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K Tateda

Publications and source records attributed to K Tateda.

At least 91 records · Page 5Linked to original sources

Detection of antibody-coated bacteria in expectorated sputum for diagnosis of lower respiratory infections.

We evaluated antibody-coated bacteria (ACB) in expectorated sputum to discriminate contaminating or colonizing organisms from true pathogens. We examined 60 expectorated sputum samples from 51 patients with lower respiratory infections (chronic obstructive pulmonary disease 25, pneumonia 20, purulent tracheobronchitis 6). All samples were examined with quantitative culture and immunofluorescent demonstration of ACB. From the results of quantitative culture, we divided specimens into pathogen-isolated and pathogen-free samples. Among pathogen-isolated samples, in which we isolated accepted pathogenic organisms at > or = 10(7) colony-forming units per ml, 16 of 23 samples were ACB-positive (69.5%). In contrast, among pathogen-free samples, in which we isolated accepted pathogens at < 10(7) colony forming units per ml or only upper respiratory flora, only 3 of 37 samples were ACB-positive (8.1%). The ACB-positive rate was significantly higher in pathogen-isolated than in pathogen-free samples (P < 0.001). Consequently, detecting ACB in expectorated sputum shows good potential as another criterion for distinguishing contaminating or colonizing organisms from true pathogens.

Adult↗

[Image diagnosis of vasculitis--ultrasound].

Ultrasound is widely used for the diagnosis and follow-up of patients with many kinds of vasculitis. Transcutaneous or transesophageal two-dimensional ultrasound images can depict vascular wall lesions associated with vasculitis such as stenosis, aneurysm or wall thickening. Pulsed Doppler and color Doppler are useful for the assessment of stenoses and changes in blood flow. Recent progress in intravascular ultrasound apparatus made it possible to more precisely assess morphological changes in vascular wall. Intravascular ultrasound of a 27-year old male patient suffering from inferior myocardial infarction with right coronary aneurysms revealed calcification and fibrosis of the intima and early development of atherosclerosis in both right and left coronary arteries suggestive of the sequelae of Kawasaki disease.

Adult↗

Effect of clearance of bacteria from the blood on the development of systemic bacteraemia in mice.

Clearance of various bacteria isolated from portal and systemic blood of mice was evaluated and compared. All portal blood strains, including Escherichia coli and enterococci were eliminated more rapidly from the circulation than were strains isolated from systemic blood, including Pseudomonas aeruginosa. With mannose-type lectin, mannose or fucose residues that mediated lectinophagocytosis were detected on the surfaces of most portal strains by agglutination tests. Blood clearance of Esch. coli H21 was inhibited by prior injection of mannose into mice, suggesting that the clearance of this strain was mediated by mannose-type lectin on the surface of tissue macrophages. However, no inhibition of clearance of any other strains was observed by the injection of mannose, galactose, or fucose into mice, nor by pre-incubation of bacteria with mannose. Blood clearance of some portal strains was significantly faster in CBA/J mice than in CBA/N mice with B cell immune deficiency, indicating that immunoglobulin was involved in their clearance. Among portal strains only enterococci showed high cell-surface hydrophobicity. These data suggest that initial bacteria blood clearance may be critical in determining whether latent portal bacteraemia progresses to systemic bacteraemia and that the rapid clearance of most strains is multifactorial.

Agglutination Tests↗

Mortality rates amongst mice with endogenous septicaemia caused by Pseudomonas aeruginosa isolates from various clinical sources.

Mice that had been treated with cyclophosphamide and ampicillin were fed with Pseudomonas aeruginosa. These procedures induced an endogenous septicaemia under conditions mimicking the pathophysiology of the disease in man. This model was used to compare the mortality rates in mice infected with P. aeruginosa isolates from various clinical sources. Mortality rates in mice given isolates from blood cultures had a broad range (0-100%), but the mean rate was significantly higher than with isolates from other infection sites. Moreover, blood isolates persisted in the intestines of mice after oral inoculation, whereas most isolates from other sources were gradually eliminated. Most P. aeruginosa isolates from blood culture produced significantly higher levels of exotoxin A and total proteases than isolates from other infection sites. Amongst the blood isolates, all but one of the lethal strains produced large quantities of exotoxin A or total proteases or both. Taken together, the results suggest that the ability of P. aeruginosa to adhere to the intestinal tract and to produce high levels of exo-enzymes may contribute to the development of fatal septicaemia.

