emaciation in well-managed farms, however, without any other overt health challenges, is really kind of startling when you think about it. All of the other pigs are doing well, but these pigs are emaciated and dying,” he relates.

“It seems to me to be more of a postweaning-location issue rather than a source farm issue. Others disagree and think it is a sow-farm-source issue. The fact is, we don’t know,” he acknowledges.

He offers this example: We can wean pigs from a sow farm onto one trailer and randomly place them at four different spots. One farm can go to heck and the other three are fine. Then, the clinical signs and mortality can disappear for long periods of time. Just about the time you get fully frustrated, it can go away and it’s gone for a while. The disease seems to wax and wane.”

Harding agrees. “One thing to keep in mind is that the location breaks are very random. We can’t predict over a long period of time which of the sources may break down. They may break down in one group, and then the next group is perfectly fine. And, in a farrow-to-finish farm with an all-in, all-out nursery and no apparent change in management, we have some groups that break down and other groups are virtually normal. It is very difficult to predict when it will come back.”

Pathology

Summarizing what they have found in pigs posted in Saskatchewan to date, Harding says the most common lesions are quite consistent across herds. They include:

  • Chronic active rhinitis (causing nasal discharge);
  • Inflammation in the stomach, but not in the esophageal region where ulcers are typically seen;
  • Fatty tissue atrophy, or a loss of fat reserves in the carcass, and mobilization of fat in the liver where it seems to stay. “There may be some enzymatic changes that would lead to fat staying in the liver and not being further metabolized,” he notes.
  • Atrophic enteritis is seen, which means in the small intestine the microscopic villi are shortened, sometimes markedly.
  • Superficial colitis, so in the large intestine and the mucosa surface, the innermost surface is inflamed.
  • Thymic atrophy. The thymus is one of the primary immune system organs located in the chest cavity as well as along the neck in the pig. “In young pigs, we would anticipate abundant thymic tissue because it is involved in the maturation of lymphocytes, which fight off infection. In cases of PFTS, the thymus is very small or non-existent,” he relates.

“A complicating issue is that many or all of these lesions can develop subsequent to anorexia and starvation. So, it’s difficult to know whether these are the primary lesions or whether they occur simply because the pig is starving and wasting away.

“We also see some other lesions — pneumonia in the anterior parts of the lungs and inflammation of multiple body surfaces. The caveat to those is they are not consistent among different farms, and, secondly, nearly all of the pigs we have looked at to date are in the terminal stages (of the syndrome).”

Generally, they go to nursery rooms that are 2-3 weeks postweaning and pick out the extremely sick pigs. “We don’t know if those last two lesions are in fact primary, or whether they are secondary to the thymic atrophy and a suppressed immune system,” he adds.

Cooperation Needed

Harding closed the emerging/reemerging disease session with these words of encouragement:

  • Collaboration is key. “We learn more by working with each other than we do by ourselves.”
  • Disease investigation involves more than just routine diagnostics.
  • Inconsistent or incomplete sampling is a missed opportunity.
  • The story is incomplete until we examine the healthy penmates.
  • Formalin (formaldehyde). “One must examine all of the major organ systems to develop a thorough understanding of the pathogenesis at hand. It is therefore essential to fix portions of virtually all organs, even if there is no apparent gross pathology,” he says.

A concerted effort will help solve this complex riddle, Harding and Henry agree.

Refocus on Biosecurity

Porcine reproductive and respiratory syndrome (PRRS) has indeed become the elephant in the room for the pork industry, forcing major changes in all aspects of biosecurity.

Producer and veterinary leaders at the Pipestone System and the Pipestone (MN) Veterinary Clinic are tightening biosecurity rules on pig production and transportation, and adding air filtration systems to stop aerosol spread of the virus in sow farm complexes across Minnesota and Iowa.

Their strategy also calls for strengthening biosecurity programs for all people who enter the farms, reports Pipestone veterinarian Gordon Spronk at the Leman Swine Conference in St. Paul in late September.

