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K Tateda

Publications and source records attributed to K Tateda.

At least 73 records · Page 4Linked to original sources
PubMed1996

Assessment of clinical significance of positive blood cultures of relatively low-virulence isolates.

In Omori Hospital, Toho University School of Medicine, relatively low-virulence blood isolates, including coagulase-negative staphylococci (CNS), enterococci and nonfermentative gram-negative rods other than Pseudomonas aeruginosa comprised c. 60% of total blood isolates. A retrospective study was conducted to assess their clinical significance by reviewing a total of 91 hospital charts. The physicians' assessments of these positive blood cultures as recorded in the charts were classified into four categories--sepsis, possible sepsis, contamination and no comment. The episodes classified as sepsis accounted for 5.0-19.6%. These episodes were also evaluated by a graded clinical significance score based on multiple factors, including number of positive cultures and clinical signs. The scores for the 91 episodes covered a wide range from 1 to 9, indicating that both contaminants and causative organisms may have been involved. The episodes judged as sepsis or possible sepsis tended to have higher scores. The scores for the episodes associated with enterococci were also higher than those involving CNS or non-fermentative gram-negative rods. The scores for episodes associated with intravenous hyperalimentation catheters were higher than those not associated with the catheters.

Bacteremia↗
PubMed1996

Experimental endogenous septicaemia caused by Klebsiella pneumoniae and Escherichia coli in mice.

Multi-resistant Klebsiella pneumoniae have recently occurred in several nosocomial outbreaks of septicaemia. An animal model resembling the pathophysiology of these infections in man would be very useful. A new model of endogenous septicaemia caused by K. pneumoniae and Escherichia coli strains in mice has been established. The mortality rate of conventional ddY mice given cyclophosphamide (CY) or fluorouracil (5-FU), each 200 mg/kg intraperitoneally, every other day was 70 and 100%, respectively. Pseudomonas aeruginosa septicaemia was observed in all dead mice treated with CY, whereas Enterobacteriaceae, including K. pneumoniae, were isolated from 90% of mice given 5-FU. Specific-pathogen-free mice, decontaminated with ampicillin and ceftazidime, were given multi-resistant K. pneumoniae CF504, CF514 or E. coli CF604, or CF614 carrying CAZ-1/TEM-5 plasmid by oral inoculation. Subsequent dosing with 5-FU induced lethal septicaemia caused by the inoculated strains in most of these mice, whereas CY did not regularly induce septicaemia. This model with 5-FU is considered to resemble closely the situation observed in man and to be beneficial for investigating pathophysiology and therapeutic strategies.

Ampicillin↗
PubMed1996

Establishment of a model of penicillin-resistant Streptococcus pneumoniae pneumonia in healthy CBA/J mice.

Examination of strain differences in the susceptibility of mice to experimental respiratory tract infection with penicillin-resistant Streptococcus pneumoniae TUM19 revealed that a fatal infection model could be induced in immunocompetent CBA/J mice, but not in C3H/HeN, C57BL/6 or ICR mice. After intranasal instillation of c. 10(6) cfu of S. pneumoniae, the bacterial counts in the lungs of CBA/J mice increased from 10(5) to 10(7) cfu after 3-5 days, and gradually increased thereafter. The challenge organisms localised mainly in the lungs until 14 days after infection. Mice began to die c. 7 days after infection, and by 3 weeks most of the mice had died. Histopathologically, infiltration of neutrophils and lymphocytes around bronchi was observed from 1 day after infection, and fibrin deposition was seen in alveolar and bronchial spaces from 5 days. This model may be useful for investigating therapy of respiratory tract infection caused by penicillin-resistant S. pneumoniae because its pathological features resemble those observed in the human disease.

Animals↗
PubMed1996

Direct evidence for antipseudomonal activity of macrolides: exposure-dependent bactericidal activity and inhibition of protein synthesis by erythromycin, clarithromycin, and azithromycin.