ADP Ribose Transferases↗

Effects of sub-MICs of erythromycin and other macrolide antibiotics on serum sensitivity of Pseudomonas aeruginosa.

We examined the effects of sub-MICs of erythromycin (EM) and other macrolide antibiotics on the serum sensitivity of Pseudomonas aeruginosa. P. aeruginosa S-6 grown for 36 and 48 h on agar with 10 micrograms of EM per ml (1/10th the MIC) showed significantly increased sensitivity to human serum bactericidal activity compared with those of bacteria grown on agar without EM (P < 0.05). No changes in serum sensitivity were observed in bacteria grown for less than 24 h. This increased sensitivity was apparent even at a concentration of 1.5 micrograms of EM per ml (1/67th the MIC) in bacteria grown for 48 h (P < 0.01). Among the other macrolide antibiotics tested, clarithromycin also enhanced sensitivity to serum, but there were no changes in the sensitivities of bacteria grown on agar with kitasamycin, josamycin, rokitamycin, or oleandomycin even at a concentration of 12 micrograms/ml (1/16th, 1/16th, 1/8th, and 1/33rd the MICs, respectively). P. aeruginosa S-6 grown on agar with subinhibitory concentrations of EM showed decreased cell surface hydrophobicity in a dose-dependent manner, whereas oleandomycin and rokitamycin, even at a concentration of 12 micrograms/ml, induced a slight decrease in hydrophobicity which was approximately equivalent to that of 1.5 micrograms of EM per ml. Among six other strains of the nonmucoid phenotype, three strains became more sensitive to serum by exposure to 10 micrograms of EM per ml for 48 h. In contrast, no evident correlation between EM treatment and a change in serum sensitivity was observed in six strains of the mucoid phenotype, as judged by the results of experiments with both 2 and 0.4% serum. These results show that EM at subinhibitory concentrations enhances the serum sensitivity of some P. aeruginosa strains. Since induced serum sensitivity was accompanied by a decrease in bacterial cell surface hydrophobicity, EM may render P. aeruginosa more serum sensitive by changing the cell surface structure(s) of this organism.

Anti-Bacterial Agents↗

In vivo production of exotoxin A and its role in endogenous Pseudomonas aeruginosa septicemia in mice.

We have examined the production of Pseudomonas aeruginosa exotoxin A (ETA) and its role in endogenous bacteremia in mice. Mice given P. aeruginosa D4 orally died of bacteremia between days 10 and 13 following cyclophosphamide-induced leukocytopenia. In this model, serum endotoxin was detected beginning on day 7 by the Limulus assay and P. aeruginosa was cultured from blood beginning on day 9. ETA and tumor necrosis factor alpha (TNF) were also detected in serum by enzyme-linked immunosorbent assay beginning on day 9. Purified ETA did not stimulate the production of TNF in normal mice primed with a synthetic derivative of muramyl dipeptide in the absence of endotoxin. However, ETA enhanced and primed endotoxin-induced TNF production in mice. The mortality rate of mice given ETA mutant PAO-PRI (5.0%) was significantly lower than that of mice given the parent strain (78.8%). These data indicate that ETA may be an important factor in the occurrence of P. aeruginosa bacteremia and/or the death of mice. Also, ETA may be responsible for enhancing the production of a lethal dose of TNF in the presence of endotoxin in P. aeruginosa bacteremia.

ADP Ribose Transferases↗

Amphotericin B-induced resistance to Pseudomonas aeruginosa infection in mice.

We evaluated the effects of amphotericin B (AmB) against Pseudomonas aeruginosa (P. aeruginosa) infection in mice. Pretreatment with 2 mg/kg of AmB 24 hours before infection significantly increased the survival rates of mice intraperitoneally infected with either P. aeruginosa or Escherichia coli. To evaluate the mechanism of this AmB-induced resistance to infection, we conducted a number of experiments. Peritoneal macrophages exposed in vitro to AmB showed superior bactericidal activity compared to that of control macrophages. Interleukin-1 production by peritoneal macrophages from mice pretreated with 2 mg/kg of AmB was significantly higher than that in control mice. Serum tumor necrosis factor level after intravenous injection of P. aeruginosa was also higher in mice pretreated with 2 mg/kg of AmB than in control mice. These data indicate that AmB induces resistance to P. aeruginosa in mice. Furthermore AmB-induced activation of peritoneal macrophages and their production of interleukin-1 and tumor necrosis factor appeared to play important roles in this phenomenon.

Amphotericin B↗

[Role of capsular polysaccharide and lipopolysaccharide of Klebsiella pneumoniae in experimental mice pneumonia model].

