In the last couple of years, there have been reports at veterinary meetings that describe variations on an overall theme of a low incidence of wasting and mortality in pigs postweaning.
Typically, weaned pigs arrive healthy and appear to get off to a good start. Within a few days, however, some pigs go off feed, lose weight rapidly and die within one or two weeks of the onset of clinical signs. Clinical enteric (diarrhea) or respiratory (cough, sneeze, “thumping”) signs are often minimal or absent, but pigs are observed with some combination of the following clinical signs: lethargy, inappetance, huddling and piling, head hanging or pressing, generalized or rear leg weakness, rapid weight loss and non-response to treatment prior to death or euthanasia.
Veterinarian reports indicate low morbidity (affecting 2-10% of weaned pigs), but a high case mortality (>50% of affected pigs).
News of this syndrome has recently circulated again and, because we have been working through a variety of diagnostic cases with this general presentation, we thought it would be timely to go through some examples to illustrate a range of diagnostic findings and suggest a diagnostic strategy. There are several well-known disease agents that are presenting somewhat novel clinical signs, but are not new diseases.
In this case, nursery performance had been excellent until pigs in one nursery developed clinical signs in three rooms in rapid succession over a three- to four-day period. Some 1-2% of pigs became lethargic, long-haired and weak with rapid weight loss and neurologic signs (generalized or rear limb weakness, with some downer pigs that remained alert). Eyelid edema was observed in a few pigs, suggesting edema disease. The diagnostic workup on this case showed:
• Postmortem gross lesions: Eyelid and mesocolonic edema, stomachs full of feed, colon with undigested feed, proximally, but formed feces distally.
• Microscopic lesions: Marked villus atrophy and villus tip necrosis consistent with viral enteritis; no brain, spinal cord or other lesions.
• Serum chemistry: Hypoproteinemia (see Table 1).
• Polymerase chain reaction (PCR) testing: positive for Groups A, B & C rotavirus. (PRRS, PCV2, TGE and Hemaggluinating encephalomyelitis virus negative).
• Electron microscopy: Many rotavirus particles observed.
• Bacterial: No significant growth.
• Liver and bone mineral analysis: Normal. Summary: Weight loss and lethargy secondary to rotavirus-induced maldigestion and malabsorption and hypoproteinemia due to a presumed protein-losing enteropathy.
This case is interesting for several reasons. First, despite significant lesions of viral enteritis, the pigs did not have diarrhea. Diarrhea had been observed in farrowing, so some of the lesions may have been chronic. However, the acute necrosis indicates active viral enteritis. The full stomachs and the undigested feed in the proximal colon suggest the colon was able to reabsorb adequate fluid out of the feces to prevent obvious diarrhea from developing, but the gut damage in the small intestine was severe enough to result in malabsorption and a protein-losing enteropathy.
Second, the edema was suggestive of an F18 E. coli/Shiga-toxin case, but no E. coli was detected. It appears in this case that the hypoproteinemia was severe enough to result in tissue edema.
Finally, three groups (A, B & C) of rotavirus were identified from intestinal contents from these pigs. This is not unique to this nursery, as we have been finding active enteritis from rotavirus involving some combination of the three groups of rotavirus in other nursery pigs. We are working to understand whether there is an actual increased incidence in postweaning rotavirus infections or if we are noticing it more because we are looking for it more routinely and other nursery problems (e.g. PRRS) have diminished.
2. Hemaggluinating encephalomyelitis virus (HEV; a.k.a. Vomiting and Wasting Disease)
This disease was named by Drs. Chuck Roe and Tom Alexander from cases first observed in Ontario in 1957. The causative virus was identified in Ontario by Dr. Grieg in 1962.
Obviously, this is a virus that has been around for a long time. Most pigs are exposed to HEV, but we don’t think too much about it because the infection is clinically silent. Pigs are exposed to this coronavirus while protected by maternal antibodies and, subsequently, develop their own active immunity without showing signs of disease. In the rare cases where clinical signs are observed, vomiting and wasting may be observed, clinical signs can be limited to neurologic signs or just general listlessness. Infected pigs apparently clear the virus quickly and virus isolation is challenging, but PCR and serology tests are available to aid in the diagnosis.
