ABSTRACT
Ceftazidime-resistant Enterobacter aerogenes was isolated from blood cultures of three patients with fever. DNA analysis using pulsed-field gel electrophoresis and ribosomal RNA gene restriction digest pattern analysis revealed that the strains were clonally similar to each other with a 79.3-96.0% homology. The same strain of E. aerogenes was isolated from a three-way stopcock connected to the indwelling catheter in one of the patients at a concentration of 45 cfu/mL. A similar strain was also isolated from the urine of one other patient on the same floor. The data suggest that E. aerogenes caused septicaemia via low bacterial contamination of a three-way stopcock in a peripheral drip intravenous infusion system in at least one patient, and that the outbreak of E. aerogenes infections was due to clonally-related strains.
Subject(s)
Cross Infection/etiology , DNA, Bacterial/analysis , Enterobacter aerogenes/isolation & purification , Enterobacteriaceae Infections/etiology , Ribotyping/methods , Sepsis/etiology , Adult , Electrophoresis, Gel, Pulsed-Field , Enterobacter aerogenes/drug effects , Enterobacter aerogenes/pathogenicity , Equipment Contamination , Female , Humans , Japan , Microbial Sensitivity Tests , Middle AgedABSTRACT
The purpose of this study was to investigate whether anisodamine could inhibit Shiga toxin-1 (Stx1)-induced cytokine production and increase the survival of Stx1-treated mice. Human monocytic cells were stimulated by Stx1 (1 to 100 ng/mL) with or without anisodamine addition (1 to 400 microg/mL). For in vivo evaluations, C57BL/6 mice were given a single intraperitoneal injection of anisodamine (1 mg) or saline solution after intraperitoneal injection of Stx1 (2.75 microg/kg). The results showed that anisodamine significantly suppressed Stx1-induced tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and IL-8 production. Reverse transcriptase-polymerase chain reaction (RT-PCR) showed that anisodamine suppressed Stx1-mediated TNF-alpha mRNA expression. Further study showed that this TNF-alpha inhibitory effect was via a prostaglandin E2-dependent mechanism. Anisodamine treatment prolonged the survival time of mice and decreased the lethality of Stx1 (94.5% to 44%). Because cytokines, in particular TNF-alpha, contribute to the pathologic process in Stx-producing Escherichia coli (STEC) infection, this study suggested that anisodamine could be a potential drug for treatment of STEC infection.
Subject(s)
Cytokines/biosynthesis , Shiga Toxin 1/toxicity , Solanaceous Alkaloids/therapeutic use , Animals , Cell Line , Cell Survival , Dinoprostone/physiology , Escherichia coli Infections/drug therapy , Gene Expression , Humans , Injections, Intraperitoneal , Interleukin-1/biosynthesis , Interleukin-8/biosynthesis , Male , Mice , Mice, Inbred C57BL , Monocytes/drug effects , Monocytes/metabolism , RNA, Messenger/analysis , Reverse Transcriptase Polymerase Chain Reaction , Solanaceous Alkaloids/administration & dosage , Solanaceous Alkaloids/pharmacology , Survival Rate , Tumor Necrosis Factor-alpha/biosynthesis , Tumor Necrosis Factor-alpha/geneticsABSTRACT
Caspase proteolytic activities, such as caspase-3, -2 and -6, of THP-1 human monocytic cells were markedly increased in a time- and dose-dependent manner by treatment with purified Shiga toxin 1 (Stx1) or Stx2. Caspase-3 activation was strictly correlated with internucleosomal DNA fragmentation and chromatin condensation of the cells. In addition, the specific caspase-3 inhibitor, Ac-DEVD-CHO, decreased the percentage of apoptotic cells. The purified B-subunit of Stx1 did not induce apoptosis in THP-1 cells. Caspase-3 activation, DNA fragmentation and chromatin condensation caused by Stx were completely blocked by pretreatment of cells with brefeldin A, an inhibitor of Golgi functions. The findings suggest that Stx1 as well as Stx2 activate caspase-3, which plays a critical role in apoptosis, and that the apoptotic signals rise after Stx is transported to the Golgi apparatus.
Subject(s)
Apoptosis/drug effects , Brefeldin A/pharmacology , Caspases/metabolism , Monocytes/drug effects , Shiga Toxin 1/metabolism , Shiga Toxin 2/metabolism , Caspase 3 , Cell Line , Chromatin , DNA Fragmentation , Enzyme Activation/drug effects , Humans , Monocytes/cytology , Monocytes/enzymology , Shiga Toxin 1/pharmacology , Shiga Toxin 2/pharmacologyABSTRACT
The motility of Helicobacter pylori was maximum at 37 degrees C and at pH 6. A newly developed proton pump inhibitor, rabeprazole (RPZ), and its thioether derivative (RPZ-TH) markedly inhibited the motility of H. pylori. The concentrations of the drug necessary to inhibit 50% of the motility were 0.25, 16, 16, and >64 microgram/ml for RPZ-TH, RPZ, lansoprazole, and omeprazole, respectively. No such inhibitory effects were observed with H(2) blockers or anti-H. pylori agents. The motilities of Campylobacter jejuni and C. coli-but not those of Vibrio cholerae O1 and O139, Vibrio parahaemolyticus, Salmonella enterica serovar Typhimurium, and Proteus mirabilis-were also inhibited. Prolonged incubation with RPZ or RPZ-TH inhibited bacterial growth of only H. pylori, except for a turbid colony mutant. The results indicate that RPZ and RPZ-TH have a characteristic inhibitory effect against the motility of H. pylori (spiral-shaped bacteria), which is distinguished from that against bacterial growth.
