S. aureus resistant to vancomycin - a new danger
From their appearance in the 1970s to the present day, methicillin-resistant staphylococci (MRSA) have been one of the main agents responsible for nosocomial infections. The frequency of MRSA in the structure of staph infections in recent years has increased significantly worldwide (for example, in the United States - from 2% in 1975 to 35% in 1996). The most effective drugs in the treatment of MRSA for a long time remained the glycopeptide antibiotics - vancomycin and teicoplanin.
The possibility of the emergence of vancomycin-resistant S.aureus began to be considered about ten years ago after reports of vancomycin resistance in coagulase-negative enterococci and staphylococci. The possibility of transmission of plasmid resistance to vancomycin by enterococci, which has been proven experimentally, was considered particularly alarming, especially since very often (according to some reports, up to 20%), these microorganisms stand out in association. However, despite this, more than ten years passed before Dr. K. Hiramatsu's first report on the release in Japan in May 1996 of MRSA with reduced sensitivity to vancomycin (CPI 8 mg / l) from a postoperative wound on 4 month-old children in the cardiovascular surgery department. The treatment of this patient with vancomycin for 29 days was inconclusive. The clinical effect was obtained with the combination of ampicillin / sulbactam (in high doses) and arbekacin aminoglycoside. Despite the BMD value for vancomycin, corresponding to a moderate resistance range, this strain was registered as VRSA (resistant to vancomycin S.aureus). None of the previously known mechanisms of resistance to vancomycin were found in this strain; only an increase in the thickness of the cell wall and in the concentration of penicillin binding proteins 2 and 2a was noted. In the United States, two S.aureus with an MPC for vancomycin of 8 mg / L and a designated VISA (S.aureus with reduced sensitivity to vancomycin) were then isolated. These strains were obtained from patients receiving long-term vancomycin treatment for bacteremia and peritonitis in the presence of chronic peritoneal dialysis. In Europe, in 1997, Dr V. Krcmery from Slovakia reported the release of VRSA with a BMD of 16 mg / l in a child with staphylococcal cellulitis and multiple abscesses in the presence of an immunodeficiency state.
Following an in-depth study of vancomycin resistance in MRSA, when screening more than 2,000 strains from various hospitals, 1% to 25% (!) Strains with heterogeneous (inducible) resistance to vancomycin expressing it with a frequency of about 1 in 106 cells have been revealed. These strains may be precursors of VRSA, which indicates a high probability of rapid growth of potentially incurable staphylococcal infections.
Experts have still not reached an agreement on the term to use (VRSA or VISA), due to the fact that, despite the IPC values corresponding to the moderate resistance range, there is clinical ineffectiveness of vancomycin in the treatment deep infections with VRSA and VISA. In other words, in the absence of resistance from a pharmacological point of view, these strains are resistant to vancomycin from a clinical and biological point of view.
The spread of vancomycin resistance in staphylococci can cause significant problems in clinical practice, as there is currently no reliable alternative to glycopeptides. Great expectations are based on new antibacterial drugs from the group of oligosaccharides (everninomycin), streptogramins (quinupristine / dalphopristine) and oxazalidinones (linezolid).
Thus, it is extremely important to develop methods for laboratory diagnosis and monitoring of vancomycin resistance, especially in patients receiving or receiving vancomycin / teicoplanin treatment and when this treatment is ineffective. Methods must be developed to control VRSA infections, and measures must be taken to isolate patients and carriers to prevent the spread of VRSA. In addition, the use of antibiotics should include a reduction in the unreasonable administration of vancomycin in the clinic and a restriction in the use of glycopeptides in veterinary practice.