Staff veterinarians, farm supervisors and technicians have spent hundreds of hours in sow barns studying human behavior and learning how to make employees more accountable for biosecurity. Some concepts are working, but Spronk admits there are still more questions to resolve.

Early Lesson

Biosecurity protocols are relatively straightforward, but the mistakes people make are a very difficult challenge to overcome, Spronk says.

“We thought we had biosecurity protocols in place in the fall of 2008 when we filtered a 3,000-sow farm,” he recalls. “While I was standing in the entrance area, a vendor came in and placed his tool belt on the counter, showered in and followed biosecurity protocols. After showering, he opened the sliding glass door, took his tool belt and headed into the hog barn, while the farm supervisor and veterinarian were standing there.”

For Spronk, that defining moment led to rethinking biosecurity to focus more on the human element.

It starts with the farm staff knowing the status of your farm — is it PRRS negative or positive? Keep it that simple for the farm staff.

The second part is assurance that staff understands the methods of disease transmission. Refer to the Pork Quality Assurance Plus manual (www.pork.org) developed by the National Pork Board. “We can talk about internal vs. external biosecurity, for instance, but at the barn level, biosecurity in the Pipestone System is about what works to keep PRRS out,” he says.

The third step is acknowledging the importance of communication and holding staff accountable when an error is made or a machine breaks down, Spronk points out.

Employees must embrace the vision of the operation and accomplish two objectives: produce pigs because that is what makes the farm go, and be a responsible employee to keep out PRRS virus.

Avoid Mistakes

There are a few cold, hard facts about farm staffs that have led to mistakes he hopes others can avoid:

  • Failure to understand, from a pure biosecurity standpoint, that 90% of people working on any project will violate their own rules. The story about the vendor and the tool belt is a good example.
  • Failure to realize it isn’t always true that once you’ve trained people right, they will correctly follow through with a biosecurity action.
  • Failure to understand that there is more than one solution to a biosecurity problem on a farm. Listen to employees and you will learn what works.
  • Failure to realize the value of training and testing. “Now we train and give a written test immediately. If the person fails, we know that maybe the teacher is the problem the first time. But if the student continually fails, then maybe it could be a student problem,” he says.
  • Failure to understand that monitoring must take place on the farm. “This is one we still struggle with in knowing what to monitor and how to improve on it,” Spronk says.

Hire Well

Be sure new staff knows your core values and goals. One tipoff: if new hires have attendance issues, there will very likely be problems with compliance of biosecurity protocols. Confront this issue as quickly as possible to correct the situation, Spronk advises.

Lack of attention to detail in performing daily tasks is another early-warning sign. “Once the right job culture was established, we had a lot better success,” he says.

Establish written protocols and make vendors participate in the same training and testing processes for biosecurity as any employee or visitor.

“Understand that your motivation is to keep PRRS out. We test staff every month on protocols,” he says. “Then we monitor, simply showing up at the farm to look for deviations from the protocols.”

Reward good behavior and punish bad behavior. “We don’t have to reward good behavior like we do production achievements, just make a point to recognize it verbally,” he says. “We learned this the hard way. It takes pig-headed determination to be successful.”

Air Filtration Systems May Become Part of Doing Business in the Future

Air filtration systems are used successfully in hospitals and nursing homes to safeguard health, and now are on the verge of becoming a vital tool in the fight against porcine reproductive and respiratory syndrome (PRRS) virus.

Four years of research at the University of Minnesota’s Swine Disease Eradication Center (SDEC) farm at remote Holloway, MN, has made it clear to veteran PRRS researcher Scott Dee, DVM, and his team of Andrea Pitkin and Satoshi Otake, DVM, that air filtration systems hold the best chance of defeating the area spread of this decades-old disease nemesis.

Dee estimates he has devoted 40% of his professional veterinary career to stopping PRRS. He is so confident of the capabilities of air filtration in blocking the pesky virus that he offers this blunt assessment:

“With the information this technology has generated in our experimental research farm design, in conjunction with our growing body of evidence from the field, I believe it has the potential to change the industry as it pertains to the control of respiratory diseases of pigs.

