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Antimicrobial resistance in community and nosocomial Escherichia coli urinary tract isolates, London 2005 – 2006
David C Bean, Daniel Krahe, David W Wareham
Annals of Clinical Microbiology and Antimicrobials , 2008, DOI: 10.1186/1476-0711-7-13
Abstract: Antimicrobial susceptibility to ampicillin, amoxicillin/clavulanate, cefalexin, ciprofloxacin, gentamicin, nitrofurantoin, trimethoprim and cefpodoxime was determined for 11,865 E. coli urinary isolates obtained from community and hospitalised patients in East London.Nitrofurantoin was the most active agent (94% susceptible), followed by gentamicin and cefpodoxime. High rates of resistance to ampicillin (55%) and trimethoprim (40%), often in combination were observed in both sets of isolates. Although isolates exhibiting resistance to multiple drug classes were rare, resistance to cefpodoxime, indicative of Extended spectrum β-lactamase production, was observed in 5.7% of community and 21.6% of nosocomial isolates.With the exception of nitrofurantoin, resistance to agents commonly used as empirical oral treatments for UTI was extremely high. Levels of resistance to trimethoprim and ampicillin render them unsuitable for empirical use. Continued surveillance and investigation of other oral agents for treatment of UTI in the community is required.Escherichia coli is the predominant cause of both community and nosocomial urinary tract infection (UTI). In the UK, trimethoprim or nitrofurantoin are usually recommended for empirical treatment of episodes of uncomplicated cystitis in the community [1], whilst parenteral cephalosporins and aminoglycosides are reserved for complicated infections or pyelonephritis. In North America a cut off point of 20% has been suggested as the level of resistance at which an agent should no longer be used empirically [2]. A UK study of the antimicrobial susceptibility of bacterial pathogens causing UTI in 1999 – 2000 showed high levels of resistance to trimethoprim, amoxicillin and oral cephalosporins [3] whilst a study of three collections of E. coli strains obtained from patients in East London in 1991, 1999 and 2004 showed rates of trimethoprim resistance of over 30% [4]. The emergence of strains producing extended spectrum β-lactamases
In vivo susceptibility of ESBL producing Escherichia coli to ceftriaxone in children with acute pyelonephritis  [PDF]
Peco-Anti? Amira,Paripovi? Du?an,Buljugi? Svetlana,Spasojevi?-Dimitrijeva Brankica
Srpski Arhiv za Celokupno Lekarstvo , 2012, DOI: 10.2298/sarh1206321p
Abstract: Introduction. The choice of empiric therapy of acute pyelonephritis (APN) in children should be based on the knowledge of Escherichia coli (E. coli) as the most common uropathogen and its antibiotic sensitivities considering that nowadays ESBL-producing [ESBL (+)] E. coli is on the rise worldwide. Objective. To examine in vivo susceptibility of ESBL (+) E. coli to ceftriaxone (CTX), and to evaluate the options for empiric therapy for APN in children. Methods. Retrospective study of CTX empiric therapy of APN in children treated at the University Children s Hospital in Belgrade from January 2005 to December 2009. ESBL phenotypic confirmatory test with ceftazidime, CTX and cefotaxime was performed for all urine isolates by disc diffusion method on Mueller-Hinton agar plates. In vivo sensitivity of CTX documented by clinical response to empiric CTX therapy was compared between two groups of children: group I with ESBL (+) E. coli and group II with ESBL (-) E. coli APN. Results. Group I with ESBL (+) APN consisted of 94 patients and group II of 120 patients with ESBL (-) APN, respectively. All patients received CTX as empiric therapy at a mean dose of 66.9 mg during 7.2±2.6 days of therapy. Clinical effect of CTX was similar in patients with ESBL (+) compared to those with ESBL (-) APN. Conclusions. In vitro resistance of ESBL E. coli to CTX determined by standard methods is not sufficiently predictive for its in vivo sensitivity. Therefore CTX may be used as empiric therapy for acute pyelonephritis in children.