Several previous investigators have reported that long-term administration of certain macrolides is efficacious in patients with persistent pulmonary Pseudomonas aeruginosa infections, even though the clinically achievable concentrations of these medications are far below their MICs. In the present study, we examined how sub-MICs of macrolide antibiotics affect the viability of and protein synthesis in several strains of P. aeruginosa. We report that 48 h, but not 12 or 24 h, of growth on agar containing a clinically achievable concentration of azithromycin (0.5 microgram/ml, 1/128 the MIC) significantly reduces the viability of strain PAO-1. Similar effects were seen with erythromycin and clarithromycin at 2 micrograms/ml (1/128 and 1/64 the respective MICs), whereas josamycin, oleandomycin, ceftazidime, tobramycin, minocycline, and ofloxacin had no effect on viability, even following 48 h of incubation with concentrations representing relatively high fractions of their MICs. The bactericidal activity of azithromycin seen following 48 h of incubation was not limited to strain PAO-1 but was also seen against 13 of 14 clinical isolates, including both mucoid and nonmucoid strains. Although viability was not decreased prior to 48 h, we found that 4 micrograms of azithromycin per ml inhibits protein synthesis after as little as 12 h and that protein synthesis continues to decrease in a time-dependent manner. We likewise found that P. aeruginosa accumulates azithromycin intracellulary over the period from 12 to 36 h. These results suggested that sub-MICs of certain macrolides are bactericidal to P. aeruginosa when the bacteria are exposed to these antibiotics for longer periods. Exposure-dependent intracellular accumulation of the antibiotic and inhibition of protein synthesis may partially account for the antipseudomonal activity of macrolides over relatively prolonged incubation periods.

Anti-Bacterial Agents↗
PubMed1996

Noncompromised penicillin-resistant pneumococcal pneumonia CBA/J mouse model and comparative efficacies of antibiotics in this model.

The present study confirms that CBA/J mice are susceptible to several clinical isolates of Streptococcus pneumoniae, including four of five penicillin-susceptible and all five penicillin-resistant strains tested, thus providing the first noncompromised animal model for penicillin-resistant S. pneumoniae pneumonia. In this model, doses of penicillin G of 0.6 mg/kg of body weight given six times at 1-h intervals produced effective pulmonary clearance of a penicillin-susceptible strain (penicillin G MIC, 0.015 microgram/ml), while doses of 40 mg/kg given six times at 1-h intervals were required to clear a penicillin-resistant strain (penicillin G MIC, 1 microgram/ml). Imipenem (MIC, 0.25 microgram/ml) was the most active antibiotic tested against the penicillin-resistant strain, with a calculated dose of 0.42 mg/kg given six times at 1-h intervals, resulting in a 2-log decrease in the number of pulmonary bacteria. Comparable effects were seen with vancomycin (MIC, 0.5 microgram/ml), cefotaxime (MIC, 0.5 microgram/ml), and penicillin G at doses of 3.3, 5.5, and 31.0 mg/kg given six times at 1-h intervals, respectively. The pharmacokinetic profile of vancomycin in infected lungs was superior to those of the other antibiotics, especially in regard to the elimination half-life (215.4 min for vancomycin versus 15.0, 14.5, and 14.5 min for penicillin G, cefotaxime, and imipenem, respectively). Both imipenem and vancomycin allowed 90% survival when 40-mg/kg doses were administered twice a day beginning 5 days after infection. Survival rates with penicillin G (160-mg/kg doses) and cefotaxime (40-mg/kg doses) were 40 and 30%, respectively, while no saline-treated mice survived. The present study shows that the CBA/J mouse pneumonia model may be useful for evaluating antibiotic efficacies against penicillin-resistant pneumococcal pneumonia in immunocompetent individuals. Our data suggest that imipenem and vancomycin may be the most active agents against penicillin-resistant S. pneumoniae pneumonia.

Animals↗
PubMed1996

Lipopolysaccharide-induced lethality and cytokine production in aged mice.