“For example, if we can prove sustainability over a sufficient period of time, along with a healthy return on investment as current buildings are retrofitted or built new, they will be equipped with filtration. As our research progresses and new technologies come forward, the systems will become cheaper to install and operate. I believe lenders will see this intervention as an effective means to reduce risk and promote it as a good investment in disease prevention that will enhance profitability.”

Airborne Spread

In 1999, Dee left private practice at Morris, MN, to study PRRS virus transmission and biosecurity at the University of Minnesota. By 2005, he had become very frustrated. Despite research on flies, mosquitoes and transport, proving that a variety of fomites and vectors could spread the PRRS virus, hog farms were still becoming infected with the virus on a regular basis.
Meanwhile, the concept of winds carrying the tiny virus from farm to farm was being hotly debated. There were skeptics who didn’t believe in aerosol spread of the virus — Dee included.

“I didn’t believe it because I couldn’t reproduce it, and it wasn’t for a lack of trying,” he recalls.

Then Dee and former graduate student Jenny Cho, DVM, embarked on a project to determine whether the virus’ ability to infect pigs via airborne spread was strain-dependent. At the time, a recently emerged, highly prevalent strain of PRRS virus, MN-184, was seemingly wafting its way across the countryside and infecting hog farms at will.

In a project comparing the ability of aerosol spread of MN-184 and a less virulent strain, the research team recorded a significant difference in the frequency of virus shed and transmissibility via the airborne route in pigs infected with the MN-184 virus.

“We showed that pigs would get infected via the air with MN-184, and we couldn’t accomplish that with the milder strains,” Dee adds.

Research Model

To build on those findings, Dee hatched the idea of building a production region model to resemble the southern Minnesota hog-dense counties that have been plagued by PRRS virus reinfections.

Using small, modular buildings from Double LL Corp., paid for by PRRS CAP 1 funds provided by the U.S. Department of Agriculture, the goal was to evaluate various routes of PRRS virus transmission and biosecurity in Year 1; Pitkin led this effort. By Year 2, Mycoplasmal pneumonia was added to the mix as industry interest and funding for the project grew. Otake then joined the team to carry on Pitkin’s efforts.

In the model, Building 1 was established as the 300-head source population, to raise pigs from 50 lb. to market weight in a continuous-flow, mechanically ventilated barn where pigs were experimentally infected with PRRS and mycoplasma.

Building 2 served as the non-filtered control unit, matched in every way to the other test barns to represent “industry standards” for biosecurity — except it lacked air filtration.

Building 3 tested mechanical filtration and electrostatic filtration. Mechanical and electrostatic filters capture particles in their fibers, preventing them from moving forward.

Building 4 tested antimicrobial filtration. Antimicrobial filters coat particles that pass through the fabric of the filter with antimicrobial compounds to kill pathogens.

Buildings 2-4 housed pigs starting at 25-30 lb., 10 pigs/building.

The filtered barns were sited about 360 ft. downwind, southeast from Building 1 (source barn), in order to maximize exposure to the northwest prevailing winds, Dee explains.

Last year, two other PRRS strains (1-18-2 and 1-26-2), common to southern Minnesota and northern Iowa, were added to the challenge.

“We wanted to see what a mixture of viruses would do as far as airborne transmission goes; it’s common for farms to have a mixture of several PRRS strains within the finishing population,” he observes. “Using this model, we have demonstrated the ability of PRRS virus to travel out to 5.5 miles in the air.”

The test buildings were outfitted with filters to reduce the risk of airborne spread of PRRS and mycoplasma, including prefilters to screen out visible objects, including dirt, dust, bugs and other debris. A double-door entry chamber was installed to prevent introduction of outside “dirty” air.

Other Biosecurity Efforts

A biosecurity program is more than just installing filters. It includes taking other precautions, training and auditing personnel, and making sure other potential routes of infection are blocked, Dee says.

“Clearly, the question is not whether the filters work or whether the data behind their validation is accurate. It’s the implementation at the farm level that will make this procedure successful,” he adds.

