scholarly journals The life and times of the Enterococcus.

1990 ◽  
Vol 3 (1) ◽  
pp. 46-65 ◽  
Author(s):  
B E Murray
Keyword(s):  
Antimicrobial Agents ◽  
Acquired Resistance ◽  
Active Agent ◽  
Bactericidal Effect ◽  
Human Pathogens ◽  
A Cell ◽  
High Level ◽  
Tract Infections ◽  
Level Resistance ◽  
Resistance Traits

Enterococci are important human pathogens that are increasingly resistant to antimicrobial agents. These organisms were previously considered part of the genus Streptococcus but have recently been reclassified into their own genus, called Enterococcus. To date, 12 species pathogenic for humans have been described, including the most common human isolates, Enterococcus faecalis and E. faecium. Enterococci cause between 5 and 15% of cases of endocarditis, which is best treated by the combination of a cell wall-active agent (such as penicillin or vancomycin, neither of which alone is usually bactericidal) and an aminoglycoside to which the organism is not highly resistant; this characteristically results in a synergistic bactericidal effect. High-level resistance (MIC, greater than or equal to 2,000 micrograms/ml) to the aminoglycoside eliminates the expected bactericidal effect, and such resistance has now been described for all aminoglycosides. Enterococci can also cause urinary tract infections; intraabdominal, pelvic, and wound infections; superinfections (particularly in patients receiving expanded-spectrum cephalosporins); and bacteremias (often together with other organisms). They are now the third most common organism seen in nosocomial infections. For most of these infections, single-drug therapy, most often with penicillin, ampicillin, or vancomycin, is adequate. Enterococci have a large number of both inherent and acquired resistance traits, including resistance to cephalosporins, clindamycin, tetracycline, and penicillinase-resistant penicillins such as oxacillin, among others. The most recent resistance traits reported are penicillinase resistance (apparently acquired from staphylococci) and vancomycin resistance, both of which can be transferred to other enterococci. It appears likely that we will soon be faced with increasing numbers of enterococci for which there is no adequate therapy.

scholarly journals Analysis of Aminoglycoside Modifying Enzyme Genes Responsible for High-Level Aminoglycoside Resistance among Enterococcal Isolates

2017 ◽  
Vol 2017 ◽  
pp. 1-5 ◽  
Author(s):  
Vishal Shete ◽  
Naveen Grover ◽  
Mahadevan Kumar
Keyword(s):  
Active Agent ◽  
Bactericidal Effect ◽  
Diffusion Method ◽  
Clinical Samples ◽  
Aminoglycoside Resistance ◽  
Enzyme Gene ◽  
A Cell ◽  
Polymerase Chain ◽  
High Level ◽  
Level Resistance

Enzymatic modification results in high-level resistance to aminoglycoside (HLAR), which eliminates the synergistic bactericidal effect of combined exposure to a cell wall-active agent and an aminoglycoside. So aim of the study was to determine prevalence of HLAR enterococcal isolate and to study distribution of aminoglycoside modifying enzyme genes in them. A total of 100 nonrepeat isolates of enterococci from various clinical samples were analyzed. As per Clinical and Laboratory Standards Institute guidelines enterococci were screened for HLAR by Kirby-Bauer disc diffusion method. Minimum inhibitory concentration of all isolates for gentamicin and streptomycin was determined by E-test. Multiplex polymerase chain reaction (PCR) was carried out for HLAR enterococcal isolates to identify aminoglycoside modifying enzymes genes responsible for resistance. 60% isolates were found to be high-level gentamicin resistant (HLGR) whereas 45% isolates were found to be high-level streptomycin resistant (HLSR). By multiplex PCR 80% HLGR isolates carried bifunctional aminoglycoside modifying enzyme geneaac(6′)-Ie-aph(2′′)-Iawhereas 18 out of 45 high-level streptomycin resistant, that is, 40%, isolates carriedaph(3′)-IIIa.However,aph(2′′)-Ib, aph(2′′)-Ic, aph(2′′)-Id,andant(4′)-Iagenes which encode other aminoglycosides modifying enzymes were not detected. Bifunctional aminoglycoside modifying enzyme geneaac(6′)-Ie-aph(2′′)-Iais the predominant gene responsible for HLAR.

scholarly journals Relationship between the Level of Acquired Resistance to Gentamicin and Synergism with Amoxicillin in Enterococcus faecalis

