Genetic Supports of blaOXA-23 in Acinetobacter baumannii and Their Clinical Significance / 中华医院感染学杂志

OBJECTIVE To study the genetic supports of OXA-23 in Acinetobacter baumannii isolates and investigate the relationship between imipenem resistance acquiring and use of antibiotics.METHODS Consecutive selection of the 24 highly susceptive A.baumannii clinical isolates by imipenem was carried out.Genes of carbapenemases were detected by PCR and the colonial relationship of these isolates was evaluated by ERIC-PCR.Plasmids conjugation experiments and blaOXA-23 hybridization were performed to explore the gene location of blaOXA-23.RESULTS From all 24 susceptible A.baumannii isolates 10 were selected,including 6 multi-colonial blaOXA23 harboring strains.Plasmid conjugation experiments and Southern blotting experiments demonstrated that blaOXA-23 was not associated with integrons.CONCLUSIONS BlaOXA-23 may exist in a certain subset of apparently carbapenem sensitive Acinetobacter strains.When under consecutive selective pressure,bacteria harboring blaOXA-23 become the predominant group and subsequently the antibiotics resistance properties appear.It highlights the reasonable use of this category of antibiotics.

VIM-2 Metallo-?-lactamase Producing Pseudomonas aeruginosa in Burn Wards / 中华医院感染学杂志

OBJECTIVE To analyze homology,antimicrobial susceptibility and metallo-?-lactamase gene type of metallo-?lactamase producing Pseudomonas aeruginosa in burn wards.METHODS Antimicrobial susceptibility tests were performed with E-tests.Using 2-mercaptoethanol disc synergy test to screen metallo-?-lactamase(positive) strains from imipenem-resistant P.aeruginosa in burn wards.Metallo-?-lactamase gene and integrase gene were amplified and sequenced.Resistance plasmid transfer and curing experiments were implemented to study the transfer of imipenem resistance and plasmid DNA was extracted and purified with Qiagen Plasmid Mini Kit.Random amplified polymorphic DNA(RAPD) typing was carried out to analyze the homology of the isolates.(RESULTS) Six strains of P.aeruginosa were suggested to produce metallo-?-(lactamase) by 2(-mercaptoethanol) disc synergy test.Using primers described for bla(VIM),the amplifications were observed among all 6 isolates and a VIM-2 metallo-?-(lactamase) gene was identified by sequencing.All isolates which producing VIM-2 metallo-?-(lactamase) had class 1 integrase gene and derived from a same clonal origin.CONCLUSIONS(VIM-2) metallo-?-(lactamase) producing P.aeruginosa is prevalent in burn wards,all isolates which producing VIM-2 metallo-?-(lactamase) have class 1 integrase gene.

Infections Caused by Enterobacter cloacae:Clinical Distribution and Antimicrobial Resistance / 中华医院感染学杂志

OBJECTIVE To investigate the clinical distribution and antimicrobial resistance of infections caused by Enterobacter cloacae in our hospital,for guiding the prophylaxis and treatment of these infections in clinical practice. METHODS Antimicrobial susceptibility tests were done by Kirby-Bauer disk diffusions method,the phenotypes of E.cloacae strains harboring AmpC ?-lactamases and extended-spectrum ?-lactamases(ESBLs) were detected by modified three-dimensional extract test. RESULTS A total of 162 strains of E.cloacae were isolated between Jan 2002 and Dec 2004,the percentages of these strains isolated from sputum,urine and wound secretion were 62.3%,11.7% and 9.9%,respectively.73.5% of all strains isolated from intensive care unit(ICU) in every endemic area.AmpC ?-lactamases,AmpC ?-lactamases combined with ESBLs and ESBLs producing strains were detected in 19.1%,11.7% and 14.2% of E.cloacae,respectively.The resistance of AmpC ?-lactamases or ESBLs producer was obviously higher than that of non-AmpC ?-lactamases and ESBLs producer,while the phenomenon of resistance was serious especially in AmpC ?-lactamases combined with ESBLs producer,but all strains were sensitive to imipenem. CONCLUSIONS E.cloacae causes infections of respiratory tract,urinary tract and wound principally in clinic,the most of which occurred in ICU.AmpC ?-lactamases and ESBLs are popular in E.cloacae,the restricted use of ?-lactams is a considerable measure which reduces prevalence of AmpC(?-lactamases) and ESBLs producing strains.The antimicrobial agents for treating infections caused by E.cloacae should be chosen according to the results of the antimicrobial susceptibility tests,imipenem is the first choice for severe infections.

