scholarly journals Cell-Wall Hydrolases as Antimicrobials against Staphylococcus Species: Focus on Sle1

2019 ◽  
Vol 7 (11) ◽  
pp. 559 ◽  
Author(s):  
Vermassen ◽  
Talon ◽  
Andant ◽  
Provot ◽  
Desvaux ◽  
...  

Some staphylococcal species are opportunistic pathogens of humans and/or animals with Staphylococcus epidermidis as one of the most important. It causes a broad spectrum of diseases in humans and animals. This species is able to form biofilms and has developed antibiotic resistance, which has motivated research on new antibacterial agents. Cell-wall hydrolases (CWHs) can constitute a potential alternative. Following a hijacking strategy, we inventoried the CWHs of S. epidermidis. The lytic potential of representative CWHs that could be turned against staphylococci was explored by turbidity assays which revealed that cell wall glycosidases were not efficient, while cell wall amidases and cell wall peptidases were able to lyse S. epidermidis. Sle1, which is encoded by chromosomal gene and composed of three anchoring LysM domains and a C-terminal CHAP (cysteine, histidine-dependent amidohydrolase/peptidase) domain, was one of the most active CWHs. The phylogeny of Sle1 revealed seven clusters mostly identified among staphylococci. Sle1 was able to lyse several staphylococcal species, including Staphylococcus aureus, both in planktonic and sessile forms, but not Micrococcus.

1968 ◽  
Vol 14 (7) ◽  
pp. 811-812
Author(s):  
Joseph T. Parisi ◽  
William J. Suling

Glycine-resistant variants of Staphylococcus aureus were obtained by successive cultivation of parent strains in increasing concentrations of glycine, and the minimal inhibitory concentrations of glycine of the parents and variants were determined. Although it has been reported that growth in glycine or certain antibiotics causes the accumulation of nucleotides involved in cell wall synthesis, a lack of cross resistance of the variants to some of these antibiotics was observed.


1999 ◽  
Vol 43 (11) ◽  
pp. 2780-2782 ◽  
Author(s):  
Nobumichi Kobayashi ◽  
Shozo Urasawa ◽  
Nobuyuki Uehara ◽  
Naoki Watanabe

ABSTRACT The distribution of insertion sequence-like element IS1272 was analyzed for clinical isolates ofStaphylococcus aureus, Staphylococcus epidermidis, and Staphylococcus haemolyticus. In each of the staphylococcal species, IS1272 was detected in both methicillin-resistant (MR) and methicillin-susceptible strains of different genetic types. In MR isolates, IS1272 was generally located downstream of the truncated mecR1 gene (ΔmecR1), with an identical junction sequence occurring between ΔmecR1 and IS1272, although insertion of an additional gene sequence in the junction sequence was detected in one S. epidermidis isolate. These findings suggest that themec element with the rearranged form of mecR1(ΔmecR1-IS1272) has been transmitted to multiple clones of staphylococci.


mBio ◽  
2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Srishtee Arora ◽  
Xiqi Li ◽  
Andrew Hillhouse ◽  
Kranti Konganti ◽  
Sara V. Little ◽  
...  

ABSTRACT Staphylococcus epidermidis is a leading cause of nosocomial infections in patients with a compromised immune system and/or an implanted medical device. Seventy to 90% of S. epidermidis clinical isolates are methicillin resistant and carry the mecA gene, present in a mobile genetic element (MGE) called the staphylococcal cassette chromosome mec (SCCmec) element. Along with the presence of antibiotic and heavy metal resistance genes, MGEs can also contain genes encoding secreted or cell wall-anchored virulence factors. In our earlier studies of S. epidermidis clinical isolates, we discovered S. epidermidis surface protein J (SesJ), a prototype of a recently discovered subfamily of the microbial surface component recognizing adhesive matrix molecule (MSCRAMM) group. MSCRAMMs are major virulence factors of pathogenic Gram-positive bacteria. Here, we report that the sesJ gene is always accompanied by two glycosyltransferase genes, gtfA and gtfB, and is present in two MGEs, called the arginine catabolic mobile element (ACME) and the staphylococcal cassette chromosome (SCC) element. The presence of the sesJ gene was associated with the left-hand direct repeat DR_B or DR_E. When inserted via DR_E, the sesJ gene was encoded in the SCC element. When inserted via DR_B, the sesJ gene was accompanied by the genes for the type 1 restriction modification system and was encoded in the ACME. Additionally, the SCC element and ACME carry different isoforms of the SesJ protein. To date, the genes encoding MSCRAMMs have been seen to be located in the bacterial core genome. Here, we report the presence of an MSCRAMM in an MGE in S. epidermidis clinical isolates. IMPORTANCE S. epidermidis is an opportunistic bacterium that has established itself as a successful nosocomial pathogen. The modern era of novel therapeutics and medical devices has extended the longevity of human life, but at the same time, we also witness the evolution of pathogens to adapt to newly available niches in the host. Increasing antibiotic resistance among pathogens provides an example of such pathogen adaptation. With limited opportunities to modify the core genome, most of the adaptation occurs by acquiring new genes, such as virulence factors and antibiotic resistance determinants present in MGEs. In this study, we describe that the sesJ gene, encoding a recently discovered cell wall-anchored protein in S. epidermidis, is present in both ACME and the SCC element. The presence of virulence factors in MGEs can influence the virulence potential of a specific strain. Therefore, it is critical to study the virulence factors found in MGEs in emerging pathogenic bacteria or strains to understand the mechanisms used by these bacteria to cause infections.


