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Page 2 of 19 Son et al. Microbiome Res Rep. 2025;4:29 https://dx.doi.org/10.20517/mrr.2025.14

INTRODUCTION
Maintaining intestinal health is important for the growth of pigs, as the intestine is the primary site for
[1,2]
nutrient digestion and absorption . It also plays a key role in immune function, housing a large number of
immune cells in pigs . However, the pig intestine is highly susceptible to infection during certain stages,
[3-5]
especially the nursery period, when it is still immature. During early weaning, piglets are unable to secrete
sufficient digestive enzymes, resulting in incomplete nutrient hydrolysis and the accumulation of undigested
nutrients in the intestine. This accumulation alters the intestinal microbiota by promoting the colonization
[6,7]
of pathogenic bacteria, which triggers intestinal inflammation . The resulting inflammatory response
[8,9]
increases oxidative stress, leading to damage of the intestinal tissue . Consequently, nutrient absorption is
impaired, delaying pig growth. During this vulnerable period, additional diseases can further compromise
intestinal health.

One major pathogen that affects intestinal health during this stage is enterotoxigenic Escherichia coli
(E. coli), to which nursery pigs are particularly susceptible. This infection significantly impairs growth and
productivity. Unlike other species, pigs express F18 receptors on the epithelial cells of the small intestine,
allowing the F18 fimbriae of enterotoxigenic E. coli to adhere [10,11] . Enterotoxigenic E. coli is classified into
two major types - F18 and F4 E. coli - based on their fimbrial antigens . A recent study reported an
+
[12]
+
increasing trend in F18 E. coli infections, while F4 infections have remained relatively stable . This shift
+
[13]
+
may be attributed to modern commercial weaning practices and differences in antimicrobial susceptibility.
Notably, the genes encoding F18 receptors are highly expressed between 3 and 4 weeks of age , which
[14]
coincides with the typical weaning period in commercial pig production. This may explain the heightened
+
susceptibility of piglets to F18 E. coli infection during weaning . The F18 fimbriae of F18 E. coli facilitate
+
[14]
attachment to the epithelial F18 receptors, promoting colonization and the secretion of enterotoxins .
[15]
+
While the antimicrobial susceptibility of F4 E. coli has remained stable, resistance has increased among
+
F18 strains, potentially contributing to their rising prevalence . The enterotoxins secreted by F18 E. coli
[13]
+
disrupt electrolyte balance, causing water efflux from epithelial cells into the intestinal lumen, which leads to
post-weaning diarrhea (PWD). For these reasons, F18 E. coli is now considered the primary cause of PWD
+
among enterotoxigenic strains . In pigs challenged with F18 E. coli, the incidence of diarrhea increased by
+
[11]
28.3%, and fecal scores rose by 0.7 on a 1-to-5 scale (1: very firm stool; 5: very watery stool), compared to
unchallenged pigs [Table 1] [16-20] .
In addition, F18 E. coli-induced PWD significantly impaired growth performance in nursery pigs, with
+
reductions in average daily gain, average daily feed intake (ADFI), and gain-to-feed ratio (G:F) by 24.1%,
+
12.5%, and 14.9%, respectively [Table 2]. Moreover, pigs suffering from PWD due to F18 E. coli exhibit
impaired intestinal morphology and a leaky gut, further heightening their susceptibility to secondary
infections and resulting in increased veterinary costs .
[38]
F18 E. coli infection can further compromise intestinal health in pigs already stressed by weaning. As a
+
result, the F18 E. coli challenge model has been widely used in nursery pigs to evaluate its effects on
+
intestinal health [23-26] . Traditionally, fecal or digesta microbiota have been assessed as indicators of intestinal
health in pigs [39,40] . However, recent research suggests that mucosa-associated microbiota - directly collected
from the mucosa layer - provide a more reliable indicator [6,41] . This is because mucosa-associated microbiota
are more intimately linked with epithelial cells than luminal microbiota, offering greater potential for host-
microbe interactions [8,42,43] .