Genetic mechanisms of variation in erythromycin resistance in Lactobacillus rhamnosus strains

Lactobacillus rhamnosus Oxy and Pen are probiotic strains capable of colonizing the human and animal gastrointestinal tract, where they are considered to exert an array of beneficial effects.¹ A growing interest has recently been observed in probiotics for the treatment of antibiotic-associated diarrhea (AAD), which is a common complication of antibiotic use. Ruszczyński et al.² have shown the efficiency of Lb. rhamnosus Oxy and Pen administration in the prevention of AAD in children receiving antibiotic treatment. To allow the use of probiotic strains along with antibiotic therapy, these strains should be intrinsically resistant to a broad group of antibiotics. Intrinsically antibiotic-resistant probiotic strains may benefit patients whose normal intestinal microbiota have become unbalanced or greatly reduced in numbers because of the administration of various antimicrobial agents.³ There have been only a few reports on the antibiotic resistance of Lb. rhamnosus strains isolated from food and those of human origin.^{4, 5, 6}

Macrolides have a broad spectrum of antimicrobial activity. Antibiotics from this family target the 23S rRNA nucleotide within the 50S ribosomal subunit tunnel, thereby blocking peptide chain elongation.⁷ Bacterial resistance to macrolides, lincosamides and streptogramins (MLS phenotype) is often due to efflux systems, methylases or inactivating enzymes, for which more than 40 genes have been reported.⁸ It can also be caused by mutations in genes encoding ribosomal proteins and in the 23S rRNA gene. These chromosomal mutations alter the erythromycin binding site in the 23S rRNA molecule.⁹ MLS resistance in Lactobacillus is frequently associated with the presence of erm genes.^{10, 11} The genes erm(A), erm(B), erm(C) and erm(F) are widely distributed among Gram-positive and Gram-negative bacteria.¹² These genes have been found in plasmids and on the chromosome of Lactobacilli spp.^{13, 14}

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