Latest Porcine Epidemic Diarrhea (PED) and Transmissible Gastroenteritis (TGE): INFLUX or REDUX?

San Miguel Animal Health Care Corner





Latest Porcine Epidemic Diarrhea (PED) and Transmissible Gastroenteritis (TGE):


Eugenio P. Mende DVM MSc

Veterinary Services Manager, San Miguel Foods Inc.


 Another Outbreak in the News

 “Mga baboy sa Bulacan, tinamaan na naman ng panibagong outbreak!”

Banner news like this especially if shown on primetime national television always create waves of panic among hog raisers and players in the industry. Shortly thereafter, text messages began to traffic my inbox. Our B-MEG text hotline (TANONG MO, I-TEXT MO and send to 0922-999-BMEG or 0922-999-2634) then became loaded with pressing questions that warranted urgent replies from our SMS Response team. Our B-Meg website consultancy box ( then click Ask Doc E section) suddenly became full. Discussions at the PCCARD website on swine issues thickened. A news item is delivered supposedly to inform. But in an industry where more than 70% is backyard, any news on disease outbreak, at least if reported to kill their pigs, will inevitably cause panic.

“Bagong sakit na naman ba ito?”; “Aabot kaya ang outbreak na yan sa area namin?” ; “Mas mainam bang ibenta ko na lang lahat ng baboy ko dahil balita ko malapit sa amin ang tinamaang farm na yan?” ; “Ano ba ang PED?”; “Ano ang gamot sa sakit na yan?”; “Paano maiiwasan ang outbreak na yan?”.



The Killer Diarrhea

It was reported in that news that the causative agent of the explosive diarrhea which infected suckling pigs was Porcine Epidemic Diarrhea (PED). As far as I can remember from watching that news segment, the reporter did not elaborate how his report came up with the definitive diagnosis. I also did not remember that news getting the side from any proper technical authorities to confirm the diagnosis, present disease prognosis and identify probable action plans (In succeeding follow-up news though, they already involved veterinarians). It was clear to me then that vaccination (I supposed to PED) was part of the control programs in that farm.


PED, if indeed true and was the agent killing pigs in that farm is nothing new. In late 2006 to early 2007, our technical group was busy dealing with Coronaviral diarrhea cases (where TGE and PED belong). We maximized the opportunities then of working with and learning from the not only few breaking farms who seek our assistance. We conducted trials as to the best protocol and practice for intestinal feedback that could provide maximum lactogenic immunity for the piglets (If you want a copy of the full feedback protocol as reference, please feel free to contact me). We also conducted a crude trial involving more than 40 sows to determine the optimum gestating days to perform the feedback program in sows. Feedback program performed at the most optimum gestating days resulted to producing hyper immune piglets as measured by survivability and morbidity up to weaning (check PVMA 2007 proceedings). B-Meg also conducted 12 regional technical forums geared towards making our customers understand the intricacies of the virus and to ensure that our customers knew that they have choices of solutions for the outbreak.


To sum it up, we’ve had many successes with the appropriate intestinal feedback program we applied or recommended in those breaking farms. I guess many practitioners could also attest that as long as feedback is executed properly, it does work very well. A few that failed, looking back, can only blame either poor execution, vague understanding of the virus, multi-factorial co-infection, poor herd immunity due to maximum herd stress or even wrong diagnosis. A major example is coccidiosis epidemic (Isospora sp.) in suckling pigs. It can show similar clinical signs but you never perform feedback in Isospora cases lest you distribute the coccidia yourself among your pigs.


 I have had issues with specific vaccination (either with PED or TGE) but that is not the point of this article. Let the gods of history in years to come blame me for not having enough confidence to recommend specific vaccination given the limitations of diagnosis and literature confidence. It may have worked for others and we all can learn from them.


But I can only testify for what worked in my practice.


Influx or Redux?

After that turbulent season of spreading and explosive diarrhea, admittedly, the incidence decreased. It was however far from viral cleansing. It’s just that producers may have gotten used to it and media found new newsworthy items. Unfortunately it was another swine outbreak that eclipsed the viral diarrhea in the headlines (High-Fever Syndrome/PRRDC/PRRSV/SIV/Hog Cholera). But in all those times, long-term diarrhea in suckling piglets, occasional increase in diarrhea-related suckling mortality and subsequent low weaning weights either persisted in many farms or entered new farms. Are these new reports cases of a viral influx or a viral redux? 


