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Vancomycin tolerant, methicillin-resistant Staphylococcus aureus reveals the effects of vancomycin on cell wall
Vicenta Cázares-Domínguez1, Ariadnna Cruz-Córdova1, Sara A Ochoa1
1Laboratorio de Investigación en Bacteriología Intestinal, Hospital Infantil de México Federico Gómez, Dr. Márquez 162, Col. Doctores, Delegación Cuauhtémoc, México D.F., México.
Abstract:
Methicillin-resistant Staphylococcus aureus (MRSA) is an important opportunistic pathogen that causes both healthcare- and community-acquired infections. An increase in the incidence of these infections may lead to a substantial change in the rate of vancomycin usage. Incidence of reduced susceptibility to vancomycin has been increasing worldwide for the last few years, conferring different levels of resistance to vancomycin as well as producing changes in the cell wall structure. The aim of the present study was to determine the effect of vancomycin on cell wall thickening in clinical isolates of vancomycin-tolerant (VT) MRSA obtained from pediatric patients. From a collection of 100 MRSA clinical isolates from pediatric patients, 12% (12/100) were characterized as VT-MRSA, and from them, 41.66% (5/12) exhibited the heterogeneous vancomycin-intermediate S. aureus (hVISA) phenotype. Multiplex-PCR assays revealed 66.66% (8/12), 25% (3/12), and 8.33% (1/12) of the VT-MRSA isolates were associated with agr group II, I, and III polymorphisms, respectively; the II-mec gene was amplified from 83.3% (10/12) of the isolates, and the mecIVa gene was amplified from 16.66% (2/12) of the isolates. Pulsed field electrophoresis (PFGE) fingerprint analysis showed 62% similarity among the VT-MRSA isolates. Thin transverse sections analyzed by transmission electron microscopy (TEM) revealed an average increase of 24 nm (105.55%) in the cell wall thickness of VT-MRSA compared with untreated VT-MRSA isolates. In summary, these data revealed that the thickened cell walls of VT-MRSA clinical isolates with agr type II and SCCmec group II polymorphisms are associated with an adaptive resistance to vancomycin.
Insights
Vancomycin-tolerant MRSA (Methicillin-resistant Staphylococcus aureus) in children shows thicker cell walls, indicating adaptive resistance. This finding is crucial for understanding and treating persistent MRSA infections.
Area of Science:
- Microbiology
- Infectious Diseases
- Pathogen Resistance
Background:
- Methicillin-resistant Staphylococcus aureus (MRSA) is a significant opportunistic pathogen causing various infections.
- Increasing vancomycin resistance necessitates understanding resistance mechanisms in MRSA.
- Vancomycin tolerance (VT) and heterogeneous vancomycin-intermediate S. aureus (hVISA) phenotypes are growing concerns.
Purpose of the Study:
- To investigate the impact of vancomycin on cell wall thickening in clinical vancomycin-tolerant MRSA isolates from pediatric patients.
- To characterize the genetic and phenotypic traits of these vancomycin-tolerant MRSA isolates.
Main Methods:
- Isolation and characterization of vancomycin-tolerant MRSA from pediatric clinical samples.
- Multiplex-PCR for agr group and SCCmec typing.
- Pulsed-field gel electrophoresis (PFGE) for genetic relatedness.
- Transmission electron microscopy (TEM) to analyze cell wall thickness.
Main Results:
- 12% of MRSA isolates were vancomycin-tolerant (VT-MRSA), with 41.66% exhibiting the hVISA phenotype.
- VT-MRSA isolates were predominantly associated with agr group II (66.66%) and SCCmec group II (83.3%).
- TEM analysis revealed a significant average increase of 24 nm (105.55%) in cell wall thickness in VT-MRSA compared to controls.
Conclusions:
- Thickened cell walls in VT-MRSA, particularly those with agr type II and SCCmec group II, are linked to adaptive vancomycin resistance.
- These findings highlight a potential mechanism for vancomycin tolerance in pediatric MRSA infections.
- Understanding cell wall alterations is critical for developing strategies against resistant MRSA strains.
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