When workers enter the research buildings, their skin, coveralls and boots are swabbed “to prove that people aren’t ‘walking’ the virus into the building,” he explains. All incoming supplies are fumigated, stored during downtime, and then swabbed prior to use. Personnel shower and work in the filtered, non-infected pig rooms first before moving into the infected control barn. The small buildings are run all-in, all-out.

A single truck picks up PRRS- and mycoplasma-negative weaner/grower pigs from an isolated, off-site area in northern Minnesota to be used in the trials. After each four-week replicate, buildings are emptied, washed and disinfected, and pigs are moved to the continuous-flow, source population finishing facility to maintain virus circulation in order to produce contaminated bioaerosols that will challenge the filtered buildings.

Air inlets are also screened to block insects. An exterminator visits monthly to keep out rodents. Although rodents don’t carry the PRRS virus, they could damage expensive filters and compromise filtration effectiveness. The feed truck only delivers hog feed to this research farm and otherwise delivers cattle feed. An on-farm incineration enclosure is used to dispose of mortalities. Manure pits are pumped out by a septic system service.

Co-investigators Pitkin and Otake, who both earned advanced degrees under Dee, have been very dedicated to developing and testing PRRS virus control and biosecurity protocols. Banks of security cameras on the farm encourage compliance.

The research farm is located 10 miles from the nearest hog farm. The owner of that farm monitors his pigs monthly, and they have remained negative for PRRS virus and mycoplasma during the four-year project.

Impact of Weather

After the first year of air filtration research, a weather station was installed to determine optimum climactic conditions for PRRS or mycoplasma transmission via the airborne route, he says. The station measures direction and speed of wind, levels of sunlight, barometric pressure, temperature and humidity.

“When there is an air-transmission event occurring in the non-filtered control facility, we can access data from the weather station and determine the meteorological events associated with this event,” Dee explains.

Conclusive data shows that spread occurs optimally on cool, cloudy, humid days when there are light, directional winds but with slight gusts, he says. The PRRS virus moves best when temperates range 30-45°F and humidity averages 80%, with 3-4 mph winds and gusts of 6-8 mph.

Dee says the common theory is that aerosols from pigs exit a building in a plume that moves slowly across the landscape. The virus survives well in low-light, cloudy and foggy conditions, but becomes dispersed on sunny, hot, windy days.

Climactic risk factors are described in Table 1.

Filtration Results
The last pigs in the air filtration trials left the research farm in early November, so the final results are being tabulated, Dee reports.

In four years of research at the site, Dee estimates there have been 1,450 days of data collection on over 4,800 pigs with 36,000-plus PCR (polymerase chain reaction) samples collected, including air, personnel, fomites, transport and insects, which were all tested for PRRS and mycoplasma.

But the evidence is clear that with all filter types used, not a single case of PRRS virus or mycoplasma infection resulted from any of the filtered facilities, he affirms.

Sow Farm Research

Further support for air filtration is provided by work with southern Minnesota veterinarians Paul Ruen at Fairmont, Gordon Spronk at Pipestone and Darwin Reicks at St. Peter. The project is funded by the USDA PRRS CAP 2, the National Pork Board and the Minnesota Pork Board.

“These clinics have been the national leaders in the application of filtration, first to boar studs and now to sow farms in southern Minnesota and northern Iowa,” Dee says. These boar studs have remained PRRS-free for almost five years and now the focus has turned to the sow farm.

In the third year of a four-year study, 10 sow farms are filtered and 26 farms are non-filtered control herds, matched in the frequency of outbreaks, the size and the density with the surrounding area.

Interestingly, during the study period, 92% of the non-filtered sow farms have broken with PRRS, including half that broke with the virus several times, he notes.

“We have learned that while very effective at aiding in the prevention of airborne infection, air filtration is not magic. It cannot stop PRRS virus infection due to other routes, such as contaminated transport, nor can it prevent the non-compliance of personnel,” Dee adds.

