OBJECTIVE: To study the microbiology, clinical features and treatment outcomes of hospital-acquired pneumonia (HAP) caused by Acinetobacter baumannii. METHODS: Six cases of HAP, caused by Acinetobacter baumannii producing PER-1 type extended-spectrum beta-lactamase verified by molecular biological methods, were studied in Bethune International Peace Hospital, from January to August 2005. Clinical data were collected and analyzed. Pulsed-field gel electrophoresis (PFGE) were used to analyze the homology of these strains. The genes of beta-lactamase (BLA), aminoglycoside-modifying enzymes (AME), resistant to disinfectant-sulfanilamide (qacEDelta1-sul1), and class 1 integrase (intl1) were analyzed using PCR and verified by DNA sequencing. RESULTS: Among these 6 strains of Acinetobacter baumannii, five were susceptible only to imipenem, and 4 were susceptible to meropenem. The PFGE types identified from these isolates were A1 (n=2) and A2-A5 (n=1, respectively). They all were positive for PER-1, TEM-1, and genes of qacEDelta1-sull and intl1. Three of them harbored genes of aac (3)-I and aac (6')-I. Two had aac (3)-I and ant (3'')-I. One had aac (3)-I. All the patients had severe underlying diseases, and had received mechanical ventilation. They all had received broad spectrum antibiotics within 15 days before Acinetobacter baumannii were identified. Although carbapenem and/or cefoperazone/sulbactam had been used, only 3 patients survived. CONCLUSION: The 6 PER-1 type extended-spectrum beta-lactamase-producing Acinetobacter baumannii isolates were closely related and had complex mechanisms of drug resistance. The prognosis of patients infected by them was poor.
OBJECTIVE: To study the microbiology, clinical features and treatment outcomes of hospital-acquired pneumonia (HAP) caused by Acinetobacter baumannii. METHODS: Six cases of HAP, caused by Acinetobacter baumannii producing PER-1 type extended-spectrum beta-lactamase verified by molecular biological methods, were studied in Bethune International Peace Hospital, from January to August 2005. Clinical data were collected and analyzed. Pulsed-field gel electrophoresis (PFGE) were used to analyze the homology of these strains. The genes of beta-lactamase (BLA), aminoglycoside-modifying enzymes (AME), resistant to disinfectant-sulfanilamide (qacEDelta1-sul1), and class 1 integrase (intl1) were analyzed using PCR and verified by DNA sequencing. RESULTS: Among these 6 strains of Acinetobacter baumannii, five were susceptible only to imipenem, and 4 were susceptible to meropenem. The PFGE types identified from these isolates were A1 (n=2) and A2-A5 (n=1, respectively). They all were positive for PER-1, TEM-1, and genes of qacEDelta1-sull and intl1. Three of them harbored genes of aac (3)-I and aac (6')-I. Two had aac (3)-I and ant (3'')-I. One had aac (3)-I. All the patients had severe underlying diseases, and had received mechanical ventilation. They all had received broad spectrum antibiotics within 15 days before Acinetobacter baumannii were identified. Although carbapenem and/or cefoperazone/sulbactam had been used, only 3 patients survived. CONCLUSION: The 6 PER-1 type extended-spectrum beta-lactamase-producing Acinetobacter baumannii isolates were closely related and had complex mechanisms of drug resistance. The prognosis of patients infected by them was poor.