Maintained growth performance and reduced mortality of genetically resistant nursery pigs after an experimental virulent F18 enterotoxigenic Escherichia coli challenge

在实验性强毒力F18肠毒素性大肠杆菌攻击后,保持了遗传抗性保育猪的生长性能并降低了其死亡率。

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Abstract

Enterotoxigenic Escherichia coli (ETEC) is a leading cause of postweaning diarrhea (PWD) and mortality of weaned pigs. The objective of this study was to evaluate genetic resistance of the polymorphism at nucleotide 307 (M307) in the FUT1 gene, to F18 E. coli infection considering different genotypes. A total of 179 pigs were used for this study. Pigs were genotyped for susceptibility to F18+ E. coli prior to the trial. Treatments included: genotype M307(GA)-heterozygous for E. coli susceptibility (A), genotype M307(GG)-homozygous E. coli susceptibility (B), or genotype M307(AA)-homozygous for E. coli resistance (C). Pigs were weighed, assigned to pens based on genotype, and allowed to acclimate for 3 d prior to the challenge. On days 4, 5, and 6, pigs were inoculated intraorally at the oropharynx with an F18+ E. coli isolate at a geometric mean concentration of 9.8 × 10(9). Growth rate (average daily gain [ADG]), feed intake (average daily feed intake), and gain-to-feed ratio (G:F) were calculated by pen. All pigs were humanely euthanized at the end of the trial. Two fixed sections of ileum and distal jejunum were collected from a subpopulation and tested by in situ hybridization (ISH) to evaluate F18+ E. coli adherence. Fresh ileum samples were used for enumeration of F18, total E. coli, and total bacteria by real-time polymerase chain reaction. Mortality rates during the trial were 26.7% for genotype A, 18.3% for genotype B, and 0.0% for genotype C (P < 0.01). Starting weights prior to inoculation were not different (P = 0.29) among genotypes. Overall, pigs from genotype C grew 223 g/d faster (P = 0.04) than genotype A. Pigs from genotype C tended to grow 185 g/d faster (P = 0.09) than genotype B. G:F for genotype C (0.74) was 23% greater (P < 0.01) than G:F for genotype A (0.60) and tended to be 12% greater (P = 0.07) than genotype B (0.66). There were no differences in ADG or G:F between genotypes A and B. F18-specifc Cq units were decreased by 7.74 and 6.47 in genotypes A and B compared with genotype C (P ≤ 0.03). Signal by ISH was increased by 14.0-fold in genotype A compared with genotype C (P = 0.02). Adherence was not different among genotypes (P = 0.40). Genotype A had greater mortality and poorer growth performance than genotype B or C. Genotype C had no mortalities during the trial, grew faster, was more feed efficient, and had less F18 E. coli in the ileal mucosa compared with genotype A. Resistant genotypes provide an opportunity to reduce PWD and mortality due to an F18+ E. coli infection.

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