Severity of drug resistance and co-existence of Enterococcus faecalis in diabetic foot ulcer infections

. 2018 Jan ; 63 (1) : 115-122. [epub] 20170909

Jazyk angličtina Země Spojené státy americké Médium print-electronic

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/pmid28889401
Odkazy

PubMed 28889401
DOI 10.1007/s12223-017-0547-2
PII: 10.1007/s12223-017-0547-2
Knihovny.cz E-zdroje

The genes encoding aminoglycoside resistance in Enterococcus faecalis may promote collateral aminoglycoside resistance in polymicrobial wounds. We studied a total of 100 diabetic foot ulcer samples for infection and found 60 samples to be polymicrobial, 5 to be monomicrobial, and 35 samples to be culture negative. A total of 65 E. faecalis isolates were screened for six genes coding for aminoglycoside resistance, antibiotic resistance patterns, and biofilm production. Infectious Diseases Society of America/International Working Group on the Diabetic Foot system was used to classify the wound ulcers. Majority of the subjects with culture-positive wound were recommended conservative management, while 14 subjects underwent amputation. Enterococcal isolates showed higher resistance for erythromycin, tetracycline, and ciprofloxacin. Isolates from grade 3 ulcer showed higher frequency of aac(6')-Ie-aph(2″)-Ia, while all the isolates were negative for aph(2″)-Ib, aph(2″)-Ic, and aph(2″)-Id. The isolates from grade 3 ulcers showed higher resistance to aminoglycosides as well as teicoplanin and chloramphenicol. All the 39 biofilm producers were obtained from polymicrobial wound and showed higher resistance when compared to biofilm non-producers. Higher frequency of isolates carrying aac(6')-Ie-aph(2″)-Ia in polymicrobial community showing resistance to key antibiotics suggests widespread distribution of aminoglycoside-resistant E. faecalis and their role in worsening diabetic foot ulcers.

Zobrazit více v PubMed

Ann Pharmacother. 2013 Feb;47(2):159-69 PubMed

J Bacteriol. 1997 Oct;179(20):6355-9 PubMed

Diabetes Metab Res Rev. 2012 Feb;28 Suppl 1:163-78 PubMed

Science. 2003 Mar 28;299(5615):2071-4 PubMed

Int J Food Microbiol. 2005 Aug 25;103(2):191-8 PubMed

Diabetes Care. 2006 Aug;29(8):1727-32 PubMed

Nat Rev Microbiol. 2012 Mar 16;10(4):266-78 PubMed

J Hosp Infect. 2006 Mar;62 Suppl 1:S1-27 PubMed

J Med Microbiol. 2014 Oct;63(Pt 10):1377-85 PubMed

Sci Rep. 2015 Aug 17;5:13296 PubMed

Diabetes Care. 2012 Mar;35(3):617-23 PubMed

J Bacteriol. 2004 Jul;186(13):4085-99 PubMed

Nature. 2011 Aug 31;477(7365):457-61 PubMed

Antimicrob Agents Chemother. 2001 Apr;45(4):999-1007 PubMed

Science. 2003 Nov 28;302(5650):1569-71 PubMed

Front Biosci. 2002 Aug 01;7:d1825-42 PubMed

Diagn Microbiol Infect Dis. 1998 Nov;32(3):141-6 PubMed

J Antimicrob Chemother. 2012 Feb;67(2):433-9 PubMed

Foot (Edinb). 2011 Mar;21(1):6-14 PubMed

Clin Microbiol Infect. 2013 Sep;19(9):E398-404 PubMed

J Clin Microbiol. 2005 May;43(5):2291-302 PubMed

J Mol Biol. 2016 Aug 28;428(17 ):3355-71 PubMed

Nephrol Dial Transplant. 2010 Apr;25(4):1272-8 PubMed

Clin Infect Dis. 2012 Sep;55(6):764-70 PubMed

Clin Infect Dis. 2000 Aug;31(2):586-9 PubMed

J Bacteriol. 1986 Aug;167(2):631-8 PubMed

J Endod. 2006 Aug;32(8):722-6 PubMed

PLoS One. 2011;6(11):e27317 PubMed

Nature. 2005 Aug 25;436(7054):1171-5 PubMed

J Clin Microbiol. 2003 Mar;41(3):1109-13 PubMed

Clin Infect Dis. 1992 Sep;15(3):495-501 PubMed

Microb Pathog. 2010 Jan;48(1):18-27 PubMed

J Infect. 2006 May;52(5):383-6 PubMed

Clin Infect Dis. 1994 Feb;18(2):233-9 PubMed

N Engl J Med. 2000 Mar 9;342(10):710-21 PubMed

J Antimicrob Chemother. 2012 Mar;67(3):551-8 PubMed

Najít záznam

Citační ukazatele

Nahrávání dat ...

Možnosti archivace

Nahrávání dat ...