Herd Health: What to do about post-weaning pigs that fail to thrive?

Sunday, April 5, 2009

Many remedies have been tried to alleviate what some call 'Post-Weaning Catabolic Syndrome' but with limited results

by S.ERNEST SANFORD

At the last University of Minnesota Leman Swine Conference in September 2008, a panel consisting of Drs. Luc Dufresne from Seaboard Foods, Steve Henry from Abilene Animal Hospital in Abilene, Kan., and Tom Fangman from Boehringer Ingelheim (USA) presented their collective findings on an evolving syndrome of post-weaning pigs that fail to thrive. They labelled this "Post-Weaning Catabolic Syndrome." 

The "failure-to-thrive pig" is defined as a pig which appears normal and well-grown at weaning, but within the first five days post-weaning loses body condition, remains alert and maintains normal vital signs, then progressively catabolizes (metabolic breakdown of body tissues) fat and muscle tissue over the next two to three weeks, becomes emaciated and dies or has to be euthanized.

Three weeks later, a strikingly similar syndrome was described by Drs. Henry Gauvreau and John Harding at the Western Association of Swine Veterinarians annual meeting in Saskatoon. They named their case "Post-Weaning Starvation Syndrome." 

The presenters at the Leman Conference agreed on the following consensus observations:
• The pig is weaned with robust glucose and fat stores.
• The pig may not know how to eat solid food or consume water from available appliances (in other words, the pig has to learn how to do this).
• The affected pig has a large frame and relatively high body mass for its age, thus high maintenance demands.
• The pig becomes anorexic (loss of appetite), perhaps due to microbial illness, but often not.
• The anorexia, which is seemingly irreversible (even with intense feeding efforts) results in glycogen depletion, which leads to depletion of fat stores and skeletal muscle protein. The byproducts of fat metabolism accumulate in the liver, resulting in development of fatty liver disease.
• Pigs become depressed and lethargic, but only towards the terminal, end-stage of the syndrome. Ketonuria (ketones in the urine, not a good sign) is observed in some pigs.
• Death usually occurs 14-17 days post-weaning.
Death is not due to classical "starvation" as fat stores are present but could not be metabolized, leading to some suspicion that this may be an abnormality in fat catabolism.

Early intervention with glucose/glycine combinations, used sparingly and in a pulse fashion, can reverse the course in some percentage of these pigs (best results around 60 per cent, usually more like 30 per cent).

The observation that glucose-fed pigs will soon return to activity and eating pellets (at least for a couple of hours before they crash) emphasizes the importance of improving our understanding of energy metabolism in these pigs.

The panel agreed that the affected pig, in good bodily condition at weaning, becomes gaunt, anorexic and remains afebrile (no fever) for three to 10 days post-weaning while continuing to be active and alert. But it then progresses to a "thin-as-rails" condition by 14 days post-weaning and usually dies by 17 days post-weaning.

Necropsies reveal a fatty liver, liquefactive necrosis of fat around internal organs and depletion of fat reserves. Ketones are often, but not always, present in the urine. No feed is in the gastro-intestinal tract, feces are pasty and scant, and many pigs appear not to have eaten since being weaned. 

Affected pigs are unlikely to have eaten creep feed, even though it was offered. The presenters emphasized that the "catabolic syndrome" pig is well-conditioned and well-framed at weaning.

Furthermore, the smaller, less well-conditioned pigs are rarely affected by the "catabolic syndrome" unless they are crippled. Specific infectious disease agents are seldom involved. When disease-causing agents are identified, specific intervention (vaccination, strategic medication, depopulation or adjustments to pig flow) corrects the problem, leaving the true "catabolic syndrome" pigs who continue to fail to thrive.

A few other less common observations were:
• Affected pigs may be coming from certain specific sow herds.
• Males are more frequently affected than females.
• PRRS virus, rotavirus and swine influenza virus (SIV) may or may not be diagnosed in some cases, but do not appear to be major contributors to the syndrome.

So what causes the catabolic syndrome? The quick answer of course is that we do not know yet. But there are many theories, suggestions and speculations. Among these are:
Cytokines. These are cellular mediators which regulate many functions in the body at the cellular level and are critical in protection of the host. Many cytokines, however, can also have a negative effect which can lead directly or indirectly to anorexia, cachexia (loss of body condition) and even kill rather than protect the host.

Some cytokines can suppress fetal skeletal muscle growth prenatally, resulting in lower birth weight. It is hypothesized that piglets from larger litters could have higher levels of these cytokines. Chronic infections with certain disease agents (PRRSV, Mycoplasma hyopneumoniae, etc.) also release cytokines, which suppress muscle growth.

So, could we have created this syndrome by selecting for large litters? Could this, compounded by high disease challenges (PRRS, SIV, PCV2), have resulted in hyper-production of some of the cytokines with negative impacts?

Nutrition. Reduction in budgeted, nutrient-dense diets for cost saving reasons may also be contributing to a pig not being able to get off to a good start post-weaning.

Specific and non-specific interventions have been tried to alleviate this "catabolic syndrome." Some of the specific efforts have included hand feeding pellets in gruel to gaunt pigs, using milk feeders and milk replacer, supplying dextrose and electrolytes and multi-day supplementation with concentrated glucose/glycine solutions. Also returning to more high nutrient-dense diets and introducing better transition diets.

Results with any and all of these interventions have been equivocal at best. At worst, they have not resolved the problem in the majority of cases.

Non-specific interventions have included the old stand-by of mass-medication with various antibiotics at weaning, followed by individual therapy as pigs fall back post-weaning. In addition, Corticosteroids and anti-prostaglandins have been used, all of the above without significant impact on the syndrome.

Although the group at the Saskatoon meeting was in general agreement with the findings reported at the Leman Conference, one significant departure was that they identified on several occasions the presence of a calicivirus in the pigs affected with the catabolic syndrome. They went further in that they named their syndrome "Post-weaning starvation syndrome," while the Leman Conference group was emphatic in stating that it was not a starvation problem.

Caliciviruses are known to cause diarrhea in pigs and another disease similar to foot-and-mouth disease, but the calicivirus described here seems to be different from those two known caliciviruses in pigs. The significance of the calicivirus remains unknown at this time.

So are we dealing with a syndrome waiting for a specific name? One thing that is clear is that we've all seen these types of catabolic, "failure-to-thrive" pigs for decades. My simple explanation over the years has been that these are pigs which have benefited most from momma's milk while suckling, so they have had no need to go after creep feed.    

They are at a loss when they are ripped away from momma at weaning and they don't know how to fend for themselves. It takes them too long to figure out the feed and water bowl systems and by the time they do they are in a negative situation and fade.

Although a certain percentage of "catabolic syndrome" pigs do fit into this scenario, it is clear that the vast majority of pigs are not in this category and the veterinarians are describing something that is different and apparently new in these "failure to thrive" pigs.

Stay tuned, for further developments and, hopefully, explanations that will solve this latest dilemma. BP

S. Ernest Sanford, DVM, Dip. Path., Diplomate ACVP, is a swine specialist with Boehringer Ingelheim Vetmedica (Canada) in Burlington.