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Simple Summary: Diarrhea causes huge economic losses in the global swine industry. Porcine epidemic diarrhea virus (PEDV) has been identified as a direct causative pathogen of diarrheic diseases in piglets. PEDV can infect all ages of pigs; however, little is known about the prevalence and evolution of PEDV in adult pigs. Here, we explored the genomic characteristics of PEDV in both diarrheic piglets and clinically healthy adult pigs from 2019 to 2022 in China. We found that PEDV variants are not only prevalent in diseased piglets but are also circulating in adult pigs. In addition, intra- and inter-subgroup recombinants were detected in adult pigs, indicating that adult pigs may also serve as the host of viral reservoirs for rapid PEDV evolution. This study provides up-to-date information on PEDV's prevalence and evolution in both diseased piglets and healthy adult pigs in China. Porcine epidemic diarrhea virus (PEDV) is a major causative pathogen of diarrheic disease. In this study, the prevalence and evolution of PEDV was evaluated using intestinal samples collected from six provinces of China in 2019–2022. PEDV could not only be detected in diarrheic piglets but also in adult pigs without enteric diseases. The complete genomes of five temporal and geographical representative PEDV strains were determined. Genome-based phylogenetic analysis indicated that XJ1904-700 belongs to the G2-a subgroup, while the other strains are clustered within the S-INDEL subgroup. Recombination analyses supported that JSNJ2004-919 is an inter-subgroup recombinant from SD2014-like (G2-b), CHZ-2013-like (G2-b) and CV777-like (G1-b) isolates, while FJFZ2004-1017 is an intra-subgroup recombinant from XM1-2-like (S-INDEL) and LYG-2014-like (S-INDEL) isolates. Both JSNJ2004-919 and FJFZ2004-1017 were from adult pigs, providing evidence that adult pigs may also serve as the host of PEDV reservoirs for virus evolution. Overall, this study provides new insights into PEDV's prevalence and evolution in both diseased piglets and clinically healthy adult pigs. [ABSTRACT FROM AUTHOR]

Porcine epidemic diarrhea virus (PEDV) is a major causative pathogen of diarrheic disease. In this study, the prevalence and evolution of PEDV was evaluated using intestinal samples collected from six provinces of China in 2019–2022. PEDV could not only be detected in diarrheic piglets but also in adult pigs without enteric diseases. The complete genomes of five temporal and geographical representative PEDV strains were determined. Genome-based phylogenetic analysis indicated that XJ1904-700 belongs to the G2-a subgroup, while the other strains are clustered within the S-INDEL subgroup. Recombination analyses supported that JSNJ2004-919 is an inter-subgroup recombinant from SD2014-like (G2-b), CHZ-2013-like (G2-b) and CV777-like (G1-b) isolates, while FJFZ2004-1017 is an intra-subgroup recombinant from XM1-2-like (S-INDEL) and LYG-2014-like (S-INDEL) isolates. Both JSNJ2004-919 and FJFZ2004-1017 were from adult pigs, providing evidence that adult pigs may also serve as the host of PEDV reservoirs for virus evolution. Overall, this study provides new insights into PEDV’s prevalence and evolution in both diseased piglets and clinically healthy adult pigs.

Colitis-complex diarrhea (CCD) in pigs can be defined as a type of diarrhea, which is associated with colonic inflammation and disrupted colonic gut barrier functionality in growing pigs (4–16 weeks post-weaning). It is a challenge for the pig industry as it is associated with the high use of antibiotics, reduced animal welfare, and depressed growth rate. The exact etiology of CCD is still unclear; however, pathogens including Brachyspira (B.) hyodysenteriae, B. pilosicoli, and swine whipworms such as Trichuris (T.) suis have been involved in specific colitis (SC). In the absence of specific pathogens, dietary factors, such as high levels of protein, pelleted feedstuffs, and lack of sufficient antioxidants, can result in non-specific colitis (NSC). On the other hand, supplement of polyunsaturated fatty acids (PUFA) and polyphenols, sufficient supply of essential amino acids (e.g., threonine, cysteine, and proline), short-chain fatty acids (SCFA; especially butyrate), and resistant starch have shown to confer preventing/ameliorating effects on CCD. Different putative biomarkers associated with CCD have been presented. It is anticipated that a comprehensive picture of the possible causes of CCD and potential dietary interventions could cast light on the direction of future studies aimed at developing preventive and curative strategies against CCD in growing pigs.

