Background: Acinetobacter spp are present everywhere in the environment and cause many epidemics in tropical countries.\r\n', u'Objectives: This study aims to learn about the status of multidrug resistance in ubiquitous and domination acinetobacter Spp caused nosocomial infections. Subjects and method: A descriptive, epidemiologic cross-sectional study on 65 nosocomial Acinetobacter spp isolated from 244 patients hospitalized at the intensive-care units, Bach Mai hospital and burn patients from the National Burn Institute from April, 2007 to May, 2008. Results: Rates of A.baumannii were 70.8% of the isolates. Acinetobacter spp were isolated from patients in intensive-care units showed resistant to almost all commercially available antibiotics groups, among Penicillin ranged from 94.6 to 97.4%; beta- Lactam ranged from 80.5 to 90%; Cephems were 97.6%; Aminoglycosides group ranged from 62.5 to 100% and Quinolon were 100%. The isolates that were susceptible to Netilmycin was 35% and Imipenem was 34.1%. Acinetobacter spp were isolated from burn patients, which showed resistant to Penicillin was 86, 7%; beta- Lactam was 93, 3%; Aminoglyco- sides ranged from 25% to 87.5% and Quinolon was 81,3%. The isolates were susceptible to Netilmycin was 75% and Imipenem was 31.3%. \r\n', u'Conclusion: Analysis of risk factors may help the study of epidemiology Acinetobacter to prevent hospital infections and reduce the mortality rate. \r\n', u'
Acinetobacter spp ; nosocomial infections

No abstract available.
Acinetobacter Infections* ; Acinetobacter* ; Infant, Newborn ; Intensive Care, Neonatal*

Carbapenem-resistant Acinetobacter species are increasingly recognized as major nosocomial pathogens, especially in patients with critical illnesses or in intensive care. The ability of these organisms to accumulate diverse mechanisms of resistance limits the available therapeutic agents, makes the infection difficult to treat, and is associated with a greater risk of death. In this review, we provide an update on the epidemiology, resistance mechanisms, infection control measures, treatment, and outcomes of carbapenem-resistant Acinetobacter infections.
Acinetobacter ; Acinetobacter baumannii ; Acinetobacter Infections ; Colistin ; Critical Illness ; Drug Therapy ; Epidemiology ; Humans ; Infection Control ; Critical Care

OBJECTIVETo study the changes in expression of quorum sensing gene aba I in Acinetobacter baumannii (AB) strains isolated from burn patients during biofilm formation process, and its influences on the extracellular matrix of biofilm and drug resistance of AB.

METHODSSix drug-resistant and five drug-sensitive AB strains isolated from wound excretion, blood and venous catheter were collected from burn patients hospitalized in Ruijin hospital of Shanghai Jiao Tong University School of Medicine from January to October 2011. The AB standard strain ATCC 19606 was used as control. (1) Clinical strains and standard strain were normally cultured 10, 24, and 48 h respectively in vitro. The bacteria samples were stained with propidium iodide to measure biofilm thickness with confocal laser scanning microscope. (2) Clinical strains and standard strain were cultured in tubes 10, 24, and 48 h respectively in vitro under shaking condition. The bacteria floating in the medium were regarded as free bacteria, while those adhered to the tube wall as the bacteria within biofilm (biofilm bacteria). Relative expression value of genes aba I and pgaB was detected by real-time fluorescent quantitative PCR with the expression value of the standard strain set at 1. Data were processed with analysis of variance.

