Abstract

Study of the emergent properties and paths of spreading of PEDV was carried out in a model experiment on newborn non-immune piglets obtained from a PED virus-free pig-breeding enterprise. The piglets were kept in separate specialized containers, with a volume of 1.0 m3, with access only through the opening at the top of the containers. The experimental group of the animals was infected with PEDV isolate extracted on one of the pig farms from the central region of Ukraine. Infection was carried out orally in a dose of 1–10 genome equivalents of virions. The control piglets, which were situated in the same room as the infected animals, were not deliberately infected. The study of biological material from piglets was carried out using the methods of bacteriology, histology and RT-PCR. To confirm the capability of PEDV to spread through house flies, specimens of Musca domestica vicina Mcq. were caught in the building where the experiment was carried out. The washings from the surface of their bodies were collected with sterile saline. Individually, 28 specimens of flies were selected. They were divided into two parts and the amount of virus in the homogenate of the fly bodies in these groups was determined with an interval between measurements of 72 hours. Study of PEDV in the washings and in flies body homogenates were carried out using RT-PCR. It is established that the field strain PEDV, belonging to the North American grouping II of the second group of the PED virus strains, is an emergent highly pathogenic agent for non-immune newborn piglets. In the model of piglets’ infection it is established that the tested PEDV strain has a high virulence for newborn piglets, DCL is 1–10 virions and the incubation period is 18–26 hours. PED is acute with lethality to 100% within 68–72 hours after infection. According to the results of RT-PCR in washing from the surface of the bodies of flies, it is established that one of the ways piglets are infected and the environment contaminated with the PED virus is the spread of the pathogen by the flies M. domestica vicina Mcq. This leads to the induction of the emergent form of PED in piglets. The presence of PEDV in the homogenate from bodies of M. domestica caught in the focus of infection and the absence of virus reproduction in their body confirms the role of the house fly in the mechanical spread of PEDV in the external environment.

Highlights

  • The virus of epidemic diarrhea of pigs (Porcine epidemic diarrhea virus – PEDV) was recently identified as a new infection and is considered as the causative agent of an emergent nosological unit in infectology

  • Non-immune newborn piglets which had not been fed colostrum were randomly selected in a pig enterprise immediately before the start of study

  • The flies could have been an effective PEDV carrier in these conditions. In favour of this assumption is the correspondence between the time from infection till the appearance of clinical symptoms and the temporal difference in the lethal outcome of the infected and control groups. This assumption was confirmed by the results of PCR-RT analysis of the PED virus on the surface and in the body of houseflies

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Summary

Introduction

The virus of epidemic diarrhea of pigs (Porcine epidemic diarrhea virus – PEDV) was recently identified as a new infection and is considered as the causative agent of an emergent nosological unit in infectology. Pigs of all age groups are affected by PED, though the most susceptible to PEDV are newborn piglets up to 10 days of age. In newborn piglets there is practically no immunity, and this is the main cause of their high susceptibility to infection with PEDV. When an infectious agent of PEDV reaches a farm, suckling piglets fall sick in the first days of life and die within 2–4 days. Such a progressive development of the infectious process determines the ineffectiveness and uselessness of vaccinating piglets. Under the circumstances of the infection propagation, the specific immune-biological protection with colostral immunoglobulins can form lactogenic immunity only (Annamalai et al, 2015)

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