| Objectives: Acinetobacter is an opportunistic pathogen. It widely spreads in nature, hospital and skin surface. Now, it becomes one of the main prevalent pathogenic bacteria of nosocomial infectious pathogen because it's strongly environmental survivability and tolerance of soap. In recent years, Acinetobacter baumannii have been increasingly resistant toβ-lactamase, quinolones, macrolides, aminoglycoside drugs. We defined these to Multi-drug Resistant Acinetobacter Baumannii (MDR-Aba). Some of them had been resistant to imipenem and meropenem. This means it have been resistant to multiple antibiotic and caused highly fatality rate. So, we should pay close attention to this situation.Acinetobacter baumannii isolates collected from 2006 to 2008 were screened for surveying epidemic trend and homology in our hospital for better understanding of these aspects to optimize both infectious control and clinical treatment. Here we studied OXA-23-like, OXA-51-like and ISAbal by molecular biotechnology and mechanisms of carbapenem resistance in Acinetobacter baumannii.Methods: (1) We retrospectively investigated clinical isolates ranking from 2006 to 2008 and dynamic observation of resistance trends of Acinetobacter baumannii. (2) Forty consecutive MDR-Aba isolates collected from July 2007 to December 2008 were screened from The PLA of ShenYang Military General Hospital, all specimens respectively coming from 9 departments including sputum, pharynx-swab, blood, urine and secretion; but the most were sputum samples. (3) Bacteria was identified by API of manual identified plate of French Biomerieux Company. Drug sensitivity test used K-B of disc diffusion method. (4) Pulsed-field gel electrophoresis (PFGE) was used to detect homology of Acinetobacter baumannii. (5) Polymerase Chain Reaction, PCR was used to examine the sequences OXA-23-like, OXA-51-like and ISAba1 gene for these isolates and four sensitive isolates.Results: (1) The detective rate of Acinetobacter baumannii from sputum was the most, but in 2006 there were only 2.6%. The next two years, the rates were 8.6% and 15.7% respectively. At this period, drug resistance rate raised year by year, but sensitive was just down to 30% in 2008. The sensitive of cefoperazone/sulbactam which was the most effective drug drop to 47.2% in 2008 from 91.4% in 2006. The detective rate of other three strains of Acinetobacter were not significant difference in three years. Drug resistance of change tendency was almost the same as those of Acinetobacter baumannii, but to a lesser degree. (2) All of forty isolates belonged to three PFGE pulsotypes (A, B, C), indicating clonal spread. Majority of pulsotype A were 37 isolates (28 of Type A1, 2 of Type A2, 6 of Type A3), 2 pulsotype B and 2 pulsotype C isolates. (3) All isolates of OXA-23-like, OXA-51-like and Int1 gene were detected by PCR. For the sensitive isolates, all carried Int1 gene. Only one is detected OXA-23-like and OXA-51-like is none of four isolates.Conclusions: (1) From 2006 to 2008, Acinetobacter of clinical infection rate got much and significantly increased resistance., which were accordant. A. baumannii was the more severe resistant than other Acinetobacter spp. It's indicated that there was different mechanism of antibiotic resistance. (2) MDR-Aba isolates collected between October 2007 and December 2008 basically belonged to the same pulsotype, Type A. The primary pulsotype was A1 and a small quantity of subtype was A2 and A3. There were occasionally pulsotype B and C. (3) The mechanism of antibiotic resistance possibly closed connected with this gene of OXA-23-like, OXA-51-like and Int1, but the details need more research. |
PDF Full Text Request