2019 ◽  
Vol 63 (10) ◽  
Author(s):  
Bibek G C ◽  
Gyan S. Sahukhal ◽  
Mohamed O. Elasri

ABSTRACT Staphylococcus aureus is an important human pathogen in both community and health care settings. One of the challenges with S. aureus as a pathogen is its acquisition of antibiotic resistance. Previously, we showed that deletion of the msaABCR operon reduces cell wall thickness, resulting in decreased resistance to vancomycin in vancomycin-intermediate S. aureus (VISA). In this study, we investigated the nature of the cell wall defect in the msaABCR operon mutant in the Mu50 (VISA) and USA300 LAC methicillin-resistant Staphylococcus aureus (MRSA) strains. Results showed that msaABCR mutant cells had decreased cross-linking in both strains. This defect is typically due to increased murein hydrolase activity and/or nonspecific processing of murein hydrolases mediated by increased protease activity in mutant cells. The defect was enhanced by a decrease in teichoic acid content in the msaABCR mutant. Therefore, we propose that deletion of the msaABCR operon results in decreased peptidoglycan cross-linking, leading to increased susceptibility toward cell wall-targeting antibiotics, such as β-lactams and vancomycin. Moreover, we also observed significantly downregulated transcription of early cell wall-synthesizing genes, supporting the finding that msaABCR mutant cells have decreased peptidoglycan synthesis. More specifically, the msaABCR mutant in the USA300 LAC strain (MRSA) showed significantly reduced expression of the murA gene, whereas the msaABCR mutant in the Mu50 strain (VISA) showed significantly reduced expression of glmU, murA, and murD. Thus, we conclude that the msaABCR operon controls the balance between cell wall synthesis and cell wall hydrolysis, which is required for maintaining a robust cell wall and acquiring resistance to cell wall-targeting antibiotics, such as vancomycin and the β-lactams.


2014 ◽  
Vol 12 (6) ◽  
pp. 881-886 ◽  
Author(s):  
Nicholas V. Borrero ◽  
Fang Bai ◽  
Cristian Perez ◽  
Benjamin Q. Duong ◽  
James R. Rocca ◽  
...  

We have discovered a novel class of bromophenazines with potent antibacterial activity against Staphylococcus aureus and Staphylococcus epidermidis.


2021 ◽  
pp. 1588-1593
Author(s):  
Yulia Horiuk ◽  
Mykola Kukhtyn ◽  
Serhiy Kernychnyi ◽  
Svitlana Laiter-Moskaliuk ◽  
Sergiy Prosyanyi ◽  
...  

Background and Aim: Mastitis, an inflammation of the mammary gland, is an ongoing problem in dairy herds. In this study, we determined the sensitivity of Staphylococcus aureus cultures of different biological origins to commercial bacteriophages and phages of S. aureus var. bovis which were isolated on dairy farms, to create a drug for the treatment of mastitis in cows. Materials and Methods: We used cultures of S. aureus isolated from different habitats, and other types of staphylococci isolated on dairy farms. As antibacterial agents, the commercially available bacteriophages staphylococcal bacteriophage and Intestifag and field strains of phages Phage SAvB07, Phage SAvB08, Phage SAvB12, and Phage SAvB14 were used. Evaluation of their lytic properties was performed using the drip method. Results: The drug Intestifag lysed cultures isolated from human habitats and archival strains of S. aureus No.209-P and S. aureus (ATCC 25923) in 91.8%–100% of cases. Staphylococcal bacteriophage killed 3.6 times fewer cultures of S. aureus isolated from humans than Intestifag and did not affect the growth of archival strains. Neither drug lysed cultures isolated from cows or cultures isolated from dairy products sold in agri-food markets. Phage SAvB14 lysed 92.7±8.3% of S. aureus isolated from the mammary glands of cows and 69.2±6.4% of cultures isolated from dairy products sold in agri-food markets. Phage SAvB12, Phage SAvB08, and Phage SAvB07 lysed 1.2-1.7 times fewer cultures isolated from the mammary glands of cows and 6-18 times fewer cultures isolated from dairy products, compared with Phage SAvB14. Phages of S. aureus var. bovis can infect staphylococcal species such as Staphylococcus epidermidis, Staphylococcus haemolyticus, Staphylococcus saprophyticus, and Staphylococcus xylosus. The widest range of hosts was found for Phage SAvB14, which indicates its polyvalence. Conclusion: The biological origin of staphylococcal strains must be considered when developing effective phage therapy. Phage SAvB14 appears to be a good candidate for the development of a drug for the treatment of mastitis in cows.