2005 ◽  
Vol 49 (10) ◽  
pp. 4144-4148 ◽  
Author(s):  
Elisabeth Aslangul ◽  
Raymond Ruimy ◽  
Françoise Chau ◽  
Louis Garry ◽  
Antoine Andremont ◽  
...  
Keyword(s):  
Enterococcus Faecalis ◽  
Acquired Resistance ◽  
Bactericidal Effect ◽  
A Cell ◽  
Enzymatic Inactivation ◽  
High Level ◽  
The Impact ◽  
Level Resistance

ABSTRACT In enterococci, intrinsic low-level resistance to gentamicin does not abolish synergism with a cell wall-active antibiotic while high-level resistance due to acquired aminoglycoside-modifying enzymes does. To study the impact of intermediate levels of resistance to gentamicin (64 < MIC < 500 μg/ml), we selected in vitro three consecutive generations of mutants of Enterococcus faecalis JH2-2 with MICs of gentamicin at 128 μg/ml for G1-1477, 256 μg/ml for G2-1573, and 512 μg/ml for G3-1688. E. faecalis 102, which is highly resistant to gentamicin by enzymatic inactivation was used as control. In in vitro killing curves experiments, gentamicin concentrations allowing bactericidal activity and synergism in combination with amoxicillin increased from 4 μg/ml (1/16th the MIC), 16 μg/ml (one-eighth the MIC), 64 μg/ml (one-quarter the MIC), and 256 μg/ml (one-half the MIC) for strains JH2-2, G1-1477, G2-1573 and G3-1688, respectively. As expected, no bactericidal effect of the combination or synergism could be obtained with strain 102. In rabbits with aortic endocarditis caused by strain G1-1477 or G2-1573, combination therapy with amoxicillin and gentamicin was significantly more active than amoxicillin alone (P < 0.05) but not in those infected with the strains G3-1688 and 102. Thus, intermediate levels of resistance to gentamicin was not associated with a loss of a beneficial effect of the gentamicin-amoxicillin combination in vivo even though higher concentrations of gentamicin were necessary to achieve in vitro synergism. Therefore, the use of an MIC of 500 μg/ml as a clinical cutoff limit to predict in vivo benefit of the combination remains a simple and effective tool.

scholarly journals Transferable high-level trimethoprim resistance among isolates ofEscherichia colifrom urinary tract infections in Ontario, Canada

1992 ◽  
Vol 109 (3) ◽  
pp. 473-481 ◽  
Author(s):  
N. Harnett
Keyword(s):  
Nalidixic Acid ◽  
Antimicrobial Agents ◽  
Acid Resistance ◽  
The Public ◽  
E Coli ◽  
High Level ◽  
Tract Infections ◽  
K 12 ◽  
Level Resistance ◽  
Nalidixic Acid Resistance

SUMMARYOf 1171 isolates ofEscherichia coliisolated from urine samples at the Public Health Laboratory, Toronto, Ontario, Canada, between May 1990 and December 1991, 120 (10·3%) were resistant to trimethoprim (TMP), cotrimoxazole (TMP/SMX), sulfamethoxazole (SMX) and other antimicrobial agents; 110 of the 120 isolates (91·7%) were resistant to four or more agents. The majority of resistant isolates (91·7%) exhibited high-level resistance (MIC > 1000 mg/L) to TMP. The MIC of TMP/SMX for all 120 isolates was > 2·0/38·0 mg/L and for SMX > 1024 mg/L. High-level resistances were also present among the β-lactam antimicrobials with MICs ranging from 16- > 256 mg/L. Forty-three of 120 TMP-resistant (35·8%) isolates conjugally transferred TMP-resistance toE. coliK-12. Co-transfer of several other resistances was observed. SMX cotransferred from 86% of the 43 donors and β-lactams together with SMX cotransferred from 70%. Nalidixic acid resistance was present among 22 (18·3%) of the 120 resistant isolates, however, nalidixic acid resistance was not transferred toE. coliK-12.

scholarly journals 2493. Real-World Utilization of Ibalizumab (IBA) Without an Optimized Background Regimen (OBT)

