Profiling Antibiotic Susceptibility among Distinct Enterococcus faecalis Isolates from Dental Root Canals

Abstract

Enterococcus faecalis, a leading multi-resistant nosocomial pathogen, is also the most frequently retrieved species from persistently infected dental root canals, suggesting that the oral cavity is a possible reservoir for resistant strains. However, antimicrobial susceptibility testing (AST) for oral enterococci remains scarce. Here, we examined the AST profiles of 37 E. faecalis strains, including thirty-four endodontic isolates, two vanA-type vancomycin-resistant isolates, and the reference strain ATCC-29212. Using Etest gradient strips and established EUCAST standards, we determined minimum inhibitory concentrations (MICs) for amoxicillin, vancomycin, clindamycin, tigecycline, linezolid, and daptomycin. Results revealed that most endodontic isolates were susceptible to amoxicillin and vancomycin, with varying levels of intrinsic resistance to clindamycin. Isolates exceeding the clindamycin MIC of the ATCC-29212 strain were further tested against last-resort antibiotics, with 7/27 exhibiting MICs matching the susceptibility breakpoint for tigecycline, and 1/27 reaching that of linezolid. Both vanA isolates confirmed vancomycin resistance and demonstrated resistance to tigecycline. In conclusion, while most endodontic isolates remained susceptible to first-line antibiotics, several displayed marked intrinsic clindamycin resistance, and MICs matched tigecycline’s breakpoint. The discovery of tigecycline resistance in vanA isolates highlights the propensity of clinical clone clusters to acquire multidrug resistance. Our results emphasize the importance of implementing AST strategies in dental practices for continued resistance surveillance.

Occurrence of Antimicrobial-Resistant Enterococcus spp. in Healthy Chickens Never Exposed to Antimicrobial Agents in Central Italy

“…Resistance to tetracycline is an important threat because these antimicrobials are largely employed in the treatment of animal and human infections. Moreover, the finding of about 30% of isolates resistant to tigecycline, a last-resort antimicrobial, is relevant, because it shows a gradually rising trend of resistance, as also observed by other studies [50].…”

Current Knowledge of Enterococcal Endocarditis: A Disease Lurking in Plain Sight of Health Providers

“…Chronic endocarditis, which is similar to the classic enterococcal endocarditis, is often much more ambiguous [ 96 , 101 ]. A variety of causes have been proposed, varying from colonisation of the oral cavity in endodontic disease to translocation of commensal enterococci in the gastrointestinal tract [ 97 , 98 ]. Enterococcus is the second leading cause of hospital-acquired bacteraemia, due in part to its ability to thrive in challenging environments.…”

“…Indirect infection can also occur through colonisation of the urinary or gastrointestinal tracts. Endogenous infections can also result from translocation through the epithelium of the GI tract [ 97 , 98 , 99 , 100 , 102 , 103 ] ( Figure 3 ).…”

“…Protein/Function Year of Publication srtC Sortase C/an enzyme that anchors surface proteins to the cell wall 2006 [47] atn Autolysin 2004 [83] salB Secretory antigen-like B/cell-shape determinant 2004 [83] bee Biofilm enhancer in Enterococcus/a putative cell wall-anchored protein 2006 [95] salA Secretory antigen-like A 2004 [83] bop Biofilm on plastic surface/a putative sugar-binding transcriptional regulator 2004 [96] gelE Secretory metalloprotease gelatinase E 2004 [8,83,97] dltA D-alanine lipoteichoic acid/D-alanine-D-alanyl carrier protein ligase 2006 [98] ebpA, ebpB, ebpC Endocarditis and biofilm-associated pili 2006 [47] ebpR Transcriptional regulator of ebpABC 2007 [99] epa (orfde4) Enterococcal polysaccharide antigen/a putative glycosyltransferase involved in polysaccharide synthesis 2004 [83] esp Enterococcal surface protein 2001, 2004 [94,100] etaR Enterococcal two-component system regulator 2004 [83] fsrA, fsrB, fsrC E. faecalis regulator/two-component quorum-sensing signal transduction system, regulates the expression of gelatinase and serine protease.…”

“…Indirect infection can also occur through colonisation of the urinary or gastrointestinal tracts. Endogenous infections can also result from translocation through the epithelium of the GI tract [97][98][99][100]102,103] (Figure 3). This process is facilitated by conventional antibiotic regimens, which can drastically increase the number of enterococci in the intestinal flora [104,105].…”