Special Issue "Antimicrobial Resistance in Nosocomial Clinical Microorganisms: from Vitro to Molecular"

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Antimicrobial Agents and Resistance".

Deadline for manuscript submissions: 30 November 2021.

Special Issue Editors

Dr. Matthew Donadu
E-Mail Website
Guest Editor
Department of Chemistry and Pharmacy, University of Sassari, 07100 Sassari SS, Italy
Interests: clinical microbiology; antimicrobial resistance; sexually transmitted infections; pathogen; virulence; bacteriology; essential oils; mycology
Dr. Donatella Usai
E-Mail Website
Guest Editor
Department of Biomedical Sciences, University of Sassari, Sassari, Italy
Interests: clinical microbiology; antimicrobial resistance; sexually transmitted infections; pathogenic; virulence; bacteriology; mycology
Prof. Stefania Zanetti
E-Mail Website
Guest Editor
Department of Biomedical Sciences, University of Sassari, Sassari, Italy
Interests: clinical microbiology; antimicrobial resistance; sexually transmitted infections; pathogenic; virulence; bacteriology; mycology

Special Issue Information

Dear Colleagues,

Infectious diseases are the second leading cause of death worldwide and 17 million people die each year from bacterial infections. In Europe, 25,000 people die from drug-resistant infections. In the United States, infections are the fourth most common cause of death, with 2.8 million people infected each year and 35,000 deaths from drug-resistant infections. Multiple mechanisms are involved in the natural and acquired resistance to many of the antimicrobial agents commonly used in clinical practice. Rates of multidrug-resistant infections have increased compared to previous years, especially among nosocomial clinical pathogens.

In this Special Issue, we wanted to address the issue of nosocomial infections caused by multidrug-resistant infectious agents and their pathogenic and virulent mechanisms.

Dr. Matthew Donadu
Dr. Donatella Usai
Prof. Stefania Zanetti
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Microorganisms is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mechanisms of pathogenicity
  • virulence mechanisms
  • new antimicrobial
  • antimicrobial effects
  • clinical applications
  • the antifungal properties
  • antiviral properties
  • antimicrobial mechanisms
  • the combination with other antimicrobials
  • the effects and possible global changes of the human microbiome

Published Papers (3 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Article
Antimicrobial Resistance Mechanisms and Virulence of Colistin- and Carbapenem-Resistant Acinetobacter baumannii Isolated from a Teaching Hospital in Taiwan
Microorganisms 2021, 9(6), 1295; https://doi.org/10.3390/microorganisms9061295 - 14 Jun 2021
Viewed by 645
Abstract
Acinetobacter baumannii, a Gram-negative bacterium, is an important nosocomial pathogen. Colistin-resistant A. baumannii is becoming a new concern, since colistin is one of the last-line antibiotics for infections by carbapenem-resistant A. baumannii. From 452 carbapenem-resistant isolates collected in a teaching hospital in [...] Read more.
Acinetobacter baumannii, a Gram-negative bacterium, is an important nosocomial pathogen. Colistin-resistant A. baumannii is becoming a new concern, since colistin is one of the last-line antibiotics for infections by carbapenem-resistant A. baumannii. From 452 carbapenem-resistant isolates collected in a teaching hospital in Taipei, Taiwan, we identified seven that were resistant to colistin. Carbapenem resistance in these isolates is attributed to the presence of carbapenemase gene blaOXA-23 in their genomes. Colistin resistance is presumably conferred by mutations in the sensor kinase domain of PmrB found in these isolates, which are known to result in modification of colistin target lipid A via the PmrB–PmrA–PmrC signal transduction pathway. Overexpression of pmrC, eptA, and naxD was observed in all seven isolates. Colistin resistance mediated by pmrB mutations has never been reported in Taiwan. One of the seven isolates contained three mutations in lpxD and exhibited an altered lipopolysaccharide profile, which may contribute to its colistin resistance. No significant difference in growth rates was observed between the isolates and the reference strain, suggesting no fitness cost of colistin resistance. Biofilm formation abilities of the isolates were lower than that of the reference. Interestingly, one of the isolates was heteroresistant to colistin. Four of the isolates were significantly more virulent to wax moth larvae than the reference. Full article
Show Figures

