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Analysis of plasmids in nosocomial strains of multiple-antibiotic-resistant Staphylococcus aureus
Abstract:
Nosocomial infections caused by Staphylococcus aureus strains resistant to methicillin and multiple antibiotics have reached epidemic proportions in Melbourne, Australia, over the past 5 years. Plasmid analysis of representative clinical isolates demonstrated the presence of three classes of plasmid DNA in most strains. Resistance to gentamicin, kanamycin, and tobramycin was usually mediated by an 18-megadalton plasmid but could also be encoded by a related 22-megadalton plasmid. Two distinguishable plasmids of 3 megadaltons each endowed resistance to chloramphenicol, and the third class consisted of small plasmids, each approximately 1 megadalton in size, with no attributable function. An extensive array of resistance determinants, including some which have usually been associated with a plasmid locus, were found to exist on the chromosome. Evidence that resistance to gentamicin, kanamycin, and tobramycin is chromosomally encoded in some clinical isolates suggests that this determinant may have undergone genetic translocation onto the staphylococcal chromosome.
Insights
Methicillin-resistant Staphylococcus aureus (MRSA) strains with multiple antibiotic resistance are epidemic in Melbourne. Plasmid and chromosomal analysis reveals complex resistance mechanisms, including potential genetic translocation of resistance genes.
Area of Science:
- Microbiology
- Infectious Diseases
- Molecular Biology
Background:
- Nosocomial infections caused by multi-drug resistant Staphylococcus aureus, particularly methicillin-resistant strains (MRSA), have become a significant public health concern.
- Epidemic proportions of these resistant strains have been observed in Melbourne, Australia, over the last five years, necessitating investigation into their genetic basis.
Purpose of the Study:
- To investigate the plasmid and chromosomal genetic elements responsible for antibiotic resistance in epidemic Staphylococcus aureus strains.
- To understand the mechanisms underlying the spread of multi-drug resistance in clinical isolates.
Main Methods:
- Plasmid DNA analysis of representative clinical isolates.
- Characterization of plasmid sizes and associated resistance determinants.
- Investigation of chromosomal resistance genes.
Main Results:
- Most strains contained three classes of plasmid DNA.
- Resistance to gentamicin, kanamycin, and tobramycin was typically mediated by 18- or 22-megadalton plasmids.
- Chloramphenicol resistance was linked to two distinct 3-megadalton plasmids, while small 1-megadalton plasmids had no attributable function.
- Numerous resistance determinants, usually plasmid-associated, were found on the chromosome.
- Evidence suggests potential chromosomal encoding and genetic translocation of gentamicin, kanamycin, and tobramycin resistance.
Conclusions:
- Antibiotic resistance in epidemic Melbourne Staphylococcus aureus strains is mediated by a combination of plasmid-borne and chromosomally encoded resistance genes.
- The findings suggest that resistance determinants, particularly for aminoglycosides, may have undergone genetic translocation onto the bacterial chromosome.
- Understanding these genetic mechanisms is crucial for combating the spread of multi-drug resistant infections.