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Pirt, S. Download references. The authors thank D. Kotsanas Monash Health , M. Hickey Ireland , A. Boulos Northern Ireland and K. Greenwood Quaintance, S. Schmidt-Malan and Y. Wi United States for their submission of isolates used in this study. Jean Y. Lee, Ian R. You can also search for this author in PubMed Google Scholar. All authors reviewed and contributed to the final manuscript. Correspondence to Benjamin P. Isolate metadata. Sheet A: clinical metadata. Sheet B: accession information.
Sheet C: sequencing and assembly statistics. Sheet D: resistome data. Sheet E: SRA strain metadata. Reprints and Permissions. Global spread of three multidrug-resistant lineages of Staphylococcus epidermidis. Nat Microbiol 3, — Download citation.
Received : 30 January Accepted : 27 July Published : 03 September Issue Date : October Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. BMC Microbiology Nature Communications Expanding on this growing prevalence, the investigators tested 32 rifampicin-resistant clinical S epidermidis isolates from 13 institutions in Australia and global isolates from 61 institutions across Europe and the United States.
Isolates from a total of 96 institutions in 24 countries helped to identify the genomic changes that caused The lineage that was dominant in Australia was found in 25 institutions in 4 countries. The other 2 lineages found to have near pan-drug resistance were found in dozens of other institutions across 7 countries.
The results of this study reveal not only the genomic mutations and different lineages that result in resistant S epidermidis, but also the global spread. Given that resistance to rifampicin encourages resistance to other antibiotics, these findings should be weighed seriously as we consider what bacteria are considered normal and often ignored. Thus, the current research was done to study the prevalence rate, distribution of virulence factors, and antimicrobial resistance properties of S.
The present investigation was done to assess the antibiotic resistance properties and distribution of virulence genes amongst the S. Table 2 represents the antibiotic resistance pattern of the S. Reversely, S. The prevalence of resistance against ciprofloxacin, clindamycin, azithromycin, and rifampin antibiotic agents were Figure 1 represents the prevalence of multi-drug resistant S.
Multidrug-resistant S. Table 3 represents the distribution of antibiotic resistance genes amongst the S. We found that aacA-D The prevalence of msrA and msrB antibiotic resistance genes were Table 4 represents the distribution of virulence factors amongst the S. We found that clfA Virulence factors for coa , X-region , and IgG-binding region were negative.
While S. Most S. However, recently published data revealed the high prevalence of S. Additionally, nosocomial S. The present study was done to assess the antibiotic resistance pattern and distribution of antibiotic resistance and virulence genes amongst the S. Relatively high prevalence of S. Because of the ubiquitous prevalence of S. Unauthorized and illegal prescription of antibiotics is the main reason for the high prevalence of antibiotic resistance.
Mohaghegh et al. Eladli et al. Ma et al. High prevalence of multidrug-resistant S. Similar patterns of antibiotic resistance of the S.
One of the most imperative mechanisms involving resistance against clindamycin is modulated by methylase enzyme which is often encoded by ermA and ermC genes [ 27 ].
The prevalence of ermA and ermC antibiotic resistance genes amongst the S. The majority of isolates carried two tetracyclines, two erythromycins, one macrolide, and several streptogramin resistance determinants revealed a great diffusion of these types of resistance. Eksi [ 28 ] revealed the higher prevalence of ermA than ermc antibiotic resistance genes amongst the clindamycin, erythromycin, and telithromycin-resistant and also higher prevalence of tetM than tetK antibiotic resistance genes amongst the tetracycline-resistant MRSA strains.
Duran et al. Adwan et al. High prevalence of tetK and tetM antibiotic resistance genes in the S. The presence of tetK gene on small multicopy plasmids and tetM on conjugative transposons contribute to the spread of these determinants [ 30 ]. Some of the S. This gene is often located on small multicopy plasmids which are present in many different staphylococcal species [ 30 ].
The ermA gene is usually carried by transposons which could explain its high prevalence amongst the S. Resistance to aminoglycosides which are encoded by the aacA-D gene It is because this gene is usually more diffused in staphylococci of human origin [ 30 ]. Amongst all virulence markers found in the S.
