The risk of viral transmission in feed:


What do we know, what do we do? By Scott Dee DVM MS PhD Dipl;ACVM, Director, Pipestone Applied Research


PART 1: WHAT DO WE KNOW? Effective biosecurity protocols are essential towards protecting the health status of swine farms. In the US, tremendous resources have been invested to reduce the risk of viral pathogens, such as porcine reproductive and respiratory virus entry into susceptible populations. Protocols including shower in-shower out, transport sanitation, quarantine and testing of incoming genetics and the filtration of incoming air are commonplace throughout the US swine industry, particularly at the level of the sow farm [1]. In contrast, prior to the entry of porcine epidemic diarrhea virus (PEDV) in the US swine population during May 2013 [2], the role of feed as a vehicle for pathogen transport and transmission had not been considered, despite the fact that feed is delivered to swine farms on a daily basis in the absence of any biosecurity protocols. Since the identification of this novel risk factor, scientists across North America have conducted numerous studies to understand its relevance. Therefore, the purpose of this paper is to review the literature on the risk of feed (what do we know?) and the protocols that have been developed to reduce this risk (what do we do?), in an effort to develop a comprehensive document to raise awareness, facilitate learning and identify knowledge gaps for future studies.


PEDV changes the paradigm Upon its entry to the US, PEDV spread rapidly throughout the country at an unprecedented rate [3]. Following phylogentic analysis, it was determined that it most likely originated from China [4]. During the initial outbreak, the American Association of Swine Veterinarians, the National Pork Producers Council and the USDA Center for Epidemiology and Animal Health conducted an epidemiological investigation involving porcine epidemic diarrhea (PED) affected case and control herds, and of the 100 variables surveyed, seven were significantly associated with acquiring PEDV during the process of feeding animals [5]. In 2014, the risk was confirmed when it was proven that ingestion of contaminated complete feed could serve as a vehicle for PEDV transmission to naïve pigs [6]. This study involved the detection of the virus in feed dust samples from the interior walls of feed bins that had provided feed for the index cases of PED in sows across a subset of farms, followed by a demonstration of virus viability using a bioassay model involving pigs consuming this material via natural feeding behavior [6]. Within 3-4 days post-ingestion, clinical signs of PED (vomiting and diarrhea) and the detection of PEDV RNA in rectal swabs along with lesions in the gastrointestinal tract suggestive of PED were documented. Shortly thereafter, the minimum infectious dose of PEDV in feed was determined to be 5.6 x 101 TCID50/g using the 10-day old piglet bioassay [7]. Another important finding was the potential for widespread PEDV


contamination of surfaces in an animal food manufacturing facility [8]. In this study, a U.S. virulent PEDV isolate was used to inoculate 50 kg of swine feed, which was then mixed, conveyed, and discharged into bags using pilot-scale feed manufacturing equipment. Subsequent collection of environmental swabs demonstrated widespread distribution of virus via feed dust, with the presence of PEDV RNA in 100% of dust


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samples collected from animal food-contact surfaces and in 89% of dust samples from non-animal food-contact surfaces. Once contamination of the feed mill environment was demonstrated, the question of whether viral survival would differ across the various feed ingredients found in a milling environment was investigated [9,10]. Interestingly, viable PEDV was detected out to 180 days post-inoculation (DPI) in conventional (high protein/low fat) soybean meal, as well as out to 30 DPI in DDGS, meat & bone meal, RBCs, lysine HCL, D/L methionine, choice white grease, choline chloride, and out to 7 DPI in limestone and 14 DPI in threonine. In contrast, viable PEDV was not present in several other ingredients, including corn, various animal protein sources, and vitamin/ trace mineral mixes. These data, along with observations from the field, posed the


question of whether certain ingredients could serve as vehicles for the movement of PEDV between countries. This issue was raised in January 2014, when PEDV was detected for the first time in Ontario, Canada [11]. Following extensive epidemiologic investigation, the source of the virus appeared to be contaminated samples of spray dried plasma protein originating from the US [12,13]. However, while infectious PEDV was demonstrated in samples of case-specific plasma by swine bioassay, transmission of the virus to pigs following consumption of feed containing PEDV-positive plasma was not successful [14]. Building on the potential for transboundary movement of PEDV, a Trans-Pacific model, simulating the movement of cargo from Beijing, China, to the Anquin terminal in Shanghai, China to port of San Francisco, CA, US, and then to Des Moines, IA, US was developed [15]. The model utilized transport times, environmental conditions and feed ingredients (www.hs.usitc.gov) representative of transport of cargo from China to the US. Under the conditions of this study, PEDV survived the trans-oceanic simulation in soy-based products, lysine, choline, and vitamin D [16]. Surprisingly, the virus did not survive in the absence of a feed matrix, suggesting that survival is dependent upon the presence of the ingredient, not the container (tote) per se.


Expanding the viral portfolio Based on these collective data involving PEDV, the transboundary experiment was repeated across 11 other viruses, including Foot and Mouth Disease Virus (FMDV), Classical Swine Fever Virus (CSFV), African Swine Fever Virus (ASFV), Influenza A Virus of Swine (IAV-S), Pseudorabies virus (PRV), Nipah Virus (NiV), Porcine Reproductive and Respiratory Syndrome Virus (PRRSV), Swine Vesicular Disease Virus (SVDV), Vesicular Stomatitis Virus (VSV), Porcine Circovirus Type 2 (PCV2) and Vesicular Exanthema of Swine Virus (VESV) [17]. In certain cases, surrogate viruses were employed including Senecavirus A (SVA) for FMDV, Bovine Viral Diarrhea Virus (BVDV) for CSFV, Bovine Herpesvirus Type 1 (BHV-1) for PRV, Canine Distemper Virus (CDV) for Nipah Virus, Porcine Sapelovirus (PSV) for SVDV and Feline Calicivirus (FCV) for VESV. Since ASFV had not been reported in China at the time of the study


and was actively circulating in Eastern Europe, a Trans-Atlantic model was developed involving representative feed ingredients, transport times


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