Looking for ways to get relief from PED

Porcine epidemic diarrhoea (PED) is caused by a coronavirus somewhat similar to that which causes transmissible gastroenteritis. The PED virus was first recognized in the UK in 1971 and has spread throughout most of Europe and Asia where it is in many countries considered to be endemic (AASV, 2013). Severe outbreaks with high mortality are typically rare in Europe, but are recently reported to be common in Asia. China has seen a large increase in outbreaks since 2010 which has been attributed to the emerging of new strains (Geiger et al., 2013). It was not present in the US until spring 2013, when the first confirmation of the virus took place. In the meantime, the virus has emerged in Canada and the total number of US states with at least one confirmed case of PED has risen to 27. Reports from Latin America and Asia indicate that the virus might be present there as well.

Pigs are the only known hosts of the PED virus. The virus is shed in the faeces and is usually transmitted orally. Most commonly, the introduction of infected pigs into susceptible farms causes outbreaks of PED within 4 to 5 days. Virus may also be introduced into a susceptible herd through contaminated personnel, equipment and other fomites (Pospischil et al., 2002).

After the recent outbreaks in the US and Canada, imported porcine blood and blood products are being investigated as to their possible role in introduction of the disease.

Clinical signs of PED may vary widely and are dependent on previous exposure and the immunological and endemic status of the farm, region or area affected (Geiger et al., 2013).

Acute outbreaks occur when the virus is first introduced into a susceptible (i.e. naïve) population (epidemic situation). The main clinical sign in all age groups is watery diarrhoea, vomiting and loss of appetite. Morbidity approaches 100%. Infected piglets up to 1 week old die from dehydration after 3 to 4 days (mortality averages about 50%). Older piglets recover in about 1 week.

Feeders, finishers and adult swine have diarrhoea, depression, anorexia and signs of abdominal pain. Outbreaks often start in these age groups. Although recovery usually follows, there may be some mortality (1-3%).

If introduced in herds where the virus is endemic, persistent diarrhoea is observed with lower morbidity in predominantly suckling and recently weaned pigs.

Figure 1: Runt piglets, vomiting, wasting and diarrhoea typical of PED.

  Figure 2: Severe dehydration and death are typical of acute viral diarrhoea.

The underlying cause for the clinical signs is that the virus replicates in enterocytes on villi of the small intestine and to a lesser degree in cryptal cells of both small intestine and colon. Viral replication subsequently causes degeneration and necrosis of enterocytes, resulting in loss of tissue fluid into the lumen and failure of the intestine to adequately absorb water. Diarrhoea follows and leads to dehydration and depletion of electrolytes.

Figure 3: Intestinal villi from a normal neonatal pig. The villi are very long (indicated by the black arrow), with a large surface area to absorb nutrients and water. The crypts of absorptive epithelium approximately 36 hours after infection of a neonatal pig with PED virus. The crypts are increasing in length (black circle) are where new cells are produced. Source: http://nationalhogfarmer.com

 

Figure 4: Severe decrease in the height of villi (villus atrophy, see the black arrow) and loss as they produce more cells in attempt to rebuild the absorptive cells of the villi. Source: http://nationalhogfarmer.com 

To prevent infection, the number one focus point remains, as always, good biosecurity.

With highly contagious diseases such as PED, this is however not easy at all. If the virus is introduced, maternal antibodies via colostrum from previously exposed sows may protect neonates against oral infection until about 4 to 13 days of age (Song and Park, 2012).

Licensed PED vaccines are currently only available in South Korea, Japan and China. Immunity can also be induced via feedback of intestinal contents and faeces to sows and replacement gilts; however, so far immunity is not lifelong, herds can re-break. Furthermore, depending on local legislation, people applying this method may be violating law as transporting infected materials brings additional risk of spreading the disease.

Treatment focusses on supportive therapy to prevent dehydration (electrolytes, warmth) and if needed on the control of secondary infections.

Apart from the above mentioned approaches, producers are looking for other options to strengthen the animal’s defense and to help the pigs dealing with the negative consequences from the disease. Owing to its specific effects on enteric development and intestinal health, one of those options is butyrate.