This study was designed to define the lipopolysaccharide (LPS) sensitivity of aged mice in terms of lethality and cytokine production and to determine down-regulating responses of corticosterone and interleukin 10 (IL-10). The 50% lethal doses of LPS in young (6- to 7-week-old) and aged (98- to 102-week-old) mice were 601 and 93 microg per mouse (25.6 and 1.6 mg per kg of body weight), respectively. Aged mice were approximately 6.5-fold more sensitive to the lethal toxicity of LPS in micrograms per mouse (16-fold more sensitive in milligrams per kilogram) than young mice. Levels in sera of tumor necrosis factor-alpha (TNF-alpha) IL-1alpha, and IL-6 after intraperitoneal injection of 100 microg of LPS peaked at 1.5, 3, and 3 h, respectively, and declined thereafter in both groups of mice. However, the peak values of these cytokines were significantly higher in aged than in young mice (P < 0.05). Gamma interferon (IFN-gamma) was detectable at 3 h, and sustained high levels were still detected after 12 h in both age groups. Although there were no significant differences in levels of IFN-gamma in sera from both groups, aged mice showed higher IFN-gamma levels throughout the 3- to 12-h study period. Administration of increasing doses of LPS revealed that aged mice had a lower threshold to IL-1alpha production than young mice. In addition, aged mice were approximately 4-fold more sensitive to the lethal toxicity of exogenous TNF in units per mouse (10-fold more sensitive in units per kilogram) than young mice. With regard to down-regulating factors, corticosterone amounts were similar at basal levels and no differences in kinetics after the LPS challenge were observed, whereas IL-10 levels in sera were significantly higher in aged mice at 1.5 and 3 h than in young mice (P < 0.01). These results indicate that aged mice are more sensitive to the lethal toxicities of LPS and TNF than young mice. We conclude that a relatively activated, or primed, state for LPS-induced cytokine production, in spite of full down-regulating responses by corticosterone and IL- 10, may explain at least in part LPS sensitivity in aged mice.

Aging↗
PubMed1996

[Coronary ectasia].

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Coronary Angiography↗
PubMed1996

[Primary right atrial hemangiosarcoma manifesting as cardiac tamponade: a case report with transesophageal echocardiography].

A 39-year-old woman presented with a right atrial hemangiosarcoma manifesting as cardiac tamponade with complaints of chest discomfort and dyspnea. Transthoracic echocardiography revealed remarkable pericardial effusion and a right atrial mass. Transesophageal echocardiography disclosed the tumor extending into the right atrial cavity. Surgery found the tumor was poorly demarcated, immobile and adhered to the adjacent right atrial wall and septum. The echocardiographic findings correlated well with the surgical and autopsy findings.

Adult↗
PubMed1995

Abrupt augmentation of ST segment elevation associated with successful reperfusion: a sign of diminished myocardial salvage.

To investigate the significance of abrupt augmentation of ST segment elevation immediately after reperfusion, 36 patients with an initial acute anterior myocardial infarction successfully treated with thrombolysis were studied. Immediately after reperfusion was performed, 17 (47%) patients showed abrupt augmentation of ST segment elevation of anterior area (E group), and 19 (53%) patients did not (N group). The time to reperfusion was not significantly different between the two groups. In the E group the peak level of creatine kinase MB isozyme was higher (p < 0.05) than in the N group. The left ventricular ejection fraction (EF) did not increase in the E group from acute to chronic phase. However, in the N group EF increased significantly. The difference in EF in the chronic phase was significant between the two groups (p < 0.05). The infarcted regional wall motion (RWM) did not increase in the E group, whereas in the N group it increased markedly (p < 0.05). In addition, the infarcted RWM in the chronic phase was worse in the E group than in the N group (p < 0.05). Abrupt augmentation of ST segment elevation associated with successful reperfusion appears to reflect diminished myocardial salvage.

Aged↗
PubMed1995

Influence of various immunosuppressive agents on the occurrence of endogenous bacteraemia in mice.