2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S865-S865 ◽  
Author(s):  
Jeannette Bouchard ◽  
Caroline Derrick ◽  
Joseph Horvath
Keyword(s):  
Real World ◽  
Active Agent ◽  
Multidrug Resistant ◽  
Phase Iii ◽  
Hiv Virus ◽  
Oral Agents ◽  
Patient Table ◽  
Tenofovir Alafenamide ◽  
High Level ◽  
Level Resistance

Abstract Background It is difficult to treat multidrug-resistant (MDR) human immunodeficiency virus (HIV). Trogarzo® (ibalizumab) a novel monoclonal antibody was approved in 2018 for heavily treatment-experienced HIV patients. Data support IBA use with at least one fully active agent, an OBR. Real-world IBA data are lacking. We report a successful case of reaching and maintaining suppression with IBA in a patient without an OBR. Methods Mutations were reviewed for the patient, Table 1, and evaluated for treatment. The patient is a 52- year old male, diagnosed in 1994, with MDR HIV secondary to non-adherence. Upon re-presenting to care, the patient was non-compliant with ART. Genotypic interpretation via the Stanford/ANRS algorithm was performed and interpreted, resulting in the addition of IBA intravenous administration every other week. IBA was obtained through patient assistance and costs were covered by the institution for infusion. Results Evaluation of the resistance profile indicated varying resistance to all available ART. More specifically, high-level resistance to all FDA-approved INSTIs, PIs, and low to high-level resistance to all NNRTIs and NRTIs. Table 2 outlines the ART history and viral load (VL) trends. The patient was initiated on daruanvir/ritonavir twice daily, etravirine twice daily, emtricitabine/tenofovir alafenamide and did not reach suppression. IBA was added off-label to a failing regimen. The patient reached VS (VL < 200 copies/mL) at Week 4 and has had an undetectable VL for 8 weeks. Notably his CD4 count has risen to 46, first detectable number since re-presenting to care. Conclusion We describe a heavily treatment experienced patient with an MDR HIV virus who achieved an undetectable VL without an OBT and the addition of intravenous IBA. Fostemsavir, was utilized in IBA’s phase III trial for similar patients, however, it is not currently FDA-approved nor available. Further data are needed to ensure continued susceptibility to IBA without an OBT. This patient required high-level coordination to reach each visit and receive this therapy alongside his oral agents. We conclude, IBA has allowed this patient to reach and maintain VS. Disclosures All authors: No reported disclosures.

scholarly journals Antimicrobial Resistance of Listeria monocytogenes Strains Isolated from Humans in France

2010 ◽  
Vol 54 (6) ◽  
pp. 2728-2731 ◽  
Author(s):  
A. Morvan ◽  
C. Moubareck ◽  
A. Leclercq ◽  
M. Hervé-Bazin ◽  
S. Bremont ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Antimicrobial Resistance ◽  
Resistant Strain ◽  
Temporal Evolution ◽  
Acquired Resistance ◽  
Mechanisms Of Resistance ◽  
Resistant Strains ◽  
High Level ◽  
Level Resistance ◽  
Microbiological Surveillance

ABSTRACT Susceptibility to antibiotics of 4,816 clinical L. monocytogenes strains isolated since 1926 was studied, and the temporal evolution of susceptibility to antibiotics was analyzed through several decades. The mechanisms of resistance in each resistant strain were studied. The prevalence of resistant strains was estimated at 1.27% among isolates from humans. Resistance to tetracyclines+ and fluoroquinolones was more common and has recently emerged. Although acquired resistance in clinical L. monocytogenes did not implicate clinically relevant antibiotics, the possibility of resistance gene transfers, the description of the first clinical isolate with high-level resistance to trimethoprim, and the recent increase in penicillin MICs up to 2 μg/ml reinforce the need for microbiological surveillance.

scholarly journals Plasmid-Mediated High-Level Resistance to Aminoglycosides in Enterobacteriaceae Due to 16S rRNA Methylation

2003 ◽  
Vol 47 (8) ◽  
pp. 2565-2571 ◽  
Author(s):  
Marc Galimand ◽  
Patrice Courvalin ◽  
Thierry Lambert
Keyword(s):  
16S Rrna ◽  
Multiple Antibiotic Resistance ◽  
Human Pathogens ◽  
Aminoglycoside Resistance ◽  
New Host ◽  
Gram Negative ◽  
Infection Resistance ◽  
New Gene ◽  
High Level ◽  
Level Resistance