Figure 1

Article
Molecular Epidemiology and Characterization of Carbapenem-Resistant Klebsiella pneumoniae Isolated from Urine at a Teaching Hospital in Taiwan
Microorganisms 2021, 9(2), 271; https://doi.org/10.3390/microorganisms9020271 - 28 Jan 2021
Cited by 1 | Viewed by 810
Abstract
Urinary tract infections (UTIs) are common in clinics and hospitals and are associated with a high economic burden. Enterobacterium Klebsiella pneumoniae is a prevalent agent causing UTIs. A high prevalence of carbapenem-resistant K. pneumoniae (CRKP) has emerged recently and is continuing to increase. [...] Read more.
Urinary tract infections (UTIs) are common in clinics and hospitals and are associated with a high economic burden. Enterobacterium Klebsiella pneumoniae is a prevalent agent causing UTIs. A high prevalence of carbapenem-resistant K. pneumoniae (CRKP) has emerged recently and is continuing to increase. Seventeen urinary CRKP isolates collected at a teaching hospital in Taiwan from December 2016 to September 2017 were analyzed to elucidate their drug resistance mechanisms. Two-thirds of the isolates were obtained from outpatients. Antimicrobial susceptibility tests demonstrated multidrug resistance in all the isolates. Multilocus sequence typing analysis showed high diversity among the isolates. PCR analysis demonstrated the presence of carbapenemases in three isolates. All isolates carried at least one other extended-spectrum β-lactamase, including TEM, DHA, and CTX-M. Fifteen isolates contained mutations in one of the outer membrane porins that were assessed. The expression levels of the acrB and/or oqxB efflux pump genes, as determined by qRT-PCR, were upregulated in 11 isolates. Six isolates might have utilized other efflux pumps or antimicrobial resistance mechanisms. These analyses demonstrated a highly diverse population and the presence of complex resistance mechanisms in urinary isolates of K. pneumoniae. Full article
Show Figures

Figure 1

Article
Epidemiology and Characterization of CTX-M-55-Type Extended-Spectrum β-Lactamase-Producing Salmonella enterica Serovar Enteritidis Isolated from Patients in Shanghai, China
Microorganisms 2021, 9(2), 260; https://doi.org/10.3390/microorganisms9020260 - 27 Jan 2021
Viewed by 515
Abstract
The emergence of extended-spectrum β-lactamase-producing Salmonella enterica serovar Enteritidis (ESBL-SE) in humans and foods has gained global attention. In particular, CTX-M-type ESBL-SE are increasingly being detected from various sample types. The aim of this study was to comprehensively analyze the epidemiology and characteristics [...] Read more.
The emergence of extended-spectrum β-lactamase-producing Salmonella enterica serovar Enteritidis (ESBL-SE) in humans and foods has gained global attention. In particular, CTX-M-type ESBL-SE are increasingly being detected from various sample types. The aim of this study was to comprehensively analyze the epidemiology and characteristics of blaCTX-M-55-carrying ESBL-SE isolates of clinical origin in Shanghai, China. A total of 292 S. Enteritidis isolates were recovered from the feces and blood of outpatients and inpatients between 2006 and 2014. Overall, there was a high frequency of cefotaxime-resistant isolates (97.3%), which was significantly higher (p < 0.01) than that of isolates resistant to the other tested antibiotics. All S. Enteritidis isolates exhibited resistance to ≥1 antibiotic, and 98.0% were multidrug resistant. A total of 233 isolates were identified as ESBL-SE, 166 of which were CTX-M type. Six subtypes of CTX-M-encoding genes were detected, among which blaCTX-M-55 (91.6%, 152/166) was the most prevalent genotype. There was high genetic similarity among blaCTX-M-55-positive ESBL-SE. The blaCTX-M-55 gene in the ESBL-SE donor strains could be easily transferred into Enterobacteriaceae recipient strains. This study highlights that CTX-M-55 should be considered an important surveillance target in Shanghai, China. Cephalosporins, especially cefotaxime, must be used with caution in empirical treatment for Salmonella infections. Full article
Show Figures

Figure 1

Back to TopTop