Porcine circovirus type 2 (PCV2) is the major swine pathogen associated with Porcine circovirus associated disease (PCVAD) including post-weaning multisystemic wasting syndrome (PMWS). Currently, there are 4 subtypes of PCV2 (PCV2a, b, c and d) and some epidemiological evidences demonstrated that virulence of PCV2 may relate to its subtypes. Recently, PMWS was observed more frequently in swine farms in Thailand; however, the information regarding to PCV2 subtype involved was limited. Therefore, this study was aimed to determine the association between occurrence of PMWS and PCV2 subtypes as well as genetically characterize PCV2 in Thailand. PCV2 DNA was isolated from faecal swabs and whole blood of piglets from PMWS-affected and -negative farms. The full length ORF2 sequences were compared using multiple alignment. The results showed that PCV2 DNA was detected more frequently in PMWS-affected farms. The nucleotide identities of the ORF2 from 9 PCV2 isolates representing each PMWS-affected farm and one from the negative farm ranged from 92.4 to 99.5% suggesting that there is some genetic variation of PCV2 in Thai swine. The 10 PCV2 isolates were classified into 2 clusters, in which the 7 isolates from PMWS-positive farms were in PCV2b cluster 1 A/B. The remaining isolates were separated in the new subtype called PCV2e. The results suggest the presence of new PCV2 subtypes in addition to PCV2a and PCV2b in Asian swine population. However, correlation between subtypes and virulence of PCV2 infection is not conclusive due to limited number of the PCV2 sequences from PMWS negative farms.

Background and Aim: Thai pig farmers have suffered huge financial losses from porcine epidemic diarrhea (PED) since 2007. PED, caused by the PED virus (PEDV), leads to severe diarrhea, vomiting, and subsequent dehydration in suckling piglets. Lactogenic immunity derived from colostrum and milk is very important because immunoglobulins (Ig) cannot cross the placenta in pregnant sows. The aim of this study was to investigate the immunological correlation of the sample-to-positive (S/P) ratios of IgA and IgG against PEDV between colostrum, sow serum, and their piglet serum. Materials and Methods: A total of 43 sows were divided into three groups according to the experience of PEDV infection: Negative sow group (n=7) and treatment group (n=36, sows previously infected with PEDV). The treatment group was subdivided into two groups: Sows immunized with live-attenuated PEDV vaccine (n=15) and sows immunized with feedback (n=21) at 3 weeks before farrowing. The 7-day-old piglets (n=425) were obtained from negative sows (n=89), vaccinated sows (n=150), and feedback sows (n=275). Colostrum, sow serum, and their piglet serum were collected and analyzed for S/P ratios of their IgA and IgG levels against PEDV using an enzyme-linked immunosorbent assay. Results: The piglets from sows immunized with live-attenuated PEDV vaccine had a higher S/P ratio of IgG against PEDV (p<0.001), whereas the piglets from the feedback group had a higher S/P ratio of IgA against PEDV (p<0.001) compared with piglets from the negative sows. In addition, the S/P ratios of PEDV-specific IgA and IgG between sow serum and colostrum showed a positive correlation (Pearson's coefficient r=0.61 and 0.75, respectively). Both S/P ratios of PEDV-specific IgA and IgG in sow serum and colostrum had a positive correlation to those in piglet serum. Conclusion: Overall, this study suggested that pregnant sows immunized with the live-attenuated vaccine against PEDV and feedback may provide maternal immunity against PEDV to their offspring.

Background and Aim: Porcine epidemic diarrhea (PED) is a severe infectious disease that causes very high mortality in newborn piglets up to 2-3 weeks age. The main cause of repeated outbreaks of PED in infected farms is the continuing circulation of the PED virus (PEDV). Improper gilt management, including inappropriate gut feedback, commingling, and inadequate immunization, causes a prolonged virus circulation in breeding herds. Moreover, insufficient transfer of passive immunity through the colostrum to newborn piglets can also increase infection risk. Therefore, a gilt management program that controls infection should focus on infection monitoring and acclimatization. We investigated the source of recurrent PEDV outbreaks and examined how the effect of immunization methods, specifically using gut feedback mechanism and vaccination, can reduce PEDV circulation and improve immune responses in replacement gilts. Materials and Methods: The study site was a segregated commercial production farm with endemic PEDV. The acclimatization methods included gut feedback and vaccination. This longitudinal study evaluated two strategies of gilt acclimatization against PEDV: Program 1 (routine farm management) and Program 2 (early feedback program and all-in-all-out system). Levels of PED RNA in fecal samples were measured using quantitative reverse transcription-polymerase chain reaction, and the PEDV S gene was sequenced. Porcine epidemic diarrhea-specific immune responses were assessed using enzyme-linked immunosorbent assay and the serum neutralization test. Results: Porcine epidemic diarrhea outbreaks occurred in the farrowing, nursery, and finishing units and farrowed litters 5–10 days old were symptomatic of PED. Phylogenetic analyses of the S gene showed PEDV sequence divergence between PEDV field strains and vaccine strain, which may contribute to periodic outbreaks and continued persistence of PEDV in the farm. After gut feedback and acclimatization, replacement gilts from Program 1 continued to shed PEDV before being introduced to sow herds, while those from Program 2 did not shed PEDV before being introduced to sow herds. However, the components of the immune response against PEDV in serum samples, including specific immunoglobulin (Ig)G, specific IgA, and neutralizing antibodies were lower in gilts of Program 2 than those in Program 1. Conclusion: We speculate that implementing the appropriate gilt acclimatization program can control PEDV circulation in farm. However, the acclimatization methods in Program 2 did not induce a strong and adequate immune response in replacement gilts. Therefore, maternal immunity levels and the degree of protection against PEDV require further study. Keywords: acclimatization, gilt, immune response, phylogenetic tree, porcine epidemic diarrhea.