ABSTRACT A self-transferable plasmid of ca. 80 kb, pIP1204, conferred multiple-antibiotic resistance to Klebsiella pneumoniae BM4536, which was isolated from a urinary tract infection. Resistance to β-lactams was due to the bla TEM1 and bla CTX-M genes, resistance to trimethroprim was due to the dhfrXII gene, resistance to sulfonamides was due to the sul1 gene, resistance to streptomycin-spectinomycin was due to the ant3"9 gene, and resistance to nearly all remaining aminoglycosides was due to the aac3-II gene and a new gene designated armA (aminoglycoside resistance methylase). The cloning of armA into a plasmid in Escherichia coli conferred to the new host high-level resistance to 4,6-disubstituted deoxystreptamines and fortimicin. The deduced sequence of ArmA displayed from 37 to 47% similarity to those of 16S rRNA m7G methyltransferases from various actinomycetes, which confer resistance to aminoglycoside-producing strains. However, the low guanine-plus-cytosine content of armA (30%) does not favor an actinomycete origin for the gene. It therefore appears that posttranscriptional modification of 16S rRNA can confer high-level broad-range resistance to aminoglycosides in gram-negative human pathogens.

scholarly journals In Vitro Antimicrobial Activity of Fosfomycin, Rifampin, Vancomycin, Daptomycin Alone and in Combination Against Vancomycin-Resistant Enterococci

2021 ◽  
Author(s):  
Wei Yu ◽  
Yiheng Jiang ◽  
Hao Xu ◽  
Li Zhang ◽  
Xuehang Jin ◽  
...  
Keyword(s):  
Virulence Genes ◽  
Therapeutic Option ◽  
Bactericidal Effect ◽  
Resistance Determinant ◽  
Vancomycin Resistant Enterococci ◽  
Vancomycin Resistant ◽  
High Level ◽  
Time Kill ◽  
Level Resistance

Abstract OBJECTIVESThe emergence of vancomycin resistant enterococci (VRE) is shortening the choices for clinical anti-infective therapy. The aim of this study was to investigate the mechanism of vancomycin resistance and evaluate the effect of fosfomycin (FM), rifampin (RIF), vancomycin (VAN), linezolid (LNZ), daptomycin (DAP) alone or in combination against VRE.METHODSEight VRE isolates were collected. A total of 18 antibiotics susceptibility tests were further done for VRE. Whole genome sequencing and bioinformatics analysis were performed. The effect of FM, RIF, VNA, LNZ, DAP alone or in combination was determined using anti-biofilm testing and the time-kill assay.RESULTSAll isolates were susceptible to LNZ and DPA. The high-level resistance determinant of VAN in these strains was due to VanA-type cassette. MLST revealed two different STs for vancomycin-resistant Enterococcus faecium (VREm) and four different STs for vancomycin-resistant E. faecalis (VREs). Virulence genes in VREs were more than VREm, especially for 4942 isolated from blood. Gene acm and uppS were only identified in VREm, while virulence genes related to cytolysin were only found in E. faecalis. Further in vitro anti-biofilm testing and time-kill assay found FM (83 mg/L) combined with DAP (20.6 mg/L) and DAP monotherapy (47.1 mg/L) showed bactericidal effect against 8 tested VRE strains at 24h. CONCLUSIONSThe high-level resistance determinant of VAN in these strains was due to VanA-type cassette. FM combined with DAP might be greater potential therapeutic option against VRE.

Canadian national survey of prevalence of antimicrobial resistance among clinical isolates of Streptococcus pneumoniae. Canadian Bacterial Surveillance Network.

1996 ◽  
Vol 40 (9) ◽  
pp. 2190-2193 ◽  
Author(s):  
A E Simor ◽  
M Louie ◽  
D E Low
Keyword(s):  
Streptococcus Pneumoniae ◽  
Antimicrobial Agents ◽  
Clinical Isolates ◽  
Beta Lactam ◽  
Surveillance Network ◽  
Antibiotic Resistant ◽  
Intermediate Resistance ◽  
Resistant Strains ◽  
High Level ◽  
Level Resistance

