Abstract
BackgroundColistin resistance is mainly driven by alterations in the Gram-negative outer membrane lipopolysaccharides and is caused, in most cases, by mutations in mgrB gene. However, the recent emergence of plasmid-encoded colistin resistance among Enterobacteriaceae strains represents a serious threat to global public health. In this paper we have investigated the rates of colistin resistance and the underlying mechanisms in 450 Klebsiella pneumoniae and Escherichia coli isolates obtained from cancer patients in Egypt.MethodsColistin susceptibility and minimum inhibitory concentrations were determined according to the European Committee on Antimicrobial Susceptibility Testing, by broth microdilution, and by E-test. The mcr-1, mcr-2 and mgrB genes were detected by PCR and then sequenced. Clonal diversity in colistin-resistant K. pneumoniae was evaluated by multilocus sequence typing.ResultsForty (8.8%) colistin-resistant isolates, including 22 K. pneumoniae and 18 E. coli, were isolated over 18 months. Of these, 50% were carbapenem-resistant, out of which nine were blaOXA-48 and seven blaNDM-1 positive. The mechanisms of colistin resistance could be revealed only in three of the 40 resistant strains, being represented by mcr-1 in one blaNDM-1-positive E. coli strain and in one K. pneumoniae ST11 and by mgrB mutations, detected in one K. pneumoniae isolate. None of the studied isolates harbored mcr-2.ConclusionsOur results demonstrate a high frequency of colistin resistance in enterobacterial strains isolated from cancer patients, but a low prevalence of the most well known resistance mechanisms.
Highlights
Antibiotic resistance is one of the most important public health issues worldwide
We have evaluated the rates of colistin resistance in clinical enterobacterial infectious isolates from tertiary Cancer Hospital in Cairo, Egypt, to assess the presence of mcr-1 and mcr-2, as well as of mutations in mgrB
Minimum inhibitory concentrations of 3–64 mg/L were reported in 2.4% and 0.7% of isolates in France and Nigeria [22]. mcr-1 was first detected in human isolates in 2011 in Denmark, Germany, Italy, the Netherlands, Spain, Sweden, and the United Kingdom [23]. mcr-1 has since been detected in clinical isolates in Malaysia [7], South Africa [24], Egypt [9], the US [25], and China [26, 27]
Summary
Structural modifications of bacterial lipopolysaccharide are the main routes of colistin resistance in gram-negative bacteria. These modifications include addition of 4-amino-4-deoxy-l-arabinose or phosphoethanolamine following chromosomal mutations in genes encoding the two-component systems PhoPQ and PmrAB, or in mgrB, a negative regulator of PhoPQ [2]. Colistin resistance is mainly driven by alterations in the Gram-negative outer membrane lipopoly‐ saccharides and is caused, in most cases, by mutations in mgrB gene. In this paper we have investigated the rates of colistin resistance and the underlying mechanisms in 450 Klebsiella pneumoniae and Escherichia coli isolates obtained from cancer patients in Egypt
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