Regardless of the efforts put into preventing or reducing fungal growth, extensive mycotoxin contamination has been reported in animal feeds. In the case of pigs, one of the mycotoxins of major concern is deoxynivalenol (DON). The use of adsorbents as feed additives represents one of the strategies to control mycotoxins' contamination in feedstuff. Therefore, the aim of the study was to verify the ability of chlorophyllin (CHL) to reduce the absorption rate of DON in swine mucosa explants. Intestine was obtained from routinely slaughtered adult pigs. The mucosa explants were studied by means of Ussing chamber technique. The effect of DON (10 and 30 μg/ml) on mucosa viability and permeability and CHL (100 μg/ml) impact on DON (30 μg/ml) absorption was verified. The results revealed that mucosa explants isolated from adult animals remained unaffected for 90 min in the presence of DON in the lower concentration (10 μg/ml). Mycotoxin in the higher dose (30 μg/ml) increased mucosa permeability (decreased transepithelial electrical resistance value) and enhanced paracellular transport of lucifer yellow and mannitol but did not affect lactate dehydrogenase leakage. The introduction of CHL neither diminished the absorption rate of DON across swine mucosa explants nor prevented the toxic effects of DON on intestine. In conclusion, the results confirm the negative effect of DON on pig jejunum mucosa. However, the toxic effect of DON was observed only when it was used in relatively high doses. A promising adsorbent agent, CHL, failed to reduce the intensity of DON transport across intestine under in vitro conditions. [ABSTRACT FROM AUTHOR]

Simple Summary: Diarrhea in growing pigs is a challenge for the pig industry since it is associated with reduced animal welfare, retarded growth, increased feed conversion ratio, and is often treated with antibiotics. One of the major causes of diarrhea in the growing period is large intestinal inflammation, often referred to as colitis. The exact causes of colitis-complex diarrhea are still to be understood, but dietary factors and/or pathogens have been recognized as the major factors in developing colitis-complex diarrhea. In this review, a thorough picture of pathogens, dietary factors, and a number of possible biomarkers related to colitis-complex diarrhea is presented. Colitis-complex diarrhea (CCD) in pigs can be defined as a type of diarrhea, which is associated with colonic inflammation and disrupted colonic gut barrier functionality in growing pigs (4–16 weeks post-weaning). It is a challenge for the pig industry as it is associated with the high use of antibiotics, reduced animal welfare, and depressed growth rate. The exact etiology of CCD is still unclear; however, pathogens including Brachyspira (B.) hyodysenteriae, B. pilosicoli, and swine whipworms such as Trichuris (T.) suis have been involved in specific colitis (SC). In the absence of specific pathogens, dietary factors, such as high levels of protein, pelleted feedstuffs, and lack of sufficient antioxidants, can result in non-specific colitis (NSC). On the other hand, supplement of polyunsaturated fatty acids (PUFA) and polyphenols, sufficient supply of essential amino acids (e.g., threonine, cysteine, and proline), short-chain fatty acids (SCFA; especially butyrate), and resistant starch have shown to confer preventing/ameliorating effects on CCD. Different putative biomarkers associated with CCD have been presented. It is anticipated that a comprehensive picture of the possible causes of CCD and potential dietary interventions could cast light on the direction of future studies aimed at developing preventive and curative strategies against CCD in growing pigs. [ABSTRACT FROM AUTHOR]