Evaluation of the Susceptibility profiles, genetic similarity and presence of qnr gene in Escherichia coli resistant to ciprofloxacin isolated in Brazilian hospitals
Pereira, Andrea S.;Andrade, Soraya S.;Monteiro, Jussimara;Sader, Helio S.;Pignatari, Antonio C.C.;Gales, Ana C.;
Brazilian Journal of Infectious Diseases , 2007, DOI: 10.1590/S1413-86702007000100011
Abstract: increasing quinolone resistance has been reported worldwide, mainly among clinical isolates of escherichia coli. the objectives of this study were to determine the susceptibility profile, the genetic relatedness, and the prevalence of the qnr gene among ciprofloxacin-resistant escherichia coli isolated from distinct brazilian hospitals. a total of 144 ciprofloxacin-resistant escherichia coli were isolated from 17 brazilian hospitals between january/2002 and june/2003. the antimicrobial susceptibility testing was performed by microdilution according to nccls. the presence of the qnr gene was initially screened by colony blotting, and then confirmed by pcr followed by dna sequencing. ninety-five urinary ciprofloxacin-resistant escherichia coli were further selected for molecular typing by pulsed-field gel electrophoresis (pfge). imipenem and meropenem showed the highest susceptibility rates (100.0% for both compounds) followed by amikacin (91.0%) and piperacillin/tazobactan (84.8%). a single ciprofloxacin-resistant escherichia coli isolate was positive for qnr among the 144 ciprofloxacin-resistant escherichia coli. forty-six pfge patterns were observed among the 95 ciprofloxacin-resistant escherichia coli type. this study shows that therapeutic options are limited for treatment of ciprofloxacin-resistant escherichia coli due to the presence of additional mechanisms of antimicrobial resistance, such as esbl production. the qnr gene was uncommon among ciprofloxacin-resistant escherichia coli clinical isolates, but its identification might indicate the emergence of this mechanism of quinolone resistance in brazil. the great genomic variability found among the ciprofloxacin-resistant escherichia coli highlights the importance of the appropriate use of quinolone to restrict the selection of resistant isolates.
Ciprofloxacin Causes Persister Formation by Inducing the TisB toxin in Escherichia coli  [PDF]
Tobias D?rr,Marin Vuli?,Kim Lewis
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.1000317
Abstract: Bacteria induce stress responses that protect the cell from lethal factors such as DNA-damaging agents. Bacterial populations also form persisters, dormant cells that are highly tolerant to antibiotics and play an important role in recalcitrance of biofilm infections. Stress response and dormancy appear to represent alternative strategies of cell survival. The mechanism of persister formation is unknown, but isolated persisters show increased levels of toxin/antitoxin (TA) transcripts. We have found previously that one or more components of the SOS response induce persister formation after exposure to a DNA-damaging antibiotic. The SOS response induces several TA genes in Escherichia coli. Here, we show that a knockout of a particular SOS-TA locus, tisAB/istR, had a sharply decreased level of persisters tolerant to ciprofloxacin, an antibiotic that causes DNA damage. Step-wise administration of ciprofloxacin induced persister formation in a tisAB-dependent manner, and cells producing TisB toxin were tolerant to multiple antibiotics. TisB is a membrane peptide that was shown to decrease proton motive force and ATP levels, consistent with its role in forming dormant cells. These results suggest that a DNA damage–induced toxin controls production of multidrug tolerant cells and thus provide a model of persister formation.
Ciprofloxacin Causes Persister Formation by Inducing the TisB toxin in Escherichia coli  [PDF]
Tobias D?rr,Marin Vuli?,Kim Lewis
PLOS Biology , 2010, DOI: 10.1371/journal.pbio.1000317
Abstract: Bacteria induce stress responses that protect the cell from lethal factors such as DNA-damaging agents. Bacterial populations also form persisters, dormant cells that are highly tolerant to antibiotics and play an important role in recalcitrance of biofilm infections. Stress response and dormancy appear to represent alternative strategies of cell survival. The mechanism of persister formation is unknown, but isolated persisters show increased levels of toxin/antitoxin (TA) transcripts. We have found previously that one or more components of the SOS response induce persister formation after exposure to a DNA-damaging antibiotic. The SOS response induces several TA genes in Escherichia coli. Here, we show that a knockout of a particular SOS-TA locus, tisAB/istR, had a sharply decreased level of persisters tolerant to ciprofloxacin, an antibiotic that causes DNA damage. Step-wise administration of ciprofloxacin induced persister formation in a tisAB-dependent manner, and cells producing TisB toxin were tolerant to multiple antibiotics. TisB is a membrane peptide that was shown to decrease proton motive force and ATP levels, consistent with its role in forming dormant cells. These results suggest that a DNA damage–induced toxin controls production of multidrug tolerant cells and thus provide a model of persister formation.