Cost Factors

The knock on air filtration systems for hog barns has been the big cost, Dee admits. When amortized over five years, the cost averages about $2/pig. Well-publicized data shows PRRS breaks cost in the range of $5-15/pig, not to mention the emotional toll of dealing with high mortality rates.

“As we accumulate more data, there is a growing interest in adapting technology of air filtration to farms, especially those in swine-dense regions with a history of annual breaks and the high-level frustration that goes with it,” he points out. “We have been making regular visits to the filtered farms in the study, asking them how it is going, and if the new level of biosecurity has caused them any problems. Basically, they are so happy not to have PRRS and are willing to work very hard to keep a break from happening again.”

Filters cost $125 apiece, prefilters $3-4 or more each.

The disease-free cull gilts or barrows used in the trials were provided at no charge by Genetiporc.

Results are Promising

A commitment to shutting down PRRS transmission can succeed using air filtration, provided biosecurity is solid, according to results at the Minnesota swine research farm that are being validated in the field.

“Filtration works. There is no doubt about this. We have proven that here at the farm and in the field under very challenging conditions,” Dee says. “While we still need more time to truly assess its value, the preliminary results are very exciting.

“It’s the implementation that is the current challenge; however, we feel that with proper training and oversight of highly motivated farm personnel, this tool will enhance the long-term success of area/regional control and elimination programs for this economically significant disease, as well as others that travel between farms via the airborne route.”

Suckling Pig Diarrhea Drains Profits from Farrowing Operations

Suckling Pig Diarrhea Drains Profits from Farrowing Operations

In these times of tight margins, every 50 cents to a dollar earned from every pound of pork produced is important to the financial stability of a hog operation, says swine veterinarian Doug Groth of the Carthage (IL) Veterinary Service, Ltd. (CVS).

“This year we are just trying to make more money to make up for the last couple of bad years,” he said in a talk at the CVS 20th Annual Swine Conference at Western Illinois University in Macomb, IL. “The goal is all about getting pounds of pork out the door.”

In the past few years, baby pig diarrhea has emerged as a major contributor to burned-out pigs and elevated preweaning mortality, Groth says.

Rotavirus Tops the List

The big three contributors in CVS’ clientele of herds in the mid-south and southern United States consist of rotavirus, clostridium and coccidia, often linked to secondary infections of E. coli.

“Rotavirus Type A has been the traditional rotavirus we have seen for a long time, and the oral vaccine has been effective in the sow herd to reduce suckling pig diarrhea,” Groth states.

Complicating that scenario has been the appearance of Type B and C rotavirus, which produce the same watery diarrhea and vomiting as Type A in young piglets, but which can’t be reproduced in the laboratory to determine their true pathology or means of causing disease, he says.

Summary data from the University of Minnesota Veterinary Diagnostic Laboratory for 2009-2010 (Figure 1) shows that cases have spiked in the last 6-12 months. “That reflects what we have been seeing in our practice, a doubling of cases that shows this is a significant disease factor in the industry,” Groth says.

Equally troubling is the fact that once pigs are infected with rotavirus, there is severe damage to intestinal villi, (tiny hair-like structures in its intestine that help the pig retain fluids), with this viral infection, which produces the watery diarrhea and severe dehydration.

“The infection just has to run its course, and work its way through the pig. You treat that type of scours with antibiotics for the secondary problems like E. coli. This provides time to restore the damaged pig’s villi,” Groth explains. Injections are sometimes easier to administer than picking up pigs for the oral drench and waiting that extra second to make sure they have swallowed it, he adds.

Feedback is one of the standard practices for rotavirus control. Common practice is to grind up intestinal tracts from pigs that have died from the disease, mix in scour material and feed the contents to sows before farrowing. This helps establish good immunity in sows and provides protection to the piglets via colostrum.

“This method still works for traditional Type A rotavirus, but we have found that it does not provide very good immune generation for the Type B and C strains,” Groth points out.

All of the types of rotavirus described typically strike at 2 days of age. If the pigs are 3-4 lb., they have a better chance of surviving than if they are 2.5 lb. or less, he explains.

