RESUMO
This report presents the prevalence of Palestinian isolates of methicillin-resistant Staphylococcus aureus (MRSA) in nosocomial infections and their antibiotic resistant pattern. A total of 321 clinical isolates of S. aureus were identified from different patients. The prevalence of methicillin resistance among S. aureus isolates was 8.7% (28 isolates). Resistance rates of MRSA to other antibiotics were as follows: 82.1% resistant to erythromycin, 67.9% to clindamycin, 64.3% to gentamicin, and 32.1% to ciprofloxacin. No co-trimoxazole- and vancomycin-resistant isolates were identified in this study. The proportion of methicillin resistance was highest among S. aureus isolates associated with upper respiratory specimens (42.8%); the proportion of methicillin resistance was 39.3% among skin ulcer isolates, 10.7% among urinary tract infection isolates, and lowest among isolates associated with blood and prostate discharge (3.6% each).
Assuntos
Infecção Hospitalar/microbiologia , Resistência a Meticilina , Infecções Estafilocócicas/microbiologia , Staphylococcus aureus/efeitos dos fármacos , Infecção Hospitalar/epidemiologia , Farmacorresistência Bacteriana , Humanos , Prevalência , Infecções Estafilocócicas/tratamento farmacológico , Infecções Estafilocócicas/epidemiologia , Staphylococcus aureus/isolamento & purificação , Staphylococcus aureus/fisiologiaRESUMO
Eighty isolates of Escherichia coli were collected in Northern Palestine throughout the 1996 to 2000 period from hospitalized patients with urinary tract infections (UTIs). Resistance rates were ampicillin, 65%; co-trimoxazole, 55%; cefuroxime, 10%; cefotaxime, 7.5%; ceftazidime, 2.5%; ciprofloxacin, 12.5%; gentamicin, 6.25% and amikacin, 1.25%. No imipenem-resistant isolates were identified. To determine whether this was due to intra-hospital transmission of resistant strains, clonal structure of 10 multiple-resistant isolates was examined by genomic DNA fingerprinting by enterobacterial repetitive intergenic concensus-polymerase chain reaction (ERIC-PCR) and all were clonally distinct. Thus, these strains are likely resistant due to convergent acquisition of resistance determinants by genetically unrelated uropathogenic strains rather than epidemic spread of resistant isolates.