Vaginal Colonization by papG Allele II+ Escherichia coli Isolates from Pregnant and Nonpregnant Women as Predisposing Factor to Pyelonephritis  [PDF]
Sareaa Maseer Gatya Al-Mayahie
Infectious Diseases in Obstetrics and Gynecology , 2013, DOI: 10.1155/2013/860402
Abstract: Vaginal (61) and fecal (61) Escherichia coli isolates from pregnant and nonpregnant women (18–45 years old) were surveyed for papG alleles by PCR technique. papG allele II was the most prevalent among both vaginal (32.7%) and fecal (3.2%) isolates, whereas other alleles were found only among vaginal isolates (1.6% for alleles I and III and 3.2% for alleles II + III). papG+ pregnant women's isolates did not differ significantly from those of nonpregnant in possession of papG allele II (90% versus 73.3%), whereas both (32.7%) differed significantly ( ) in comparison with fecal isolates (3.2%). The vast majority of papG allele II+ vaginal isolates were clustered in group B2 (81.8%) and much less in group D (18.1%). Also, most of them were positive for fimH (100%), papC (100%), iucC (90.9%), and hly (72.7%), and about half of them were positive for sfa/foc (45.4%). In addition, the mean of VFs' gene possession was 3.5 (range from 2 to 5). It can be concluded that vaginal colonization by papG allele II+ E. coli is possibly one of the predisposing factors of both pregnant and nonpregnant women to pyelonephritis, but its potential may be modified by other factors especially host factors. 1. Introduction Bacterial adherence is an essential step in all infections which involves surface interactions between specific receptors on the mammalian cell membrane and ligands on the bacterial surface. Tissue specificity of infection is determined significantly by the presence or absence of specific receptors on mammalian cells [1]. The ability of uropathogenic Escherichia coli (UPEC) to adhere to host uroepithelia is an important stage in the successful colonization of the urinary tract and pathogenesis of urinary tract infection (UTI). The principal adherence organelle of UPEC is P fimbriae, which mediates Gal(α1-4)Gal-specific binding via the adhesin molecule PapG [2]. The three molecular variants (I to III) of the adhesin are coded by the adhesin gene papG of which there are three known alleles [3]. These variants exhibit different receptor binding specificities [4]. Naturally, papG alleles occurin four combinations, that is, class Ι plus III, class III only, class II plus III, and class II only [2, 5]. According to the receptor specificity of the PapG adhesin, p-fimbriated uropathogenic E. coli is clinically divided into two subtypes: papG allele II+ strains associated with pyelonephritis and bacteremia, and papG allele III+ strains associated with cystitis but have been found in pyelonephritis and bacteremia [2, 5–7]. The most common extraintestinal E. coli
Antibacterial Derivatives of Ciprofloxacin to Inhibit Growth of Necrotizing Fasciitis Associated Penicillin Resistant Escherichia coli  [PDF]
Ronald Bartzatt,Suat L. G. Cirillo,Jeffrey D. Cirillo
Journal of Pharmaceutics , 2013, DOI: 10.1155/2013/517638
Abstract: Escherichia coli (E. coli) is associated with necrotizing fasciitis (type I) and can induce enough damage to tissue causing hypoxia. Three ester derivatives of the broad-spectrum antibiotic ciprofloxacin were placed into bacteria culture simultaneously with the parent ciprofloxacin (drug 1) to ascertain the level of antibacterial activity. The n-propyl (drug 2), n-pentyl (drug 3), and n-octyl (drug 4) esters of ciprofloxacin were synthesized under mixed phase conditions and by microwave excitation. The formation of ester derivatives of ciprofloxacin modified important molecular properties such as Log P and polar surface area which improves tissue penetration, yet preserved strong antibacterial activity. The Log P values for drugs 1, 2, 3, and 4 became ?0.701, 0.437, 1.50, and 3.02, respectively. The polar surface areas for drugs 1, 2, 3, and 4 were determined to be 74.6 Angstroms2, 63.6 Angstroms2, 63.6 Angstroms2, and 63.6 