The antimicrobial susceptibilities of 1,089 clinical isolates of Streptococcus pneumoniae obtained from 39 laboratories across Canada between October 1994 and August 1995 were determined. A total of 91 isolates (8.4%) demonstrated intermediate resistance (MIC, 0.1 to 1.0 microgram/ml) and 36 (3.3%) had high-level resistance (MIC, > or = 2.0 micrograms/ml) to penicillin. Penicillin-resistant strains were more likely to have been recovered from normally sterile sites (P = 0.005) and to be cross-resistant to several beta-lactam and non-beta-lactam antimicrobial agents (P < 0.05). These results indicate that there has been a recent significant increase in the prevalence of antibiotic-resistant S. pneumoniae in Canada.

scholarly journals Prevalence of moderate penicillin resistant invasive Neisseria meningitidis infection in Scotland, 1994–9

2001 ◽  
Vol 128 (2) ◽  
pp. 149-156 ◽  
Author(s):  
M. H. KYAW ◽  
J. C. BRAMLEY ◽  
S. CLARKE ◽  
P. CHRISTIE ◽  
I. G. JONES ◽  
...  
Keyword(s):  
Antimicrobial Agents ◽  
Health Interventions ◽  
Penicillin Resistance ◽  
Drug Resistant ◽  
Geographic Variations ◽  
Resistance To Penicillin ◽  
Low Incidence ◽  
High Level ◽  
B 52 ◽  
Level Resistance

We examined the serological characteristics of 774 invasive meningococcal isolates collected through an active laboratory-based surveillance system in Scotland from 1994 to 1999. Of these, 72–73% of isolates were tested for susceptibility to several antimicrobial agents. Meningococci with high-level resistance to sulphadiazine had a prevalence of 10% and incidence of 0·22 per 100000 population. High-level resistance to penicillin and other antibiotics was not detected. The prevalence of moderate penicillin resistant meningococci was 8·3%. There was no increase in moderate penicillin resistant meningococcal isolates during the study period, but there were temporal and geographic variations. The estimated incidence of moderate penicillin resistant meningococci was 0·15 per 100000 population. High and low incidence of moderate penicillin resistant meningococci appeared to correlate with the number of doses of penicillin prescribed in some geographic locations. The majority of moderate penicillin resistant isolates belonged to serogroups B (52·2%) and C (39·2%). However, the prevalence of moderate penicillin resistance in serogroup W135 was substantially higher (51·7%) than serogroups B (7·8%) and C (7·6%). Serogroup W135 accounted for a higher proportion of moderate penicillin resistance (8·7%) than disease (1%). There was no predominant penicillin resistant serotype/subtype within any serogroup. Constant surveillance is necessary to monitor the emergence and spread of resistance and to guide appropriate public health interventions in preventing drug resistant meningococci.

scholarly journals A Comparison of High-Level Aminoglycoside Resistance in Vancomycin-Sensitive and Vancomycin-Resistant Enterococcus Species

2002 ◽  
Vol 30 (5) ◽  
pp. 529-534 ◽  
Author(s):  
H Yazgi ◽  
M Ertek ◽  
S Erol ◽  
A Ayyildiz
Keyword(s):  
Brain Heart Infusion ◽  
Bactericidal Effect ◽  
Vancomycin Resistance ◽  
Glycopeptide Antibiotics ◽  
Aminoglycoside Resistance ◽  
Significant Difference ◽  
Vancomycin Resistant ◽  
High Level ◽  
Infusion Agar ◽  
Level Resistance

The aim of this study was to investigate whether there was a significant difference in high-level aminoglycoside resistance (HLAR) between vancomycin-sensitive enterococci (VSE) and vancomycin-resistant enterococci (VRE). Vancomycin resistance was determined in 116 Enterococcus isolates using brain-heart infusion agar containing 6 μg/ml vancomycin. HLAR was determined by both standard agar screening and disk diffusion methods. Streptomycin and gentamicin were used as predictors of HLAR. Vancomycin resistance and HLAR were found in 17 (14.7%) and 41 (35.3%) of the Enterococcus strains, respectively. HLAR was found in 11 of 17 VRE and 30 of 98 VSE strains. HLAR in VRE strains was significantly higher than in VSE. More enterococcal strains were found to be resistant to both gentamicin and streptomycin (29) than to gentamicin (one) or streptomycin (11) alone. The HLAR rate in VRE was two-fold higher than in VSE. The synergistic bactericidal effect of aminoglycosides and β-lactam or glycopeptide antibiotics is lost if there is high-level resistance to aminoglycosides.

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