RESULTS(1) At post culture hour (PCH) 10, 24, 48, biofilm thickness of clinical strains was thicker than that of standard strain; biofilm thickness of drug-resistant strains [(28.8 ± 0.6), (31.7 ± 1.1), and (38.1 ± 3.1) µm] was respectively thicker than that of drug-sensitive strains [(17.1 ± 0.4), (20.1 ± 1.6), and (25.8 ± 1.7) µm, with F value respectively 1274.38, 206.60, and 61.73, P values all below 0.05]. (2) Biofilm bacteria: at PCH 10, 24, 48, expression values of aba I in drug-resistant strains (6.6 ± 1.7, 25.7 ± 3.5, 9.8 ± 3.6) were much higher than those of drug-sensitive strains (2.7 ± 1.0, 15.0 ± 3.5, 4.7 ± 3.2, with F value respectively 21.82, 25.24, and 6.22, P values all below 0.05); expression values of pgaB in drug-resistant strains (37.4 ± 1.1, 44.5 ± 3.6, 33.1 ± 11.5) were obviously higher than those of drug-sensitive strains (14.6 ± 0.8, 20.0 ± 6.9, 18.7 ± 6.8, with F value respectively 1488.44, 57.26, and 6.01, P values all below 0.05). (3) Free bacteria: at PCH 10, 24, 48, there was no significant statistical difference between drug-resistant strains and drug-sensitive strains in expression value of aba I (with F value respectively 0.24, 2.33, and 0.11, P values all above 0.05); expression values of pgaB in drug-resistant strains (13.8 ± 3.8, 12.5 ± 2.9, 23.7 ± 2.1) were obviously higher than those of drug-sensitive strains (7.0 ± 5.9, 5.0 ± 1.3, 15.6 ± 6.7, with F value respectively 5.44, 28.42, and 7.76, P values all below 0.05). (4) Comparison between biofilm bacteria and free bacteria in resistant strains: expression value of aba I in biofilm bacteria at each time point was respectively higher than that of free bacteria (with F value respectively 43.69, 286.61, and 9.98, P values all below 0.05); expression values of pgaB in biofilm bacteria at PCH 10, 24 were higher than those in free bacteria (with F value respectively 214.26 and 283.20, P values below 0.05). (5) Comparison between biofilm bacteria and free bacteria in sensitive strains: expression value of aba I in BF bacteria at PCH 24 was higher than that of free bacteria (F = 70.28, P < 0.05); expression values of pgaB in biofilm bacteria at PCH 10, 24 were higher than those of free bacteria (with F value respectively 8.03 and 22.62, P values below 0.05).

CONCLUSIONSDuring biofilm formation process, the increasing expression of quorum sensing gene aba I in drug-resistant AB strains isolated from burn patients may up-regulate the expression of gene pgaB, which leads to high production of extracellular matrix and biofilm formation, and enhances drug resistance of AB.

Acinetobacter Infections ; Acinetobacter baumannii ; genetics ; isolation & purification ; Biofilms ; Burns ; microbiology ; Drug Resistance, Bacterial ; Genes, Bacterial ; Humans

OBJECTIVETo observe expressions of pgaABC gene clusters and changes in biofilm (BF) phenotype in Acinetobacter baumannii (AB) isolated from burn patients.

METHODSFrom January 2009 to October 2010, 24 strains of AB isolated from burn patients hospitalized in our burn wards were collected for the study, while the standard strain ATCC 19606 was used as control. Expressions of pgaABC gene clusters were detected by real time fluorescence quantitative RT-PCR. All strains were cultured for 16 hours in vitro, BF with semi-quantitative detection was respectively evaluated by modified microtiter-plate test under stable condition and tube test under shaking condition for expression of absorbance value. All strains were cultured for 48 hours in vitro, then stained with fluorescent agent and collected for measurement of BF thickness with confocal laser scanning microscopy (CLSM). Data were processed with t test.

RESULTS(1) The expression of pgaB gene (27.91 ± 7.93) in clinical AB strains was much higher than that of standard strain ATCC 19606 (1.00, t = 5.77, P < 0.05). There was no statistical difference in expression of pgaA and pagC genes between standard strain ATCC 19606 (1.00) and clinical AB strains (1.01 ± 0.28, 1.15 ± 0.38, with t value respectively 0.04, 0.64, P values all above 0.05). (2) After being cultured for 16 hours, BF of clinical AB strains cultured under shaking condition formed distinct "purple circle", and its absorbance value (1.25 ± 0.31) was higher than that in standard strain ATCC 19606 (0.76 ± 0.03, t = 2.67, P < 0.05). There was no obvious difference in absorbance value between clinical AB strains and standard strain ATCC19606 cultured under stable condition. (3) After being culture for 48 hours, green fluorescence intensity and distribution in extracellular matrix of clinical AB strains were stronger as compared with those of standard strain ATCC 19606, and BF thickness in clinical AB strains [(27.3 ± 9.4)µm] was thicker than that in standard strain ATCC 19606 [(15.6 ± 1.7) µm, t = 2.09, P < 0.05].