Eftekhar et al. Additionally, amongst all the examined genes, clfB The prevalence of tsst-1 gene amongst the S. Similar findings have also been reported from Iran Tsst-1 gene is a pyrogenic toxin that encodes a It is known as a severe acute disease distinguished by symptoms such as fever, rash, hypotension, and dysfunction of multiorgan systems.
In addition, TSS secretion into the human blood may raise the rate of neonatal TSS-like exanthematous disease, Kawasaki syndrome, and sudden infant death syndrome [ 32 ]. Regarding the other detected genes, the eta gene was presented in 6.
The prevalence of etb gene was The incidence rate of the eta and etb in the present study was higher than that reported in other investigations conducted on Iran 0. A higher prevalence of eta gene was reported in studies conducted in Czech Ghasemian et al. The incidence of the clfA gene in the bacterial strains of our research was relatively high A higher prevalence of this gene was reported from Brazil [ 39 ] and China [ 40 ].
Another important detected gene amongst the S. Agr virulence gene was also predominant amongst the S. The accessory gene regulator agr locus influences the expression of many virulence genes in the S.
Four allelic groups of agr , which generally inhibit the regulatory activity of each other, have been identified within the species. Interference in virulence gene expression caused by different agr groups has been suggested to be a mechanism for isolating bacterial populations and a fundamental basis for subdividing the species [ 43 ]. It encodes a two-component signal transduction system that leads to downregulation of surface proteins and upregulation of secreted proteins during in vitro growth.
A role for agr in virulence has been demonstrated by the attenuated virulence of agr mutants in different animal infection models [ 43 ]. The present investigation is the first report of the phenotypic and genotypic analysis of antibiotic resistance in the S. The total prevalence of S. Considerable prevalence of resistance against penicillin, tetracycline, erythromycin, cefazolin, and trimethoprim-sulfamethoxazole and high distribution of aacA-D , tetK , mecA , and tetM antibiotic resistance genes may pose a potential public health threat.
A high prevalence of multi-drug resistant S. Moreover, the presence of antibiotic resistance genes and also virulence factors in some S. Further researches are required to understand additional epidemiological aspects such as the exact relations between antibiotic resistance genes and virulence factors of the S. From February to July , a total of various types of hospital infectious samples were randomly collected from several private hospitals of the Ahvaz city, Iran.
Hospital infectious samples were defined as those which were collected from hospitalized patients with severe infections such as UTIs, WIs, and RIs. Furthermore, samples were taken from the site of infection. Samples were immediately transferred to the Clinical Microbiology Research Center of the Islamic Azad University of Shahrekord in a cooler with ice packs. The sample was enriched in a tryptic soy broth, and grown on mannitol salt agar, and then catalase, tube coagulase and urease tests, and carbohydrate fermentation were performed.
Patterns of antimicrobial resistance of the S. A simple disk diffusion technique on the Mueller-Hinton agar Merck, Germany medium was used for this purpose. The instructions of the Clinical and Laboratory Standards Institute were used for this purpose [ 46 ]. The diameter of the zone of inhibition produced by each antibiotic disc was measured and interpreted using the CLSI zone diameter interpretative standards [ 46 ]. Table 1 represents the list of primers and PCR conditions used for the amplification of virulence factors and antibiotic resistance genes [ 47 ].
Statistical analysis was done using the SPSS Prevalence, identification of virulence factors, O-serogroups and antibiotic resistance properties of Shiga-toxin producing Escherichia coli strains isolated from raw milk and traditional dairy products.
Antimicrob Resist Infect Control. Phenotypic analysis of antibiotic resistance and genotypic study of the vacA, cagA, iceA, oipA and babA genotypes of the Helicobacter pylori strains isolated from raw milk. Phenotypic and genotypic characterization of antibiotic resistance of methicillin-resistant Staphylococcus aureus isolated from hospital food.
Article Google Scholar. Shiga Vero -toxin producing Escherichia coli isolated from the hospital foods; virulence factors, o-serogroups and antimicrobial resistance properties.
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