The influence of six immunosuppressive agents on the occurrence of endogenous bacteraemia in mice was evaluated. The mortality rates in conventional ddY mice given cyclophosphamide (CY), fluorouracil (5-FU), methotrexate (MTX), cisplatin (CDDP) or FK-506 intraperitoneally, or dexamethasone (DXM) subcutaneously were 70, 100, 100, 100, 0 and 0%, respectively. Pseudomonas aeruginosa was isolated from 70% of mice treated with CY but from only 10% of mice treated with 5-FU and 30% treated with MTX. Enterobacteria were isolated from 90% of mice treated with 5-FU. Specific-pathogen-free (SPF) mice fed P. aeruginosa were also treated with these agents. All mice in the CY, 5-FU, MTX and CDDP groups died whereas mice treated with DXM and FK-506 showed 20% and 0% mortality, respectively. Pure cultures of P. aeruginosa were obtained from all of the mice treated with CY. Polymicrobial bacteraemia with P. aeruginosa and enterobacteria occurred in 5, 25, 5 and 5% of mice treated with 5-FU, MTX, CDDP and DXM, respectively. Enterobacterial bacteraemia was observed in 70% of mice treated with CDDP and in 5% of the DXM group. Different types of bacteraemia were induced by different immunosuppressive agents. The mechanism of immunosuppression may affect the frequency of bacteraemia and the causative organism.

Animals↗
PubMed1995

A protective role for lymphocytes in cyclophosphamide-induced endogenous bacteraemia in mice.

Cyclophosphamide (CY) is used in many animal studies, including models of bacteraemia, to deplete peripheral neutrophils and induce a compromised state. Although CY also influences lymphocyte function, the protective role of lymphocytes in bacteraemia is unclear. Therefore, CY (200 mg/kg) was administered to ddY mice and its influence on the number, cellular composition, and function of lymphocytes in the spleen and Peyer's patches was examined. A single dose of CY reduced the number of lymphocytes in a time-dependent fashion. Flow cytometry showed that B cells carrying B220 antigen decreased significantly. The production of IgA in Peyer's patches, as measured by enzyme-linked immunosorbent assay, was also suppressed in a time-dependent fashion. Blastogenic responses of splenic lymphocytes to Concanavalin-A, lipopolysaccharide and heat-killed Pseudomonas aeruginosa were suppressed 48 h after CY administration. The results suggest that CY suppresses the number and function of lymphocytes, especially B cells. This may lead to bacterial overgrowth in the gut and result in bacteraemia. Intravenous transfusion of normal lymphocytes or oral inoculation of IgA to mice with P. aeruginosa D4 endogenous bacteraemia significantly increased survival rates, indicating that lymphocytes and their products have a protective role in bacteraemia in mice.

Administration, Oral↗
PubMed1995

Role of exotoxin A in inducing severe Pseudomonas aeruginosa infections in mice.

The effects of exotoxin A (EXA) from Pseudomonas aeruginosa on polymorphonuclear leucocytes (PMNLs) were studied in a mouse model and in vitro. P. aeruginosa PA103, which produced EXA, was 20 times more virulent for normal mice than was its EXA-deficient mutant, PA103-29. EXA was detected in the plasma of mice infected with P. aeruginosa PA103, and its presence correlated with increasing numbers of bacteria in the blood and internal organs. A monoclonal antibody (MAb) against EXA prevented the death of the mice if it was given simultaneously with, or 2 h before, infection with strain PA103. The number of PMNLs in murine blood decreased by 50% within 30 min of intravenous injection of EXA, but this decrease was prevented by simultaneous or prior injection of MAb to the toxin. EXA inhibited in-vitro phagocytosis and killing of P. aeruginosa by human and murine PMNLs and decreased the number of the PMNLs by between 60 and 68%. Collectively, these results not only confirm that EXA is toxic in vivo, but also suggest that this toxin accelerates the growth of virulent P. aeruginosa in mice.

ADP Ribose Transferases↗
PubMed1995

The influence of exo-enzyme S and proteases on endogenous Pseudomonas aeruginosa bacteraemia in mice.