In a recent case at the Minnesota Veterinary Diagnostic Lab, HEV was detected by PCR from the tonsil of a postweaning pig that was observed vomiting in a nursery with a history of wasting pigs. The PCR tests for HEV were negative on pigs chronically affected with wasting, but these chronic pigs had HEV HI serology titers as high as 1:640, whereas, acutely affected pigs had negative or low HEV HI titers. Gilts and sows in the breeding herd have been mostly negative by serology even though HEV was detected in neonates with encephalitis in the last year.
In this instance, it appears that HEV could be a factor in the chronic wasting observed in nursery pigs. Other disease agents or management factors did not show up in the diagnostic investigation. The negative HEV serology in the sow herd raises the possibility that the normal cycle of passive maternal immunity and silent infection may have been interrupted in this herd. More work is needed to understand the significance of the HEV detection, but there is a history of HEV activity associated with typical clinical signs on this farm that strongly suggests a role for this 50-plus-year-old virus.
3. F18 E. coli
Another familiar disease agent, F18 E. coli, has been associated with a low prevalence of wasting in nursery pig cases from multiple states. Pigs in these cases were reported as lethargic (standing with their heads down) and lost body condition due to not eating. Only a low percentage of pigs were affected and the pigs did not have diarrhea or respond to treatment with antibiotics. The unique aspect in these cases has been the genotype of the E. coli bacteria – positive for Shiga-like toxin 2e gene, but negative for enterotoxin genes. In one case, pigs improved after oral vaccination for F18 E. coli. It bears noting that had intestine not been submitted (because pigs did not have diarrhea), the diagnosis could not have been made.
It has been tempting to try to come up with a single cause of this syndrome. However, we have identified several different causes or combination of causes that wind up with pigs looking very similar. A variety of known infectious agents can be involved in addition to other feed and management possibilities.
Reduced feed intake can result from a variety of non-infectious causes (e.g. hypo- or hyperthermia induced by transport or housing, social competition for feeder space, mycotoxins in the feed, etc.) in addition to the infectious causes identified in the case examples. The combination of careful clinical observations and a complete diagnostic sample submission is critical for identifying the cause in each case.
Diagnostic investigations must be thorough. The diagnostic testing at a lab starts with animal and tissue selection back at the farm. Kent Schwartz, DVM, indicated in his article last month ( nationalhogfarmer.com/weekly-preview/0201-six-agents-postweaning-diarrhea), samples should be taken from acutely affected pigs; sample submissions from chronically affected pigs have little or no value in determining the initial cause of the clinical disease.
For some disease agents, we need samples from very acutely affected pigs because the agent is cleared very quickly after infection (e.g. influenza and HEV). Fever is a good predictor of finding viruses if they are present.
For many viruses, virus loads are higher in younger pigs, so it’s preferable to include samples from the youngest pigs affected with acute clinical signs. Using tools such as clinical chemistries can be of value in understanding the mechanisms of unique disease processes. A full complement of tissues from at least three pigs is preferable. As noted in the cases described, failure to submit intestine from pigs without diarrhea would have resulted in a failure to diagnose the cause of the problem. Finally, it may take more than one submission to get a complete picture.
It’s unlikely, but there could also be a truly new infectious agent at work rather than just new behaviors by some old ones. Pigs have been affected by quite a few of them over the past 50 years and we’ll keep looking for more. However, after a thorough diagnostic investigation, we are able to identify known disease agents and processes to account for the clinical disease observed in most cases.
Click to view graphs.
Kurt Rossow, DVM;
Albert Rovira, DVM;
Jeremy Schefers, DVM;
Jerry Torrison, DVM
University of Minnesota Veterinary Diagnostic Laboratory