scholarly journals Resistance to Autolysis in Vancomycin-Selected Staphylococcus aureus Isolates Precedes Vancomycin-Intermediate Resistance

2003 ◽  
Vol 47 (6) ◽  
pp. 2036-2039 ◽  
Author(s):  
Susan Boyle-Vavra ◽  
Mamatha Challapalli ◽  
Robert S. Daum
Keyword(s):  
Staphylococcus Aureus ◽  
Clinical Isolate ◽  
Resistance Phenotype ◽  
Low Level ◽  
Single Passage ◽  
Intermediate Resistance ◽  
Triton X ◽  
Induced Autolysis

ABSTRACT Four clinical U.S. glycopeptide intermediate resistant Staphylococcus aureus (GISA) isolates were resistant to Triton X-100-induced autolysis. Similar resistance was demonstrated in an isolate obtained after a single passage of a susceptible clinical isolate in low-level vancomycin. Strains with the vancomycin-induced Triton X-100 resistance phenotype produced active murein hydrolases but were resistant to lysis by murein hydrolases.

Antimicrobial Activity of Galangin and Its Effects on Murein Hydrolases of Vancomycin-Intermediate Staphylococcus aureus (VISA) Strain Mu50

Chemotherapy ◽  
2017 ◽  
Vol 63 (1) ◽  
pp. 20-28 ◽  
Author(s):  
Jing Ouyang ◽  
Fengjun Sun ◽  
Wei Feng ◽  
Yonghong Xie ◽  
Lijuan Ren ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Antimicrobial Activity ◽  
Cell Wall ◽  
Morphological Changes ◽  
Control Group ◽  
Cellular Division ◽  
Murein Hydrolase ◽  
Triton X ◽  
Cell Wall Hydrolysis ◽  
Induced Autolysis

Backgroud: Antibiotic treatment for infections caused by vancomycin-intermediate Staphylococcus aureus (VISA) strains is challenging, and only a few effective and curative methods have been developed to combat these strains. This study aimed to investigate the antimicrobial activity of galangin against S. aureus and its effects on the murein hydrolases of VISA strain Mu50. This is the first report on these effects of galangin, and it may help to improve the treatment for VISA infections by demonstrating the effective use of galangin. Methods: Firstly, the minimum inhibitory concentration (MIC) and growth curve were used to investigate the antimicrobial activity of galangin against S. aureus. Secondly, transmission electron microscopy (TEM) was used to observe morphological changes of VISA strain Mu50. Thirdly, Triton X-100-induced autolysis and cell wall hydrolysis assays were performed to determine the activities of the murein hydrolases of Mu50. Finally, fluorescence real-time quantitative PCR was used to investigate the expression of the murein hydrolase-related Mu50 genes. Results: The results indicated that the MIC of galangin was 32 μg/mL against ATCC25293, N315, and Mu50, and galangin could significantly suppress the bacterial growth (p < 0.05) with concentrations of 4, 8 and 16 μg/mL, compared with control group (0 μg/mL). To explore the possible reasons of bacteriostatic effects of galangin, we observed morphological changes using TEM which showed that the division of Mu50 daughter cells treated with galangin was obviously inhibited. Considering the vital role of murein hydrolases in cellular division, assays were performed, and galangin markedly decreased Triton X-100-induced autolysis and cell wall hydrolysis. Galangin also significantly inhibited the expression of the murein hydrolase genes (atl, lytM, and lytN) and their regulatory genes (cidR, cidA, and cidB). Conclusions: Our findings indicated that galangin can effectively inhibit murein hydrolase activity as well as the growth of VISA strain Mu50.

scholarly journals Opposing Roles of the Staphylococcus aureus Virulence Regulators, Agr and Sar, in Triton X-100- and Penicillin-Induced Autolysis

1998 ◽  
Vol 180 (14) ◽  
pp. 3724-3726 ◽  
Author(s):  
David F. Fujimoto ◽  
Kenneth W. Bayles
Keyword(s):  
Staphylococcus Aureus ◽  
Virulence Factor ◽  
Regulatory Genes ◽  
Critical Aspect ◽  
Mutant Strains ◽  
Murein Hydrolase ◽  
Triton X ◽  
Induced Autolysis

ABSTRACT The regulation of murein hydrolases is a critical aspect of peptidoglycan growth and metabolism. In the present study, we demonstrate that mutations within the Staphylococcus aureusvirulence factor regulatory genes, agr and sar, affect autolysis, resulting in decreased and increased autolysis rates, respectively. Zymographic analyses of these mutant strains suggest thatagr and sar exert their effects on autolysis, in part, by modulating murein hydrolase expression and/or activity.

scholarly journals Interaction of the GraRS Two-Component System with the VraFG ABC Transporter To Support Vancomycin-Intermediate Resistance in Staphylococcus aureus