CONCLUSIONSThe high expression of pgaB gene in AB strains isolated from burn patients can induce production of extracellular matrix, which may be related to increase in the ability and thickness of BF formation.

Acinetobacter Infections ; microbiology ; Acinetobacter baumannii ; genetics ; isolation & purification ; Biofilms ; Burns ; microbiology ; Genes, Bacterial ; Humans ; Multigene Family

Acinetobacter Infections ; diagnosis ; therapy ; Acinetobacter baumannii ; Child ; Drug Resistance, Bacterial ; Humans

Acinetobacter baumannii is a source of opportunistic infection in hospital and can cause central nervous system infection mainly by neurosurgical operation. Community acquired infection by Acinetobacter baumannii is very rare. A 58-year-old man was presented with fever, decreased consciousness and seizure. Acinetobacter baumannii was identified in the CSF culture, and colistin was administered intravenously. Patient's clinical symptoms improved after treatment. We report a case of successful treatment of Acinetobacter baumannii meningitis with colistin.
Acinetobacter baumannii* ; Acinetobacter* ; Central Nervous System Infections ; Cerebrospinal Fluid ; Colistin* ; Consciousness ; Fever ; Humans ; Meningitis* ; Middle Aged ; Opportunistic Infections ; Seizures

A cystic mass of lid is occasionally diagnosed as a sebaceous cyst. But 20% of the clinically diagnosed sebaceous gland cystic mass wasbenign tumors or inflammations. So final diagnosis of cystic mass was often made by histologic examination. Acinetobacter species are gram negative, anaerobic rods and mainly cause nosocomial infection. Most species are resistant to antibiotics so that careful selection of antibiotics is needed. We experienced a 12 year-old girl who had a palapable and tender mass on the right upper lid similar to sebaceous cyst. The mass was confirmed as a acinetobacter abscess. The authors present a case of acinetobacter infection of the upper lid that was treated with excision and antibiotics.
Abscess ; Acinetobacter Infections* ; Acinetobacter* ; Anti-Bacterial Agents ; Cellulitis ; Child ; Cross Infection ; Diagnosis ; Epidermal Cyst ; Female ; Humans ; Inflammation ; Sebaceous Glands

In recent years, Acinetobacter baumannii has become an increasingly common nosocomial pathogen. It causes rare, but severe, central nervous system (CNS) infection, especially in patients undergoing neurosurgical procedures or with head trauma. Multi-drug-resistant A. baumannii (MDR-AB) has emerged as a pathogen causing CNS infection. We describe A. baumannii CNS infections seen during the last 5 years and focus on MDR-AB CNS infection. Seven patients were admitted to the neurosurgical intensive care unit with serious head injuries. Imipenem-susceptible A. baumannii was identified in all four cases seen from 2003 to 2006, whereas the three cases seen from 2007 to 2008 were MDR-AB CNS infections. Two cases of MDR-AB CNS infection were cured with intraventricular or intrathecal colistin without any side effects. Therefore, intraventricular or intrathecal colistin should be considered for MDR-AB CNS infection. Studies of the dose and duration of intraventricular and intrathecal administration are needed.
Acinetobacter ; Acinetobacter baumannii ; Central Nervous System ; Central Nervous System Infections ; Colistin ; Craniocerebral Trauma ; Humans ; Intensive Care Units ; Neurosurgical Procedures

Infections caused by Acinetobacter baumannii (AB) have emerged as a knotty clinical problem in the burn wards due to its omni-resistance to antibiotics and high prevalence. Although our knowledge in regard to the pathogenesis and the resistance mechanisms of AB is increasing, the available treatment remains much limited. Measures to effectively control nosocomial infection are warranted. Meanwhile, development of novel therapeutic agents or combination of antibiotics should be considered.
Acinetobacter Infections ; epidemiology ; Acinetobacter baumannii ; drug effects ; Anti-Infective Agents ; pharmacology ; Burns ; microbiology ; Drug Resistance, Multiple, Bacterial ; Humans