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.