The role of Pseudomonas aeruginosa exo-enzymes was evaluated in a murine model of endogenous bacteraemia in which the bacteria invaded the bloodstream after oral dosing. Although an elastase mutant PAO-E64 was as virulent as its parent strain PAO1, an exo-enzyme S-deficient mutant, DG1-ExS5 and alkaline protease mutants PAKS-16, PAKS-17, PAKS-19, were less virulent than their parent strains, DG1 and PAKS-1, respectively (p < 0.01). Thus exo-enzyme S and alkaline protease, but not elastase, appear to contribute to the pathogenicity of P. aeruginosa in this model.

Animals↗
PubMed1995

Role of LPS length in clearance rate of bacteria from the bloodstream in mice.

Strains of Pseudomonas aeruginosa isolated from patients with cystic fibrosis (CF) never spread systemically. This may be due to serum sensitivity since these strains are very sensitive to complement-mediated bactericidal activity. A serum-resistant mutant, P. aeruginosa TUM3 HSR, was obtained from serum-sensitive strain TUM3 from a CF patient in order to clarify the mechanism of failure of systemic spread. LPS profiles on silver-stained gels and immunological analysis revealed that a long O-polysaccharide side chain was overproduced on the LPS molecules of TUM3 HSR as compared with the LPS of TUM3. The clearance rate from the bloodstream in mice was compared in the two strains. The number of TUM3 bacteria in 1 ml of blood, 10 min after injection into the tail vein, significantly decreased from 1.7 x 10(8) to 3.7 x 10(5) c.f.u. ml-1. In contrast, TUM3 HSR was not eliminated during the same period (decrease from 1.9 x 10(8) to 3.4 x 10(7) c.f.u. ml-1). Interestingly, these isogenic strains were not killed by 40% murine serum, probably reflecting immaturity of the complement-mediated killing system in mice. These results pointed to a correlation between LPS structure and blood clearance rate in mice. This was confirmed by examining blood clearance kinetics using the smooth-LPS strain Salmonella typhimurium LT2 and LPS-deficient mutants derived from it. S. typhimurium LT2 resisted blood clearance while the LPS-deficient mutants were cleared rapidly. None of the S. typhimurium strains were killed by murine serum. The number of P. aeruginosa TUM3 and S. typhimurium LPS-deficient mutants trapped in the liver following injection into the peripheral circulation was greater than that of their counterparts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Profiles of outer membrane proteins and lipopolysaccharide of Pseudomonas aeruginosa grown in the presence of sub-MICs of macrolide antibiotics and their relation to enhanced serum sensitivity.

We have previously reported that erythromycin at sub-inhibitory concentrations enhanced the serum sensitivity of some Pseudomonas aeruginosa strains. To explore the mechanism of this effect, we have now examined the influence of macrolide antibiotics on outer membrane proteins and lipopolysaccharide (LPS) of P. aeruginosa. The strains S-6 and PAO-1 of P. aeruginosa were used as susceptible and resistant strains respectively to assess enhancement of serum sensitivity by erythromycin. The strain S-6 became more serum-sensitive when grown on agar with sub-MICs of erythromycin or azithromycin, but not of josamycin, whereas no change was observed in the serum sensitivity of the strain PAO-1 after growth with any of these antibiotics. The analysis of outer membrane proteins showed that erythromycin treatment resulted in a reduction in the amount of the 38 kDa protein (OprF) and in a prominent increase of 41 kDa protein band in the strain S-6, but not in the strain PAO-1. By an immunoblotting assay, this 41 kDa protein was shown to be highly reactive to the immune serum against untreated P. aeruginosa. LPS of the strain S-6 were examined by SDS acrylamide gel electrophoresis. The treatment with erythromycin or azithromycin, but not with josamycin, reduced the amounts of LPS species with lower molecular weights although the levels of LPS species with high molecular weights were similar to those of untreated bacteria. These results suggest that the enhanced serum sensitivity of P. aeruginosa by erythromycin is associated with changes in bacterial surface components, such as outer membrane proteins and LPS.

Anti-Bacterial Agents↗