Background and Aim: Mycotoxin contamination in animal feeds is of considerable concern because it can affect animal health systems. As a result of contamination in the food chain, humans can indirectly come into contact with mycotoxins. The present study aimed to present mycotoxin contamination patterns in animal feeds from 2015 to 2020 and elucidate associations between the type of feed and the type of ingredient. Materials and Methods: Data were summarized from the records of the Kamphaeng Saen Veterinary Diagnosis Center from 2015 to 2020, which comprised the analyses of aflatoxin (AFL), zearalenone (ZEA), T-2 toxin (T-2), fumonisin (FUM), and deoxynivalenol (DON) contamination in feed ingredients, complete feeds, and unclassified feeds. Descriptive statistics, Chi-squared tests, and Fisher's exact tests were used for data analysis. Results: ZEA was prevalent in animal feeds. The prevalence of each mycotoxin was constant from 2015 to 2020. Approximately 20-30% of samples were positive for AFL and FUM. The highest contamination was ZEA, which was found in 50% of the samples, and the occurrence of T-2 and DON was <10%. AFL significantly contaminated complete feeds more than feed ingredients. Feed ingredients were related to mycotoxin contaminations. The highest levels of AFL, FUM, and DON contamination occurred in 2017. The data in this year consisted mostly of soybean, corn, and rice bran. Conclusion: The number of positive samples of all five mycotoxins was constant from 2015 to 2020, but the occurrence of ZEA was the highest. Mycotoxins in feedstuffs are significantly related to the type of feed and the type of ingredient.

Background and Aim: Opisthorchis viverrini infection-induced inflammation contributes to cholangiocarcinoma (CCA) development in humans and animals. Inflammation generates free radicals, such as reactive oxygen species and reactive nitrogen species (RNS), which damage the host’s DNA. However, only 5% of O. viverrini-infected individuals develop malignancy, suggesting that variations in the inflammatory response of individuals to the parasite may influence susceptibility. Due to limitations in studying human susceptibility, we used an animal model to investigate the profiles of inflammatory reactions, oxidative burst, and irreversible DNA damage. This study aimed to explore the potential role of inflammation and RNS in causing DNA damage that may predispose susceptible hosts and non-susceptible animal models to cancer development in O. viverrini infection. Materials and Methods: This experimental study was conducted on 30 Syrian golden hamsters (OV-H) and 30 BALB/c mice (OV-M) infected with O. viverrini, representing susceptible and non-susceptible models, respectively. Five animals per group were examined at six predetermined time points during the experiment. Biliary tract samples were systematically investigated using histopathological evaluation for inflammatory cell infiltration and immunohistochemical staining for RNS production and markers of DNA damage, including nitrotyrosine and 8-hydroxy-2ʹ-deoxyguanosine. These features were quantified and compared among the experimental groups. Mann–Whitney U-test was used for statistical analysis, with p < 0.05 considered statistically significant. Results: The comparison revealed that the OV-M group exhibited significantly earlier and higher rates of inflammatory cell infiltration during the acute phase, whereas the OV-H group exhibited chronic and more severe inflammation (p < 0.020). Intracellular RNS production and DNA damage were closely associated with the inflammatory response. Conclusion: This study demonstrates differential responses in susceptible and non-susceptible models of O. viverrini infection regarding disease onset and duration, as well as intracellular RNS production and DNA damage caused by inflammation. Persistent inflammation generated oxidatively damaged DNA, which is a distinct pathological characteristic of susceptible hosts and may be critical for CCA development. Keywords: cholangiocarcinoma, DNA damage, inflammatory reactions, Syrian golden hamsters.