Recently-emerged coronaviruses include the severe acute respiratory syndrome (SARS) virus that caused outbreaks of respiratory disease in humans in 2002–2003 and the Middle East respiratory syndrome (MERS) virus identified in 2012. Contemporary work suggests that bat and bird species are the natural reservoirs of coronaviruses.

Five coronaviruses are recognized in swine: three alphacoronaviruses (transmissible gastroenteritis virus (TGEV), porcine respiratory coronavirus (PRCV), and porcine epidemic diarrhea virus (PEDV)), one betacoronavirus (porcine hemagglutinating encephalomyelitis virus (PHEV)), and one species of porcine deltacoronavirus (PDCoV).

PEDV, TGEV and PDCoV primarily cause enteric infections in pigs. PRCV is the result of deletion and mutation of the spike gene of TGEV. This virus has a predilection for the respiratory tract, but also has the capacity to produce enteric disease. In contrast, PHEV infection ("vomiting and wasting disease") produces encephalomyelitis, rather than enteritis, and thus is not often considered when differentiating enteric infections.

Among the porcine coronaviruses, PEDV has received considerable attention because recently emerged highly virulent strains have caused significant morbidity and mortality in neonatal pigs. Catastrophic outbreaks of PEDV were reported in Korea (1997), China (2005), and Thailand (2007). Following its detection in the U.S. in April 2013, PEDV is estimated to have caused the deaths of 8 million piglets and economic losses of $481 to $929 million (USD) in 2014.

The primary site of PEDV replication is the cytoplasm of villous enterocytes throughout the small intestine. Infection causes epithelial cell degeneration and villous atrophy, which leads to diarrhea, dehydration, and prolonged shedding of PEDV in feces. PEDV viremia has also been reported during the acute stage of infection in young pigs. The most common clinical consequence of PEDV infection is diarrhea, i.e. watery and flocculent feces, often accompanied by vomiting. Morbidity and mortality is highly age-dependent, with neonatal pigs the most severely affected. Thus, an outbreak in a naïve swine population may result in 90% mortality in piglets ≤ 2 weeks of age and ≤ 40% mortality in 2- to 4-week-old pigs. This age-dependent variation in mortality is likely the result of slower villus-epithelial repopulation and less developed immune systems in neonatal pigs. Experimentally-infected 3-week-old pigs showed a significant reduction in average daily gain during the first week post-inoculation and no compensatory weight gain in the following 4 weeks. In the field, Olanratmanee et al. (2010) reported that PEDV infection in pregnant gilts and sows may also have contributed to reduced reproductive performance, including a 12.6% decrease in farrowing rate, a 5.7% increase in the return rate, a 1.3% increase in the abortion rate, and a 2.0% increase in the number of mummified fetuses per litter.

It is generally accepted that lactogenic immunity, i.e., anti-PEDV secretory IgA in milk, is central to limiting the replication of PEDV in the intestinal tract and protecting piglets against clinical disease.

This concept is primarily derived from research showing that sows with higher anti-TGEV SIgA levels in milk were better able to protect their piglets against clinical TGE. These observations are the foundation upon which successful TGEV prevention and control strategies have been based for over 50 years. However, dissimilarities between immunity to PEDV versus immunity to TGEV have not been closely examined and deserve investigation. The question addressed in this project was the effect of colostral (passive) antibody on the protection of neonates against PEDV. Specifically, the objective of this experiment was to quantify the impact of circulating anti-PEDV antibody on the course of PEDV replication and clinical disease in the neonatal pig using a passive transfer model.

Further Reading

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