INFLUX - Acute PED or TGE is difficult to distinguish on the basis of clinical findings and regardless of age of pigs infected. Laboratory methods are necessary for the diagnosis of the specific agent (IFT, ELISA and IHC have variable sensitivity; only RT-PCR is reported to be highly sensitive). Cell culture reportedly can not even be used for routine definitive diagnosis. Cross-protection has not been reported and therefore specific live vaccination from outside antigen eg PED vaccination to a naïve or TGE-infected herd and vice versa pose a big risk.


Clinically, acute neonatal TGE or PED will both show explosive diarrheic feces that are watery and flocculent and have characteristic fetid odor. Morbidity may approach 100% and mortality can reach from 50-80% or even more due to dehydration and metabolic acidosis. Both TGE and PED replicate in the cytoplasm of villous enterocytes throughout the small intestines. They therefore destroy the villi making the intestines fluid-filled and severely thin-walled. Only in grower or feeder PED-infected pigs can PED be characterized quite clearly different from TGE because of its high morbidity but very low mortality of only up to 1-3%.


REDUX – If both PED and TGE persist for a long time and become endemic in the herd, the clinical signs become similar to rotavirus, coccidia and colibacillosis creating more confusion in the diagnosis and proper treatment. Endemic TGE or PED are common sequelae of an epidemic or acute outbreak especially in large, continuous farrowing system herds. In these large herds, significant number of susceptible pigs escaped infection during the primary outbreak. These uninfected pigs become nidus for maintaining the infection in the herd. Furthermore, continuous addition of negative replacement pigs into an endemic herd plays vital role in the persistence of the disease.


A continuous farrowing system also provides a constant supply of susceptible piglets. The virus remains active when piglets suckle from seronegative sows, if sows have low degrees of lactogenic immunity and if sows have poor milk supply. There has to be more thorough execution of intestinal feedback in a continuous system.


Learning from Failures in Intestinal Feedback (may have caused the epidemic to become endemic)


When PED or TGE knocks at your herd, never panic. The key is to boost sow maternal immunity for them to provide maximum piglet lactogenic protection against the virus. Since the immunoglobulin IgA is responsible in providing protection, the preparation should be given orally. Since confirmatory diagnosis is always not possible (and may not even be) and your herd is single site anyway, the handiest yet effective tool is using the virus from within the herd through feedback. I trust that by now, you already have your own recipe for feedback. For the past years however, I have listed some reasons why your recipe for feedback may have failed:


  •    It’s not just simply a viral diarrhea. There were farms with endemic collibacillosis cases but wanted to join the feedback trend. Initial antibiotic medication didn’t work due to poor choice, poor treatment execution and antibiotic resistance.
  •   The producer harvested intestines after the pigs had naturally died therefore there’s no more optimum amount of infectious virus in the material. Intestines must be harvested during the acute stages, preferably 6-12 hours from the onset of clinical signs.
  •   The harvested material was kept at room temperature and was not used immediately or was not preserved in ideal temperature.
  •   Tap water or mineral water was used as diluent.
  •   Introduction of intestinal feedback in gestating sows were either too early or too late at gestating periods.
  •   Sows were group-housed making it difficult to dose individual animals. Less aggressive sows may not have received the feedback material.
  •   Intestinal-fed sows that were individually-stalled were not properly monitored for infection signs.
  •   Few viral materials but over diluted with distilled water, PBS or cell culture media.
  •   Some sows were less susceptible to the feedback material because of previous immunity from previous vaccination or natural exposure in the farrowing herd.
  •   Failure in managing transmission of the virus from affected to susceptible piglets. Strict All-In-All-Out will be very valuable. If possible, separate group of litters in the farrowing room by empty crates to decrease spread between litters.
  •   Failure to acclimatize replacement gilts. Some farms did it best by purchasing 6 months of replacement gilts and then closing the herd.
  •   Failure in maximizing supportive therapy including electrolyte supplementation, secondary bacterial medication, temperature and colostrum management.



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