2007 ◽  
Vol 51 (8) ◽  
pp. 2679-2689 ◽  
Author(s):  
Michael Meehl ◽  
Silvia Herbert ◽  
Friedrich Götz ◽  
Ambrose Cheung
Keyword(s):  
Staphylococcus Aureus ◽  
Abc Transporter ◽  
Regulatory System ◽  
Polymyxin B ◽  
Current Treatment ◽  
Peptide Antibiotics ◽  
Genetic Changes ◽  
Resistance Phenotype ◽  
Two Component ◽  
Intermediate Resistance

ABSTRACTCurrent treatment for serious infections caused by methicillin-resistantStaphylococcus aureusrelies heavily upon the glycopeptide antibiotic vancomycin. Unfortunately, this practice has led to an intermediate resistance phenotype that is particularly difficult to treat in invasive staphylococcal diseases, such as septicemia and its metastatic complications, including endocarditis. Although the vancomycin-intermediate resistance phenotype has been linked to abnormal cell wall structures and autolytic rates, the corresponding genetic changes have not been fully elucidated. Previously, whole-genome array studies listed numerous genes that are overexpressed in vancomycin-intermediate sensitive strains, includinggraRS(SACOL0716 to -0717), encoding a two-component regulatory system (TCRS), as well as the adjacentvraFG(SACOL0718 to -0720), encoding an ATP-binding cassette (ABC) transporter; but the exact contribution of these genes to increased vancomycin resistance has not been defined. In this study, we showed that isogenic strains with mutations in genes encoding the GraRS TCRS and the VraFG ABC transporter are hypersensitive to vancomycin as well as polymyxin B. Moreover, GraRS regulates the expression of the adjacent VraFG pump, reminiscent of gram-positive bacteriocin-immunity regulons. Mutations ofgraRSandvraFGalso led to increased autolytic rates and a more negative net surface charge, which may explain, in part, to their increased sensitivity to cationic antimicrobial peptides. Taken together, these data reveal an important genetic mediator to the vancomycin-intermediateS. aureusphenotype and may hold clues to the selective pressures on staphylococci upon exposure to selective cationic peptide antibiotics used in clinical practice.

scholarly journals Cell Wall Thickening Is Not a Universal Accompaniment of the Daptomycin Nonsusceptibility Phenotype in Staphylococcus aureus: Evidence for Multiple Resistance Mechanisms

2010 ◽  
Vol 54 (8) ◽  
pp. 3079-3085 ◽  
Author(s):  
Soo-Jin Yang ◽  
Cynthia C. Nast ◽  
Nagendra N. Mishra ◽  
Michael R. Yeaman ◽  
Paul D. Fey ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Parental Strain ◽  
Cell Walls ◽  
Treated Patient ◽  
Resistance Mechanisms ◽  
Wall Thickening ◽  
Surface Binding ◽  
Transmission Electron ◽  
Triton X ◽  
Induced Autolysis

ABSTRACT The mechanism(s) of daptomycin (DAP) resistance (DAPr) is incompletely defined. Thickened cell walls (CWs) acting as either a mechanical barrier or an affinity trap for DAP have been purported to be a major contributor to the DAPr phenotype. To this end, we studied an isogenic set of methicillin-resistant Staphylococcus aureus (MRSA) isolates (pulsotype USA 300) from the bloodstream of a DAP-treated patient with endocarditis in which serial strains exhibited increasing DAPr. Of interest, the DAPr isolate differed from its parental strain in several parameters, including acquisition of a point mutation within the putative synthase domain of the mprF gene in association with enhanced mprF expression, increased synthesis of lysyl-phosphotidylglycerol, an enhanced positive envelope charge, and reduced DAP surface binding. Transmission electron microscopy (TEM) revealed no significant increases in CW thickness in the two DAPr isolates (MRSA 11/21 and REF2145) compared with that in the DAP-susceptible (DAPs) parental strain, MRSA 11/11. The rates of Triton X-100-induced autolysis were also identical for the strain set. Furthermore, among six additional clinically isolated DAPs/DAPr S. aureus strain pairs, only three DAPr isolates exhibited CWs significantly thicker than those of the respective DAPs parent. These data confirm that CW thickening is neither universal to DAPr S. aureus nor sufficient to yield the DAPr phenotype among S. aureus strains.

scholarly journals Staphylococcus aureus Clinical Isolate with High-Level Methicillin Resistance with an lytH Mutation Caused by IS1182 Insertion

2007 ◽  
Vol 52 (2) ◽  
pp. 643-647 ◽  
Author(s):  
Takaji Fujimura ◽  
Kazuhisa Murakami
Keyword(s):  
Staphylococcus Aureus ◽  
Clinical Isolate ◽  
Methicillin Resistance ◽  
Clinical Isolates ◽  
Lytic Enzymes ◽  
Resistance Level ◽  
Low Level ◽  
Mrsa Strains ◽  
High Level ◽  
Level Resistance