Angstroms2, respectively. These values of Log P and polar surface area improved tissue penetration, as indicated by the determination of dermal permeability coefficient ( ) and subsequently into the superficial fascial layer. All drugs induced greater than 60% bacterial cell death at concentrations less than 1.0 micrograms/milliliter. The ester derivatives of ciprofloxacin showed strong antibacterial activity toward penicillin resistant E. coli. 1. Introduction Necrotizing fasciitis is an often fatal infection of the softtissue that will commonly begin after some form of trauma [1]. This softtissue infection involves the superficial fascial layers (or hypodermis) of the abdomen, extremities, or perineum [1]. This infection of the deep layers of skin and subcutaneous tissues easily spreads across the fascial plane. A polymicrobial infection is more common, involving gram-positive, gram-negative (i.e., Escherichia col (E. coli)), aerobic, and anaerobic bacteria [1]. Quick diagnosis, application of broad-spectrum antibiotics, and/or surgical intervention is required for successful patient outcome [1]. The three types of necrotizing fasciitis are based on anatomy; the depth of infection; and/or (3) the microbial source for the infection [2]. Type I infection is by polymicrobial incidents involving gram-positive cocci, Gram-negative rods, and anaerobes [2]. For Type I episodes, one type of bacteria can aid the survival and growth of another bacteria (this is synergy). Common type I category bacteria include E. coli, Klebsiella, Staphylococcus aureus, and Streptococcus species [2]. The Treatment of the infection requires strong
Ciprofloxacin-resistant Escherichia coli in Central Greece: mechanisms of resistance and molecular identification  [cached]
Mavroidi Angeliki,Miriagou Vivi,Liakopoulos Apostolos,Tzelepi Εva
BMC Infectious Diseases , 2012, DOI: 10.1186/1471-2334-12-371
Abstract: Background Fluoroquinolone resistant E. coli isolates, that are also resistant to other classes of antibiotics, is a significant challenge to antibiotic treatment and infection control policies. In Central Greece a significant increase of ciprofloxacin-resistant Escherichia coli has occurred during 2011, indicating the need for further analysis. Methods A total of 106 ciprofloxacin-resistant out of 505 E. coli isolates consecutively collected during an eight months period in a tertiary Greek hospital of Central Greece were studied. Antimicrobial susceptibility patterns and mechanisms of resistance to quinolones were assessed, whereas selected isolates were further characterized by multilocus sequence typing and β-lactamase content. Results Sequence analysis of the quinolone-resistance determining region of the gyrA and parC genes has revealed that 63% of the ciprofloxacin-resistant E. coli harbored a distinct amino acid substitution pattern (GyrA:S83L + D87N; ParC:S80I + E84V), while 34% and 3% carried the patterns GyrA:S83L + D87N; ParC:S80I and GyrA:S83L + D87N; ParC:S80I + E84G respectively. The aac (6’)-1b-cr plasmid-mediated quinolone resistance determinant was also detected; none of the isolates was found to carry the qnrA, qnrB and qnrS. Genotyping of a subset of 35 selected ciprofloxacin-resistant E. coli by multilocus sequence typing has revealed the presence of nine sequence types; ST131 and ST410 were the most prevalent and were exclusively correlated with hospital and health care associated infections, while strains belonging to STs 393, 361 and 162 were associated with community acquired infections. The GyrA:S83L + D87N; ParC:S80I + E84V substitution pattern was found exclusively among ST131 ciprofloxacin-resistant E. coli. Extended-spectrum β-lactamase-positive ST131 ciprofloxacin-resistant isolates produced CTX-M-type enzymes; eight the CTX-M-15 and one the CTX-M-3 variant. CTX-M-1 like and KPC-2 enzymes were detected in five and four ST410 ciprofloxacin-resistant E. coli isolates, respectively. Conclusions Our findings suggest that, ST131 and ST410 predominate in the ciprofloxacin resistant E. coli population.
