METİSİLİN DİRENÇLİ Staphylococcus aureus ÜREMESİ TESPİT EDİLEN ÇOCUK HASTALARIN, KLİNİK, EPİDEMİYOLOJİK ÖZELLİKLERİ VE VANKOMİSİN HETEROJEN VE VANKOMİSİN ORTA DUYARLI İZOLATLARIN KLİNİK YANSIMALARI
Turgutoğlu Yılmaz, Aslı
xmlui.mirage2.itemSummaryView.MetaDataShow full item record
Staphylococcus aureus is one of the most important pathogens causing both nosocomial and community-acquired infections. These infections frequently develop with methicillin-resistant Staphylococcus aureus (MRSA) strains. Glycopeptide antibiotics, such as vancomycin are the agents used in treatment of these infections. Unfortunately, increased nosocomial MRSA infections and intense use of vancomycin result in drug resistance at the various levels. Reduced sensitivity to vancomycin may develop because of many phenotypic, genetic and biochemical ways. The superficial layer adhesion and biofilm development are the most important mechanisms of virulence. In 1940’s, by the use of penicillin G treatment, a significant decrease was observed in S.aureus-induced lethal infections. Shortly after, penicillin-resistant S. aureus strains began to emerge. Since 1959, by the use of metisilin which is a beta-lactamase-resistant semisynthetic penicillin, this problem had been solved. In 1961, just two years after the first use of methicillin, MRSA was identified. Methicillin-resistant Staphylococcus aureus bacteremia is one of the most serious bacterial infections associated with significant morbidity and mortality. In Europe and the United States, since mid-2000s, the increase of infection control measures for MRSA, decreased the incidence of infection. However, the incidence of MRSA infections in Asia is still high. Vancomycin is the standard antimicrobial therapy for MRSA. Reduced sensitivity of vancomycin for MRSA strains poses dangerous consequences. These strains are; vancomycin-intermediate (medium resistance) Staphylococcus aureus (VISA) and heterogeneous vancomycin intermediate Staphylococcus aureus (hVISA). In Japan in 1996, the first MRSA isolate with reduced sensitivity for vancomycin, had been identified. The common feature of VISA cases was prolonged and several times use of vancomycin or teicoplanin six months prior to the development of resistance. Showing different susceptibility patterns of isolates, vancomycin resistance is thought to occur as a result of repeated exposure. We aimed to evaluate the clinical course of vancomycin moderate sensitive Staphylococcus aureus in Hacettepe Univercity İhsan Doğramacı Children’s Hospital. We evaluated the patients who had been vancomycin moderate sensitive Staphylococcus aureus detected in microbiological samples. Demographic characteristics, underlying diseases, prevalence of previous hospitalizations, previous antibiotic use before therapy, type and duration of antibiotic intakes, identification of community or hospital-acquired infection, chemotherapy or immunosuppressant use, responses to treatment, steroid use, intubation, intensive care unit admission, presence of foreign bodies such as central venous catheter or peritoneum dialysis catheters, MIC values of vancomycin moderate sensitive Staphylococcus aureus and treatment modalititis for the infection were determined and risk factors of developing hVISA were described. A total of 68 children under 18 years of age who had methicillin resistant Staphylococcus aureus infections were included in the study. Seventy-two percent of patients (n = 49) were males and 27.9% (n=19) were females. The mean age was 60.62±8.69 months (median: 36 months) in patients with MRSA infection. The mean age was 26.07±8.97 months (median: 11 months) in patients with hVISA infection. MRSA was found in 77.9% (n = 53) of patients in the study group and hVISA was detected in 22.1% (n = 15) of patients. None of the patients had VISA isolates. Most of the patients had underlying illnesses and prolonged hospitalization history. The mean of MIC values for vancomycin was 1.13 ± 0.41 μg/mL and the mean of E test values was 1.17 ± 0.4 μg/mL for MRSA patients. In patients with hVISA the mean of MICs for vancomycin and mean of E test values were 1.7± 0.49 μg/mL and 1.5 ± 0.3 μg/mL, respectively. Types of infection were bacteriemia in 44.1% (n = 30), pneumonia in 16.2% (n = 11), soft tissue infection in 22.1% (n = 15), meningitis in 2.9% (n=1), peritonitis in 1.5 (n=1) and catheter related bacteremia in 13.2% (n = 9) of patients. Fifty –six percent (n=38) of the patients were hospitalized in intensive care unit. Twenty percent (n=6) of patients with bacteremia, 27.2% (n=3) of patients with pneumonia, 20% (n=3) of patients with soft tissue infection and 50% of patients with meningitis and 22.2% (n=2) of patients with catheter-associated bacteraemia had hVISA infection. Overall mortality was 35.3% (n = 24); MRSA infection related mortality was 30.2% (n = 16) and hVISA infection related mortality was 53.3% (n=8). On the sixth day of antimicrobial therapy, 62.3% (n = 33) of patients with MRSA infection and 53.3% (n = 8) of hVISA infection had treatment withdrawal. The end-treatment response was 30.2% (n=16) in patients with MRSA and 60% (n=9) in patients with hVISA. Previous vancomycin, teicoplanin and cephalosporin group antibiotic exposures of patients were evaluated and no significant risk determined in terms of hVISA development. As a result of our study, the use of vancomycin in repeated doses and intensive care admision were not considered as risk factors for developing hVISA infection.