African swine fever (ASF) was officially reported in Vietnam in February 2019 and spread across the whole country, affecting all 63 provinces and cities. In this study, ASF virus (ASFV) VN/Pig/HaNam/2019 (VN/Pig/HN/19) strain was isolated in primary porcine alveolar macrophage (PAM) cells from a sample originating from an outbreak farm in Vietnam’s Red River Delta region. The isolate was characterised using the haemadsorption (HAD) test, real-time PCR, and sequencing. The activity of antimicrobial feed products was evaluated via a contaminated ASFV feed assay. Phylogenetic analysis of the viral p72 and EP402R genes placed VN/Pig/HN/19 in genotype II and serogroup 8 and related it closely to Eastern European and Chinese strains. Infectious titres of the virus propagated in primary PAMs were 10⁶ HAD₅₀/ml. Our study reports the activity against ASFV VN/Pig/HN/19 strain of antimicrobial Sal CURB RM E Liquid, F2 Dry and K2 Liquid. Our feed assay findings suggest that the antimicrobial RM E Liquid has a strong effect against ASFV replication. These results suggest that among the Sal CURB products, the antimicrobial RM E Liquid may have the most potential as a mitigant feed additive for ASFV infection. Therefore, further studies on the use of antimicrobial Sal CURB RM E Liquid in vivo are required. Our study demonstrates the threat of ASFV and emphasises the need to control and eradicate it in Vietnam by multiple measures.

A corn culture of Fusarium roseum was added to a standard corn-soybean swine gestation ration. Low, middle, and high dosage mixed feeds contained 7, 38, and 64 mg of zearalenone/kg of feed (7, 38, and 64 ppm) and 0.5, 2.5, and 4.5 mg of deoxynivalenol/kg, respectively. Control feed was the standard ration without added F roseum corn culture. Mature gilts were bred by natural service and fed control or F roseum molded feed from 3 to 34 days after breeding. The main effect of the molded feed was an inhibition of fetal development, with decreased numbers of fetuses present in treated animals at slaughter (38 to 43 days after breeding). Normal litters were present in 7 of 8 control animals, in 2 of 4 gilts given the low-dosage feed, in 1 of 4 gilts given the medium dosage, and in 0 of 4 given the high-dosage feed. Corpora lutea were maintained in all treated animals, as evidenced by serum progesterone concentrations. Serum estradiol concentrations were decreased in gilts in the middle- and high-dosage groups. The genital system of the gilts fed low- and middle-dosage feeds had a gross and microscopic appearance similar to that of the pregnant controls and reflected prolonged progesterone stimulation. Morphologic changes in the genital system of the high-dosage group were intermediate between changes induced by progesterone and those induced by estrogen. Clinical signs of hyperestrogenism and partial feed refusal were noticed in only some of the high-dosage group animals.

Two of 3 groups of Holstein-Friesian steers (groups II and III; n = 5 each) were fed a ration containing corn naturally contaminated with 800 ng of aflatoxin/g. The other group of steers (group I; n = 5) was fed a ration containing noncontaminated corn. The respective rations were fed for 17.5 weeks, except the ration given to group III; the latter's first diet (contaminated with aflatoxin) was changed to a noncontaminated diet after 15 weeks, continuing for the remaining 2.5 weeks. All steers were killed and tissues and fluids were obtained for aflatoxin analysis. Although aflatoxin B1 and M1 could be detected in blood and urine at several sampling times during the experimental period in groups II and III steers (given the diets containing aflatoxin), there appeared to be no effects on body weight gains and immune phenomena, such as lymphoblastogenesis and antibody production, but there was a waning of the delayed cutaneous hypersensitivity in steers given aflatoxin-contaminated diets. In group III animals (diet was changed to noncontaminated ration at 15 weeks), aflatoxin B1 and M1 disappeared from urine before they were slaughtered. All tissues and fluids, except the rumen contents from these group III steers, were void of detectable aflatoxins B1 and M1 at necropsy. The concentrations of aflatoxin B1 in the rumen content of the latter steers were low. All tissues collected at necropsy from the group II steers fed the aflatoxin diet throughout the 17.5 weeks had detectable aflatoxins B1 or M1 present.