ABSTRACT We previously reported that deficiency of the lytH gene, whose product is homologous to lytic enzymes, caused the elevation of methicillin resistance in Staphylococcus aureus strain SR17238, a strain of S. aureus with a low level of resistance to methicillin (low-level MRSA) (J. Bacteriol. 179:6294-6301, 1997). In this study, we demonstrated that deficiency of lytH caused the same phenomenon in four other clinical isolates of low-level MRSA, suggesting this deficiency to exist in clinical isolates. We therefore searched the region including lytH in 127 clinical isolates of MRSA by PCR and found one strain, SR17164 (methicillin MIC, 1,600 μg/ml), in which the lytH gene was inactivated by insertion sequence IS1182. lytH::IS1182 was replaced with intact lytH in this strain by integration and excision of the plasmid carrying the lytH region. Recombinants with intact lytH genes showed methicillin MICs of 800 μg/ml, twofold lower than those of the recombinants with lytH::IS1182 and the parent. In addition, S. aureus SR17164, which has a high level of methicillin resistance, had properties similar to those caused by lytH deficiency; that is, the resistance levels of strain SR17164 and lytH-deficient variants from strain SR17238 were not significantly affected by llm inactivation, which greatly lowered resistance levels in most other high-level MRSA strains. These findings suggest that lytH inactivation contributed, to some extent, to the resistance level of S. aureus SR17164. To the best of our knowledge, this strain is the first clinical isolate of MRSA for which the genetic base for high-level resistance has been clarified.

scholarly journals Genome Sequences of a Staphylococcus aureus Clinical Isolate, Strain SMA0034-04 (UGA22), from Siaya County Referral Hospital in Siaya, Kenya

2019 ◽  
Vol 8 (17) ◽  
Author(s):  
Gary Xie ◽  
Qiuying Cheng ◽  
Hajnalka Daligault ◽  
Karen Davenport ◽  
Cheryl Gleasner ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Clinical Isolate ◽  
Referral Hospital ◽  
Genome Sequences ◽  
Content Type

Here, we report the genome sequences of a Staphylococcus aureus clinical isolate, strain SMA0034-04 (UGA22), which contains one chromosome and one plasmid. We also reveal that isolate SMA0034-04 (UGA22) contains loci in the genome that encode multiple exotoxins.

scholarly journals Resistance of Streptococcus pneumoniaeto Deformylase Inhibitors Is Due to Mutations indefB

2001 ◽  
Vol 45 (9) ◽  
pp. 2432-2435 ◽  
Author(s):  
Peter Margolis ◽  
Corinne Hackbarth ◽  
Sara Lopez ◽  
Mita Maniar ◽  
Wen Wang ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Staphylococcus Aureus ◽  
Streptococcus Pneumoniae ◽  
Peptide Deformylase ◽  
Wild Type ◽  
Resistance Phenotype ◽  
Resistant Mutants

ABSTRACT Resistance to peptide deformylase inhibitors in Escherichia coli or Staphylococcus aureus is due to inactivation of transformylase activity. Knockout experiments in Streptococcus pneumoniae R6x indicate that the transformylase (fmt) and deformylase (defB) genes are essential and that adef paralog (defA) is not. Actinonin-resistant mutants of S. pneumoniae ATCC 49619 harbor mutations indefB but not in fmt. Reintroduction of the mutated defB gene into wild-type S. pneumoniaeR6x recreates the resistance phenotype. The altered enzyme displays decreased sensitivity to actinonin.

scholarly journals Evaluation of Accessory Gene Regulator (agr) Group and Function in the Proclivity towards Vancomycin Intermediate Resistance in Staphylococcus aureus

2006 ◽  
Vol 51 (3) ◽  
pp. 1089-1091 ◽  
Author(s):  
Brian T. Tsuji ◽  
Michael J. Rybak ◽  
Kerry L. Lau ◽  
George Sakoulas
Keyword(s):  
Staphylococcus Aureus ◽  
Wild Type ◽  
Accessory Gene ◽  
Time Curve ◽  
Unbound Fraction ◽  
Accessory Gene Regulator ◽  
Intermediate Resistance ◽  
And Function ◽  
Type Strains

ABSTRACT Simulated therapeutic vancomycin exposures were evaluated against agr wild-type and knockout Staphylococcus aureus groups I, II, III, and IV using an in vitro pharmacodynamic model. All agr groups developed intermediate resistance to vancomycin after subtherapeutic exposure. The free unbound fraction of the area under the concentration-time curve (fAUC/MIC) required to suppress resistance was fourfold higher (P < 0.001) in agr dysfunctional strains (112 to 169) than that in parent wild-type strains (28).

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