Abstract
Clinical disease associated with porcine epidemic diarrhea virus (PEDV) infection in naïve pigs is well chronicled; however, information on endemic PEDV infection is limited. To characterize chronic PEDV infection, the duration of infectious virus shedding and development of protective immunity was determined. On Day 0 (D0), a growing pig was challenged with PEDV and 13 contacts were commingled. On D7, 9 contact pigs (principal virus group (PG)), were selected, moved to a separate room and commingled with one sentinel pig (S1). This process was repeated weekly with S2, S3 and S4. The PG was PEDV-positive by PCR from D3-11, with some pigs intermittently positive to D42. Pigs S1 and S2 were PEDV-positive within 24 hours of commingling. Antibodies were detected in all PG by D21 and by 7 days post-contact in S1 and S2. Pigs S3 and S4 were PCR and antibody negative following commingling. To evaluate protective immunity, 5 naïve pigs (N) and the PG were challenged (N/C, PG/C) with homologous virus on D49. All N/C pigs were PEDV PCR-positive by D52 with detection out to D62 in 3/5 N/C pigs. All PG/C pigs were PEDV PCR-negative post-challenge. By D63, all N/C seroconverted. Although PEDV RNA was demonstrated in pigs after primary infection until D42, infectious PEDV capable of horizontal transmission to naïve pigs was only shed 14–16 days after infection to age-matched pigs. Homologous re-challenge 49 days post initial PEDV exposure did not result in re-infection of the pigs. This demonstrates potential for an effective PEDV vaccine.
Highlights
Porcine epidemic diarrhea virus (PEDV) was discovered in 1976 in the feces of young pigs with diarrhea, and subsequently demonstrated to induce diarrhea in pigs [1]
In 4-week-old contact pigs, mild-to-moderate diarrhea was observed for approximately one week post exposure to a PEDV experimentally-infected seeder pig
No other clinical disease was observed in the contact pigs
Summary
Porcine epidemic diarrhea virus (PEDV) was discovered in 1976 in the feces of young pigs with diarrhea, and subsequently demonstrated to induce diarrhea in pigs [1]. This virus was determined to be the cause of an enteric disease in feeder/fattening pigs that was first described in England in 1971, and characterized by severe watery diarrhea with low mortality [2]. In contrast to Europe, the clinical impact of PEDV in Asia was much higher leading to the commercialization of both killed and attenuated vaccines in the late 1990s [5]. The main method of PEDV transmission is fecal-oral; the ability of the virus to aerosolize and be transported over large distances by air is being considered as an additional important route of virus transmission [9]
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