Linezolid-Resistant Enterococcus spp. Isolates from Foods of Animal Origin—The Genetic Basis of Acquired Resistance

Abstract

Enterococci are important opportunistic pathogens with the capacity to acquire and spread antibiotic resistance. At present, linezolid-resistant enterococci (LRE) pose a great challenge. Linezolid is considered as a last resort antibiotic in the treatment of enterococcal infections, so it is important to monitor the occurrence of LRE in various environments. The aim of this study was to define the genetic mechanisms of linezolid resistance in enterococci (E. faecalis, E. faecium, E. hirae, E. casseliflavus) isolated from foods of animal origin (n = 104). Linezolid resistance (LR) was shown by 26.9% of isolates. All of them displayed linezolid MICs of 8–32 µg/mL, and 96.4% of them were multidrug multidrug-resistant. The most common acquired linezolid resistance gene in LR isolates was poxtA (64%), followed by optrA (28%) and cfr (12%). According to the authors’ knowledge, this research is the first to indicate the presence of the cfr gene among isolates from food. In 28.6% of the isolates, the point mutation G2576T in the V domain of the 23S rRNA was responsible for linezolid resistance. All isolates harbored the wild-type rplC, rplD and rplV genes. The obtained results indicate that linezolid resistance among enterococci in animal-derived food may result from various genetic mechanisms. The most worrying is that this resistance is encoded on mobile genetic elements, so there is a risk of its rapid transmission, even despite the lack of selective pressure resulting from the use of antibiotics.

Transmission of linezolid-resistant Enterococcus isolates carrying optrA and poxtA genes in slaughterhouses

“…95.65% (44/46) of strains belonged to MDR strains, similar to the MDR rate of enterococci isolated from Polish marketed animal foods (Zarzecka et al, 2022). Among them, the resistance rates of 10.3389/fsufs.2023.1179078 Frontiers in Sustainable Food Systems 07 frontiersin.org tilmicosin, sulfisoxazole, tiamulin, florfenicol and linezolid were all above 70%, which was much higher than the resistance rate of optrAor poxtA-positive enterococci isolated from retail meat and foodproducing animals in Tunisian (Elghaieb et al, 2019).…”

Detection of Genes Related to Linezolid Resistance (poxtA, cfr, and optrA) in Clinical Isolates of Enterococcus spp. from Humans: A First Report from Iran

“…Therefore, continued surveillance and implementation of effective infection control measures are crucial in preventing the dissemination of antibiotic-resistant Enterococci . [ 35 36 37 38 ]…”

The burden of antibiotic resistance of the main microorganisms causing infections in humans – review of the literature

“…The US Food and Drug Administration (FDA) approved linezolid as the first oxazolidinone antibiotic for use in clinical settings in 2000. Oxazolidinones, which are now used in hospital settings, have been regarded as a novel class of antibiotics for the last 40 years [ 82 ]. They are very effective against Gram-positive bacteria, including VRE and MRSA, and act through the suppression of protein synthesis by interacting with domain V of the 23S ribosomal RNA (rRNA) [ 83 ].…”

“…reported that 28 strains exhibited phenotypic resistance to linezolid. Two strains (7.1%) were recognised as E. faecium , one strain (3.6%) was identified as E. hirae , and the majority (89.3%) belonged to the E. faecalis strain [ 82 ]. In total, 96.4% of the linezolid-resistant isolates were resistant to antibiotics from three or more classes, primarily ansamycins, tetracyclines, and macrolides, with linezolid MICs of 8–32 µg/ml [ 82 ].…”

“…Two strains (7.1%) were recognised as E. faecium , one strain (3.6%) was identified as E. hirae , and the majority (89.3%) belonged to the E. faecalis strain [ 82 ]. In total, 96.4% of the linezolid-resistant isolates were resistant to antibiotics from three or more classes, primarily ansamycins, tetracyclines, and macrolides, with linezolid MICs of 8–32 µg/ml [ 82 ]. In eight strains (28.6%), linezolid resistance was caused by the point mutation G2576T in domain V of the 23S rRNA.…”