In our study, a clear increase in E. faecalis infections were reported between the two 5-year periods. However, the overall prevalence of E. faecalis remained almost stable ranging from 13.31% in the 2010–2014 to 11.03% during the 2017–2021 period. These data were higher than that of the 4-year summary from 2011 to 2014 reported to the national healthcare safety network at the Centers for Disease Control and Prevention of the USA, which was 7.4% . This could be explained by the study participants as the American study included patients from all the departments, various hospitals as well as rehabilitation facilities. The methods employed for the detection of E. faecalis could also attribute to the different results. In another study, E. faecalis was isolated in 24 of 200 (12%) surgical wound samples and in 2 of 100 (2%) blood cultures . All isolates were resistant to ampicillin and 19.2% were resistant to teicoplanin . The results of our study are in accordance with a recent publication from China that reported that resistance rates to ampicillin decreased gradually but to teicoplanin increased for E. faecalis .
Ampicillin is a penicillin beta-lactam antibiotic, with effectiveness against most infectious organisms like E. coli, S. pneumoniae, and H. influenzae [21, 22]. Teicoplanin is a glycopeptide antibiotic that was isolated more than 40 years ago as a product of Actionplanes teicomyceticus . It has potent bactericidal activity against a wide variety of aerobic and anaerobic gram-positive bacteria. Its adverse effects include ototoxicity, nephrotoxicity, skin rash, eosinophilia, neutropenia, and transient elevation of serum aminotransferases . It has been shown that serum levels of teicoplanin may not be predictable when administered to seriously ill patients, making cautious use in such cases mandatory .
Presently, the treatment of enterococcal infections represents one of the most arduous problems that physicians are dealing with. An increased prevalence of strains that are resistant to almost all antibiotics with in vitro bactericidal activity against enterococci has been observed, reflecting a perturbing tendency. The enterococci are intrinsically resistant to many commonly used antimicrobial agents, namely cephalosporins, aminoglycosides, clindamycin, quinupristin/dalfopristin, and trimethoprim-sulfamethoxazole . All enterococci exhibit decreased susceptibility to penicillin and ampicillin, as well as high-level resistance to most all semi-synthetic penicillins . Nonetheless, for many isolates, despite their level of resistance to ampicillin, its clinical use is not prohibited. Actually, ampicillin remains the treatment of choice for enterococcal infections that lack other mechanisms for high-level resistance . Our data are in concordance with this therapeutic trend indicating that, currently, ampicillin could be effective against E. faecalis isolates. In the second 5-year period both ampicillin and teicoplanin remained highly active against E. faecalis isolates.
Vancomycin-resistant enterococci (VRE) are a usual and difficult-to-treat reason for hospital-acquired infection . VRE are distinguished from other strains of Enterococcus by a raised minimum inhibitory concentration (MIC) for vancomycin and the presence of vancomycin-resistance gene clusters such as vanA . High-level resistance to vancomycin is encoded by different clusters of genes referred to as the vancomycin-resistance gene clusters (for example, vanA, B, D, and M gene clusters). VanA is the most common type of vancomycin resistance, usually mediates higher levels of resistance than other types, and causes cross-resistance to teicoplanin. The VanB phenotype, the second most common type, is less frequently encountered than VanA .
High-level vancomycin resistance is the most problematic resistance of enterococci because it often appears in strains already highly resistant to ampicillin. The three major phenotypes, VanA, VanB, and VanD, can sometimes be differentiated by the level of vancomycin resistance, susceptibility to the glycopeptide antibiotic teicoplanin, and whether the resistance is induced by exposure to teicoplanin .
Adherence to protocols for cleaning patient rooms should be monitored to decrease environmental contamination with VRE . Healthcare-associated VRE is transmitted in the hands of healthcare workers; as a result, good hand hygiene is considered an essential measure for reducing the spread of this pathogen. Colonization with VRE typically precedes infection. Colonization most commonly occurs in patients with previous antimicrobial therapy and residents in long-term care facilities .
A multimodal strategy is required for VRE prevention and control, including general infection prevention measures including the best care of vascular and urinary catheters, accurate and quick diagnosis and management, judicious use of antibiotics, and infection transmission prevention [32,33,34].
.An infection control program is essential to surgical site infection (SSI) prevention . A successful program may decrease the rate of SSIs by 40% [27,28,29,30]. The prompt administration of efficient preoperative antibiotics and careful attention to surgical technique rank as the most crucial elements in the prevention of SSI, along with maintaining a clean operating room environment. A variety of topical and local antibiotic delivery methods as well as wound-protecting barrier devices have been employed during surgery to lower the incidence of SSI . .The use of antimicrobial-coated sutures may minimize the risk of SSI, although the available and high-quality data are scarce .