The current antibiotic resistance epidemic is reaching levels higher than previously reported. And the roots of this epidemic can be found not only in an increase in outpatient antibiotic use, but also on the high proportions of resistant bacteria transmitted from food-producing animals.
The effects of antibiotics on human gut bacterial diversity is of particular relevance during early life. It has been found that the infants’ gut carries high amounts of antibiotic-resistance genes compared with adults, regardless of antibiotic exposure. However, the source of the infant gut resistome and mobile genetic elements involved in transferring antibiotic resistance genes between bacteria has not yet been explored.
A new study, led by Dr. Marko Virta from the Department of Microbiology at the University of Helsinki (Finland), has found that maternal gut and breast milk microbiomes may contribute to infant acquisition of antibiotic resistance genes and mobile genetic elements.
The researchers analyzed breast milk and both infant and maternal fecal microbiomes through deep metagenomic sequencing in 16 mother-infant pairs over 8 months. Sample times included 1 month and 6 months for infant feces, gestational week 32 and 1 month postpartum for maternal feces, and 7 days and 1 month postpartum for maternal breast milk.
Infants’ fecal microbiota, antibiotic resistance genes and mobile genetic element compositions were more similar to those of their own mothers than to unrelated mothers. The highest levels of shared similarity were found in breast milk, with 70% of antibiotic resistance genes detected in breast milk overlapping with those in the infant gut.
On the other hand, maternal intrapartum antibiotic prophylaxis, breastfeeding duration and bacterial phylogeny also influenced the infant gut resistome and mobile genetic elements.
Infants from mothers who received antibiotics during delivery had a larger number of specific antibiotic resistance genes as well as mobile genetic elements, which persisted until 6 months of age and did not affect the mothers.
Furthermore, breastfeeding for less than 6 months led to an increase in some antibiotic resistance genes (e.g. those conferring resistance to tetracyclines) and mobile genetic elements (e.g. plasmids) in infants, when compared with breastfeeding for 6 months or longer. The role of breast milk in reducing the antibiotic resistance gene load in the infant gut is another reason for achieving a minimum of 6 months of exclusive breastfeeding, as recommended by the World Health Organization.
Antibiotic resistance gene abundance was also associated with the microbiome composition of infants and mothers. By and large, the researchers found that bacterial phylogeny was the primary determinant of the resistome. These results suggest that interactions between different taxonomic groups in both the gut microbiome of infants and mothers and in breast milk may shape the resistome.
Escherichia coli was the commensal bacterium that strongly correlated with total antibiotic resistance gene abundances, whereas Bifidobacterium genus dominant in the infant gut showed the strongest negative correlation. These findings confirm the previous hypothesis of Gammaproteobacteria (including first colonizers of the newborn gut) being the main contributors to the high abundance of antibiotic resistance genes in the infant gut compared with adults.
In the case of E. coli, the researchers found that acquired resistance genes were shared between different families and were indeed mobile, rather than having been acquired from the infants’ own mothers.
On the whole, these findings show that both maternal genes from breast milk and gut microbiota are unnoticed contributors to the infant gut microbiota’s resistome and related mobile genetic elements. However, microbiome composition was the major determinant in the overall antibiotic resistance load.
Pärnänen K, Karkman A, Hultman J, et al. Maternal gut and breast milk microbiota affect infant gut antibiotic resistome and mobile genetic elements. Nat Commun. 2018; 9(1):3891. doi: 10.1038/s41467-018-06393-w.