Multi-drug resistant (MDR) strains of Acinetobacter baumannii are responsible for an increasing number of opportunistic infections in hospitals. This study determined the prevalence of MDR A. baumannii isolates from intensive care units in a large tertiary-care hospital in Ismailia, Egypt, and the occurrence of different beta-lactamases in these isolates. Biotyping and antimicrobial susceptibility profile was done for isolated strains. Respiratory, urine, burn wound and blood specimens were collected from 350 patients admitted to different units; 10 strains (2.9%) of A. baumannii were isolated. All isolates showed resistance to more than 3 classes of antibiotics. Among the isolates, 6 isolates were carbapenemase producers, 2 were AmpC beta-lactamase producers and no isolates were metallo-betalactamase producers. Despite the low prevalence of A. baumannii infection in this hospital, the antibiotic resistance profile suggests that prevention of health-care-associated transmission of MDR Acinetobacter spp. infection is essential. Parmi ces isolats, six produisaient des carbapénèmases, deux des bêta-lactamases AmpC mais aucun isolat ne produisait de métallo-bêta-lactamases. Malgré une faible prévalence de l'infection à A. baumannii dans cet hôpital, le profil de résistance aux antibiotiques laisse penser que la prévention de la transmission de l'infection à Acinetobacter spp. multirésistante associée aux soins de santé est essentielle.
The increasing prevalence of multidrug-resistant and pan drug-resistant Acinetobacter baumannii as a cause of nosocomial infections has led to the need for the reassessment of novel combinations of antibiotics as our only current viable option for handling such infections until a new therapeutic option becomes available. Two of the most commonly used methods for testing antimicrobial synergy are the Time-kill assay method and the E-test method, and these were the methods used in this study. Antibiotic combinations tested in this study were azithromycin and polymyxin, tobramycin and polymyxin, polymyxin and rifampicin, and tobramycin and rifampicin. The azithromycin and polymyxin combination showed synergy, while the rifampicin and polymyxin combination showed antagonism. The synergy was achieved at lower MIC values than using each of the single agents alone against the same isolates. Synergy testing results varied according to the method used, and it is difficult to establish which method is more accurate. The use of these lower MIC values as a guide to determine effective therapeutic doses used in combination therapy can help to decrease the emergence of resistance and can also minimize the side effects associated with using a single agent at a higher dose. Further research is still required to predict in vivo efficacy of such combinations.
The population structure of Pseudomonas aeruginosa is panmictic-epidemic in nature, with the prevalence of some high-risk clones. These clones are often linked to virulence, antibiotic resistance, and more morbidity. The clonal success of these lineages has been linked to acquisition and spread of mobile genetic elements. The main aim of the study was to explore other molecular markers that explain their global success. A comprehensive set of 528 completely sequenced P. aeruginosa genomes was analyzed. The population structure was examined using Multilocus Sequence Typing (MLST). Strain relationships analysis and diversity analysis were performed using the geoBURST Full Minimum Spanning Tree (MST) algorithm and hierarchical clustering. A phylogenetic tree was constructed using the Unweighted Pair Group Method with Arithmetic mean (UPGMA) algorithm. A panel of previously investigated resistance markers were examined for their link to high-risk clones. A novel panel of molecular markers has been identified in relation to risky clones including armR, ampR, nalC, nalD, mexZ, mexS, gyrAT83I, gyrAD87N, nalCE153Q, nalCS46A, parCS87W, parCS87L, ampRG283E, ampRM288R, pmrALeu71Arg, pmrBGly423Cys, nuoGA890T, pstBE89Q, phoQY85F, arnAA170T, arnDG206C, and gidBE186A. In addition to mobile genetic elements, chromosomal variants in membrane proteins and efflux pump regulators can play an important role in the success of high-risk clones. Finding risk-associated markers during molecular surveillance necessitates applying more infection-control precautions.
Informed antibiotic prescription offers a practical solution to antibiotic resistance problem. With the increasing affordability of different sequencing technologies, molecular-based resistance prediction would direct proper antibiotic selection and preserve available agents. Amikacin is a broad-spectrum aminoglycoside exhibiting higher clinical efficacy and less resistance rates in Ps. aeruginosa due to its structural nature and its ability to achieve higher serum concentrations at lower therapeutic doses. This study examines the predictive potential of molecular markers underlying amikacin susceptibility phenotypes in order to provide improved diagnostic panels. Using a predictive model, genes and variants underlying amikacin resistance have been statistically and functionally explored in a large comprehensive and diverse set of Ps. aeruginosa completely sequenced genomes. Different genes and variants have been examined for their predictive potential and functional correlation to amikacin susceptibility phenotypes. Three predictive sets of molecular markers have been identified and can be used in a complementary manner, offering promising molecular diagnostics. armR, nalC, nalD, mexR, mexZ, ampR, rmtD, nalDSer32Asn, fusA1Y552C, fusA1D588G, arnAA170T, and arnDG206C have been identified as the best amikacin resistance predictors in Ps. aeruginosa while faoAT385A, nuoGA890T, nuoGA574T, lptAT55A, lptAR62S, pstBR87C, gidBE126G, gidBQ28K, amgSE108Q, and rplYQ41L have been identified as the best amikacin susceptibility predictors. Combining different measures of predictive performance together with further functional analysis can help design new and more informative molecular diagnostic panels. This would greatly inform and direct point of care diagnosis and prescription, which would consequently preserve amikacin functionality and usefulness.
The strong bond between dogs and their owners creates a close association that could result in the transfer of antibiotic-resistant bacteria from canines to humans, potentially leading to the spread of antimicrobial resistance genes. Pseudomonas aeruginosa, a common causative agent of persistent ear infections in dogs, is often resistant to multiple antibiotics. Assessing the antimicrobial resistance profile and genotype of P. aeruginosa is crucial for the appropriate use of veterinary pharmaceuticals. However, in recent years, few studies have been conducted on this bacterium in Japan. We determined the antimicrobial resistance profile and genotype of P. aeruginosa isolated from the ear canal of dogs in Japan in 2020. Analysis of antimicrobial resistance using disk diffusion tests indicated a high frequency of resistance to most antimicrobial agents. Particularly, 29 isolates from the ear canals of the 29 affected dogs (100%) were resistant to cefovecin, cefpodoxime, and florfenicol; however, they were susceptible to cefepime and piperacillin/tazobactam. Only 3.4, 10.3, and 10.3% of the isolates were resistant to ceftazidime, tobramycin, and gentamicin, respectively. Furthermore, upon analyzing the population structure using multilocus sequence typing, a considerably large clonal complex was not observed in the tested isolates. Three isolates, namely ST3881, ST1646, and ST532, were clonally related to the clinically isolated sequence types in Japan (such as ST1831, ST1413, ST1812, and ST1849), which is indicative of dog-to-human transmission. Considering the variation in antibiotic resistance compared to that reported by previous studies and the potential risk of dog-to-human transmission, we believe that the survey for antimicrobial resistance profile and population structure should be continued regularly. However, the prevalence of multidrug-resistant P. aeruginosa in dogs in Japan is not a crisis.
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