Combined therapy of interleukin-12 and interleukin-18 against Cryptococcus neoformans infection in a murine model / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>To explore adverse effects of combined treatment of interleukin-12 (IL-12) and interleukin-18 (IL-18) against cryptococcosis in a murine model.</p><p><b>METHODS</b>Infected mice were treated with a combination of IL-12 and IL-18. Their body weight and intake of water and food were observed and recorded. Serum levels of leptin were detected with an enzyme-linked immuno sorbent assay (ELISA).</p><p><b>RESULTS</b>In the combined treatment group, the intake volume of water and food were reduced, leading to weight loss and undetectable levels of leptin in the serum. These adverse effects were more profound in mice that had received higher doses of cytokines, which sometimes led to a fatal outcome. There was a significant difference compared with the control group. Neutralization of endogenous tumor necrosis factor-alpha (TNF-alpha) by its specific mAb did not alter the wasting effect of this treatment.</p><p><b>CONCLUSIONS</b>The combined IL-12/IL-18 treatment may cause a number of adverse effects independent of TNF-alpha and leptin synthesis. Further investigations for resolving these adverse effects are required before clinical application of these cytokines.</p>

Mutations of Pseudomonas aeruginosa oprD gene in Imipenem-resistant clinical isolates / 中华传染病杂志

Objective To study the mutations of Pseudomonas aeruginosa oprD gene in Imipenem-resistant clinical isolates. Methods Random amplified polymorphic DNA typing(RAPD) was carried out to analyse the homology in 10 Imipenem-resistant clinical isolates. Pseudomonas aeruginosa oprD gene in 10 Imipenem-resistant clinical isolates were amplified by polymerase chain reaction and sequenced. Results Ten Imipenem-resistant clinical isolates were divided into four different clones which can not produce metallo ?-lactamase. As compared with sequence X63152, oprD gene of Pseudomonas aeruginosa varied greatly. The aberration rates exceed 50%. There were multiple point mutations within 276～387 bp coding region of 30, 11, 9, 20, 31 strains. Due to the mutations of 308 bp G→C and 344 bp C→A, threonine and diaminocaproic acid were replaced by serine and threonine respectively. The DNA deletion of 393～412 bp in oprD gene contributes to the frame shift mutation in the following nucleotide sequence. The deletion of 264～273 bp in the coding region of oprD gene in 13 and 21 clone strains leads to frame shift mutations forming terminal codon TAA(319～321 bp).Base substitutions and multiple point mutations were obvious in the coding regions of 1 and 22 clone strains. Their aberration rates were 54.03% and 74.89% respectively. Conclusions The mutations of Pseudomonas aeruginosa oprD gene in Imipenem-resistant clinical isolates are various.

Antimicrobial Susceptibility and Molecular Epidemiology of Imipenem-Resistant Pseudomonas aeruginosa / 中华医院感染学杂志

OBJECTIVE To study the antimicrobial susceptibility and molecular epidemiology of imipenem-resistant Pseudomonas aeruginosa isolated from patients in burn wards in a hospital of Guangzhou. METHODS A total of 48 imipenem-resistant isolates were collected,antimicrobial susceptibility was tested by KirbyBauer disk diffusion method.Random amplified polymorphic DNA(RAPD) typing was carried out to analyze the homology. RESULTS All isolates were multiresistant,the orders of sensitivity rates of antibiotics were CIP,TOB,AMK,GEN,and FEP.Forty eight strains were classified into types A,B,C,and D based on RAPD pattern,types A and B were the most epidemic clones. CONCLUSIONS The prevalence of imipenemresistant P.aeruginosa in burn wards of the hospital is due to nosocomial infection.The prevalent strains are multiresistant.