Several studies have indicated that besides providing epithelial cells with energy, butyrate markedly enhances proliferation, differentiation and maturation of enterocytes in the small intestine and improves colonic barrier function (Wang et al., 2005; Manzanilla et al., 2006; Sengupta et al., 2006). Through its influence on gene expression and protein synthesis, butyrate speeds up intestinal mucosa maturation during the development or repair after injury (Kotunia et al., 2004; Guilloteau et al., 2010).

This protective and recovering effect of butyrate has been demonstrated in in vivo challenge trials with micro-organisms (E. coli in piglets and C. perfringens in poultry) damaging the intestinal barrier like PED virus does. In the challenge trials, administration of butyrate was able to prevent to a great extent the negative effects of the intestinal challenges and allow for growth very close to the growth of uninfected animals (Bosi et al., 2009; Timbermont et al., 2010). Furthermore, butyrate modulates ion absorption and may alleviate the severity of the diarrhoea (Vidyasagar & Ramakrishna, 2002; Binder, 2010).

It is well known from literature and from field experience that the benefits of butyrate on gut development are most outspoken in the youngest animals. Studies in neonatal and in weaned piglets show that the ingestion of butyrate results in improved performance, which is further improved if butyrate is fed sooner rather than later post-birth (Kotunia et al., 2004; Mazzoni et al., 2008; Le Gall et al., 2009). This feature can be very valuable in the case of PED as the disease has the most severe impact on the young animals.

More recent research at the University of Taiwan looked into survival of PED-infected newborn piglets. These piglets were separated from the sows after one week, to evaluate interventions aiming to increase survival. While only 20% of the infected control piglets survived the second week, livability was documented to be strongly increased to 70% in the group that received a liquid creep feed including 1.5 kg/T ADIMIX®30 Coated. These results demonstrate that ADIMIX supplementation in PED affected piglets helps them to cope better with the infection.

Since the virus damages intestinal cells in the small intestine and in the colon, it is crucial that butyrate is able to reach these areas. Butyrate can only arrive in the lower luminal parts of the intestinal tract when it is protected from metabolisation in the stomach and is gradually released in the distal regions of the intestine. The most efficient way to achieve this is by administering a protected butyrate with precision delivery capacity such as ADIMIX® 30 Coated. 

Figure 5: Matrix-encapsulated Na-butyrate (ADIMIX®30 Coated) ensures precision delivery.

Different coated butyrate products are available for use in animal production. They come however in many different shapes and forms. One should make a clear distinction between high quality coatings that result in optimal protection and precision delivery of butyrate and coatings that are solely applied to cover the distinct butyrate smell.

In recent research done at the University of Illinois (Song et al., 2013) the importance of a high quality coating was demonstrated. Weanling pigs were randomly allotted to 3 dietary treatments (6 replicate pigs per treatment):

control diet
control diet + 4kg/T of a smell coated butyrate (50% Na-butyrate)
control diet + 4kg/T of a precision delivery butyrate (ADIMIX®30 Coated, 30% Na-butyrate)

Pigs were euthanized and the concentration of butyrate was analyzed in samples from different parts of the intestinal tract. Weanling pigs fed ADIMIX®30 Coated had significantly higher (P < 0.05) concentrations of butyrate in the jejunum and ileum in comparison with both the control group and the group fed the smell coated butyrate. It could therefore be concluded that administration of high quality protected butyrate (ADIMIX®30 Coated), in spite of lower percentage of Na-butyrate (30%), was effective in delivering butyrate to the lower intestinal tract of pigs, whereas supplementation of the more concentrated (50%) but less protected butyrate (smell coated) was not. 

In conclusion, thanks to its specific properties on intestinal health, butyrate may be a very valuable tool in the fight against the dramatic effects of PED on the infected pig.

However, to unlock the full potential of butyrate, it is crucial to assure its delivery in the right area. When applying protected butyrates in animal production, it is of great importance to distinguish between different types of coated products, as their in vivo efficacy will greatly differ due to their different delivery profile.

Our results demonstrate that ADIMIX®30 Coated is able to deliver butyrate to the areas most affected by PED.