Clostridium, Coccidia Causes

Clostridium bacteria (Type A and difficile) are also frequently identified with rotavirus. When these two are linked, it usually means death for the piglet. Clostridium perfringens Type A can be treated with autogenous vaccines or antibiotics with mixed results.

A third piglet type of scours is due to coccidia, a parasite that produces scours at 7-8 days of age or older. Sanitation sometimes produces mixed results, but power wash, disinfect and dry crates to achieve maximum results and attempt to prevent transmission from one litter to the next, Groth suggests.

Coccidia produces spores that can persist in the environment for long periods. High concentration of bleach along with vigorous cleaning can beat down the spore population. Flaming crates using an LP torch to achieve high temperatures is an extreme measure to kill spores and other bacteria, he suggests.

An oral paste product called Marquis from Bayer Animal Health has produced the best results. “It is the only thing we have found that works to prevent coccidia,” he says. This product is available by prescription in swine, due to off-label use.

Accurate Diagnosis is Critical

Not every case of suckling pig diarrhea can be traced to a disease pathogen, according to Groth. The sow may be sick or the energy levels of her feed could have changed — both of which can affect piglet ability to absorb nutrients and result in scouring.

That’s why the first order of business when scours appear is to determine whether it is disease- or management-related. Perform a few necropsies, send tissues to the diagnostic lab and obtain a good workup that will provide an answer, he says. The lab is best equipped to perform both bacterial and viral isolation assays. The goal is to find the primary pathogen so a course of treatment can be prescribed.

“If there is a lot of diarrhea litters, the scours could be due to Transmissible gastroenteritis (TGE),” Groth says. “At first, it may just affect a few litters, but in a very short time it will become very explosive — the whole farrowing house will be scouring and it will smell bad,” he explains. TGE is still typically a wintertime virus carried by birds. Most U.S. herds are very susceptible to TGE because they haven’t had it.

Management Factors

The severity of the nursing pig diarrhea challenge can depend on the level of care or farrowing house management. The facility, staff and stressors each play a role.

Make sure farrowing rooms are set up prior to loading sows. Heat lamps should be positioned, heat mats warmed to 85-90°F and hot boxes cleaned and disinfected. Mistral powder can be used on mats and in boxes to help dry off pigs.

“With the same genetics at two different farms, there can be a different incidence of scours, and it often ties back to people and individual pig care,” Groth says.

In Professional Swine Management (PSM) sow farm systems, the goal is to aggressively focus on individual pig care as young at Day 1-2 to find those one or two pigs starting to scour. Sometimes a small pig in the litter or one that is nursing a hind teat will start scouring, while the rest of the litter looks perfectly fine. If the whole litter is scouring the next day, that’s a much bigger challenge to correct, he notes.

At the first signs of scouring in a litter, Groth suggests flagging the litter and creating a scour treatment card. All pigs in that litter are treated for scours for three days. If there is a response during treatment, that is noted on the card. If there is no response, a different antibiotic is tried. Groth suggests treating piglets one extra day after scours dry up to ensure health.

Watch for yellow staining on pig’s butts as a sign of scours, but don’t be fooled if that is observed in full-bodied pigs actively nursing. Pigs can look healthy one day and still have scours and nurse, but not be absorbing nutrients and look dehydrated the next, he warns.

At PSM farms, preweaning mortality ranges from 8-12%, but it can quickly jump much higher, even to 25%, with severe cases of rotavirus. The goal is to hold mortalities under 8%.

At weaning, a lot of scouring litters will have recovered to become productive pigs, but they may average a pound or two less. Others will survive, but never fully recover to become viable pigs. It is these pigs that should be humanely euthanized, Groth says.

Sometimes pigs are just shy of meeting that 8-lb. minimum weight requirement at 21-day weaning. They will often be placed on a nurse sow until 25 days of age. “With that extra four days, if they definitely are not weighing 8 lb., then they are not going to be in the production flow system,” he emphasizes.