In vitro selection of resistance in Escherichia coli and Klebsiella spp. at in vivo fluoroquinolone concentrations
Lorenzo Drago, Lucia Nicola, Roberto Mattina, Elena De Vecchi
BMC Microbiology , 2010, DOI: 10.1186/1471-2180-10-119
Abstract: Frequencies of mutations for levofloxacin and ciprofloxacin were less than 10-11 at peak concentration, while for prulifloxacin they ranged from <10-11 to 10-5. The lowest number of resistant mutants after multistep selection was selected by levofloxacin followed by ciprofloxacin and prulifloxacin. Both ciprofloxacin- and prulifloxacin-resistant mutants presented mutations in gyrA and parC, while levofloxacin resistance was found associated only to mutations in gyrA.Among the tested fluoroquinolones, levofloxacin was the most capable of limiting the occurrence of resistance.Escherichia coli is worldwide the most frequent pathogen isolated from uncomplicated urinary tract infections (UTI) (70 - 95%) and, in bacteremia of nosocomial or community origin, it represents about the 15.5% and 42.1% of aetiologies, respectively [1]. Also Klebsiella spp., especially Klebsiella pneumoniae, are involved in uncomplicated UTI for 5% and represent 4.1% of bacteremias, the mortality of nosocomial infections being more than twice that of community-acquired infection [1,2].Fluoroquinolones (FQ) are potent antimicrobial agents used for the treatment of a wide variety of community- and nosocomial- infections. However, increasing resistance to FQ in E. coli isolated from community acquired UTI has been recently reported, with up to 29% of women harbouring FQ resistant E. coli, although FQ resistance rates varied significantly according to sex, age, type of urinary infection and geographic region [3-6]. Moreover, infections due to extended-spectrum beta-lactamases (ESBL) - producing Enterobacteriaceae are an emerging problem in the community since an high proportion of these microorganisms have been isolated from urine samples of women with uncomplicated UTI [7].Ciprofloxacin use and ESBL production have been shown to be significantly correlated in a study on K. pneumoniae [8]. ESBL-producing strains have been shown to be significantly more frequent among ciprofloxacin-resistant E. coli
Specific patterns of gyrA mutations determine the resistance difference to ciprofloxacin and levofloxacin in Klebsiella pneumoniae and Escherichia coli
Fu Yingmei,Zhang Wenli,Wang Hong,Zhao Song
BMC Infectious Diseases , 2013, DOI: 10.1186/1471-2334-13-8
Abstract: Background Wide use of ciprofloxacin and levofloxacin has often led to increased resistance. The resistance rate to these two agents varies in different clinical isolates of Enterobacteriaceae. Mutations of GyrA within the quinolone resistance-determining regions have been found to be the main mechanism for quinolone resistance in Enterobacteriaceae. It has been shown that only some of the mutations in the gyrA gene identified from clinical sources were involved in fluoroquinolone resistance. Whether different patterns of gyrA mutation are related to antimicrobial resistance against ciprofloxacin and levofloxacin is unclear. Methods The minimum inhibitory concentration (MIC) of ciprofloxacin and levofloxacin were determined by the agar dilution method followed by PCR amplification and sequencing of the quinolone resistance determining region of gyrA to identify all the mutation types. The correlation between fluoroquinolone resistance and the individual mutation type was analyzed. Results Resistance differences between ciprofloxacin and levofloxacin were found in 327 isolates of K. pneumoniae and E. coli in Harbin, China and in the isolates reported in PubMed publications. GyrA mutations were found in both susceptible and resistant isolates. For the isolates with QRDR mutations, the resistance rates to ciprofloxacin and levofloxacin were also statistically different. Among the 14 patterns of alterations, two single mutations (Ser83Tyr and Ser83Ile), and three double mutations (Ser83Leu+Asp87Asn, Ser83Leu+Asp87Tyr and Ser83Phe+Asp87Asn) were associated with both ciprofloxacin and levofloxacin resistance. Two single mutations (Ser83Phe and Ser83Leu) were related with ciprofloxacin resistance but not to levofloxacin. Resistance difference between ciprofloxacin and levofloxacin in isolates harboring mutation Ser83Leu+Asp87Asn were of statistical significance among all Enterobacteriaceae (P<0.001). Conclusions Resistance rate to ciprofloxacin and levofloxacin were statistically different among clinical isolates of Enterobacteriaceae harboring GyrA mutations. Ser83Leu+Asp87Asn may account for the antimicrobial resistance difference between ciprofloxacin and levofloxacin.
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