2005 ◽  
Vol 28 (11) ◽  
pp. 1186-1191 ◽  
Author(s):  
D. Campoccia ◽  
L. Montanaro ◽  
L. Baldassarri ◽  
Y.H. An ◽  
C.R. Arciola

In the last decade the rising phenomenon of resistance to most common antibiotic drugs among staphylococcal clinical isolates has been a reason for serious concern and alarm. The present study investigated the prevalence of antibiotic resistance within a large microbial collection including 530 clinical strains of S. aureus and 408 strains of S. epidermidis to a panel of 16 different drugs. All strains were isolated from orthopedic infections, either associated or non-associated with implant materials. Interestingly, our data show that the profile of the prevalence of antibiotic resistance within the two species of pathogens is extremely similar for the vast majority of the drugs screened. The only statistically significant variations in prevalence concerned, in order of relevance, the following 5 out of 16 antibiotics: sulfamethoxazole (in combination with trimethoprim), erythromycin, and, to a lesser extent, oxacillin, imipenem, and clindamycin. In the case of Staphylococcus aureus, the isolates associated to implant materials were found more frequently resistant to all 4 aminoglycosides screened as well as to ciprofloxacin.


2006 ◽  
Vol 50 (2) ◽  
pp. 428-438 ◽  
Author(s):  
Longzhu Cui ◽  
Akira Iwamoto ◽  
Jian-Qi Lian ◽  
Hui-min Neoh ◽  
Toshiki Maruyama ◽  
...  

ABSTRACT As an aggressive pathogen, Staphylococcus aureus poses a significant public health threat and is becoming increasingly resistant to currently available antibiotics, including vancomycin, the drug of last resort for gram-positive bacterial infections. S. aureus with intermediate levels of resistance to vancomycin (vancomycin-intermediate S. aureus [VISA]) was first identified in 1996. The resistance mechanism of VISA, however, has not yet been clarified. We have previously shown that cell wall thickening is a common feature of VISA, and we have proposed that a thickened cell wall is a phenotypic determinant for vancomycin resistance in VISA (L. Cui, X. Ma, K. Sato, et al., J. Clin. Microbiol. 41:5-14, 2003). Here we show the occurrence of an anomalous diffusion of vancomycin through the VISA cell wall, which is caused by clogging of the cell wall with vancomycin itself. A series of experiments demonstrates that the thickened cell wall of VISA could protect ongoing peptidoglycan biosynthesis in the cytoplasmic membrane from vancomycin inhibition, allowing the cells to continue producing nascent cell wall peptidoglycan and thus making the cells resistant to vancomycin. We conclude that the cooperative effect of the clogging and cell wall thickening enables VISA to prevent vancomycin from reaching its true target in the cytoplasmic membrane, exhibiting a new class of antibiotic resistance in gram-positive pathogens.


2020 ◽  
Vol 5 (4) ◽  
pp. 364-373
Author(s):  
Anna A. Pliska ◽  

The results of microbiological studies of the material taken from the diseased seal are presented. The taxonomic characteristics of microorganisms, their virulence and antibiotic resistance were studied. Treatment measures were developed and performed. It was found that the seal has the following types of microorganisms: Staphylococcus aureus; Enterococcus faecalis; Escherichia coli; Staphylococcus warneri; Proteus vulgaris; Clostridium perfringens, Proteushauseri, Staphylococcus epidermidis, Plesiomonas shigel-loides. All pathogens isolated from the seals were sensitive to 60.3% of antibiotics (ampicillin, cefuroxime, cefixime, gentamicin, amikacin, ciprofloxacin, ofloxacin, furadonin, Ceftriaxone, vancomycin) and resistant to 39.7% of antibiotics, two representatives of cephalosporins (cefaclor and ceftazidim) and ticarcillin.


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