In this study, role of capsular polysaccharide (CPS) and lipopolysaccharide (LPS) of Klebsiella pneumoniae was investigated in experimental mice pneumonia model. Inoculation with K. pneumoniae mucoid strain DT-S into mice lung induced expansive, voluminous lethal pneumonia characterized with thickening of the alveolar septa caused by infiltration of inflammatory cell and packing of bacteria within alveolar spaces. On the other hand, mice lung inoculated with K. pneumoniae DT-X, which was non-mucoid mutant isolated from DT-S during natural passage, showed infiltration of inflammatory cell into alveolar spaces but there was no death of mice during the course of this pneumonia. Inoculation of CPS 100 micrograms of DT-S strain into mice lung induced lesser extent of accumulation of inflammatory cell than that of LPS 4 micrograms of this strain. Stimulation of alveolar and peritoneal macrophage with CPS, even at a concentration of 100 micrograms/ml, induced weaker Interleukin-1 (IL-1) activity than stimulation with LPS 4 micrograms/ml. These results suggest that since CPS of K. pneumoniae DT-S encapsulate bacteria including LPS, CPS may inhibit chemotaxis of inflammatory cell and IL-1 production of macrophage to be induced by LPS during course of pneumonia. It is speculated that existence of CPS have important role in modulating host response to bacterial LPS, and this effect of CPS may be related with difference of pathological findings of lung and lethality between K. pneumoniae DT-S and DT-X.

Animals↗

[Effect of azithromycin on human serum sensitivity of Pseudomonas aeruginosa].

We examined the effect of azithromycin (AZM), a 15-membered azalide newly synthesized from erythromycin (EM), on serum sensitivity of 6 strains of Pseudomonas aeruginosa. Incubation for 48 h on agar with EM 12 micrograms/ml or AZM 1.6 micrograms/ml induced increased serum sensitivity in 2 of 6 strains (S-6, PA-103), but there were no changes in any strains with josamycin (JM) 12 micrograms/ml. Although EM 12 micrograms/ml induced increased serum sensitivity of S-6 after more than 36 h incubation, AZM 1.6 micrograms/ml induced increased serum sensitivity of this strain at 12 h incubation. AZM 0.8 microgram/ml (1/62.5 MIC) showed more potent activity to enhance serum sensitivity of S-6 than that of EM 12 micrograms/ml (1/8 MIC) after 48 h incubation. P. aeruginosa S-6 incubated with EM 12 micrograms/ml or AZM 1.6 micrograms/ml for 48 h was less hydrophobic than that of control bacteria, but there was little change in the hydrophobicity of the strain incubated with JM 12 micrograms/ml. These results show that AZM has more potent activity to enhance serum sensitivity of P. aeruginosa than that of EM. Since decrease of cell surface hydrophobicity of P. aeruginosa S-6 was correlated with increased serum sensitivity, EM and AZM may induce enhanced serum sensitivity by changing cell surface structure of P. aeruginosa.

Azithromycin↗

[The study of pathogenic mechanisms of chronic Pseudomonas aeruginosa lung infections by mucoid strains].

Chronic Pseudomonas aeruginosa lung infection with mucoid strains is the predominant cause of death in cystic fibrosis (CF) or diffuse panbronchiolitis (DPB). This infection is characterized by a chronic course without spread of the bacteria to the blood when compared with other infections due to the non-mucoid strains. However, the mechanism of P. aeruginosa lung infection with the mucoid strains remains obscure. Intra-tracheal and systemic infection in mice, susceptibility to the bactericidal activity of fresh human and mouse serum, and adherent activity to mouse fetal lung cell were examined for mucoid and non-mucoid strains of P. aeruginosa. After intra-tracheal infection, the mucoid strains were distributed to other organs anormously but not the non-mucoid stains, and the bacterial number of the mucoid strains in the blood were significantly lower than that of the non-mucoid strains. On the other hand, when these strains were inoculated into the tail vein of mouse, the mucoid strain was eliminated more rapidly from blood as compared with the non-mucoid strain. The mucoid strains showed reduced bacteremic virulence when compared with non-mucoid strains with a 50% lethal dose (LD50) of 1.5 x 10(7) CFU/mouse as the mean value in a systemic infection. In contrast to the non-mucoid strains, the mucoid strains were sensitive to human fresh serum but were resistant to mouse fresh serum. The mucoid strains adhered to the monolayer of the mouse fetal lung cell 7-fold better than did non-mucoid strains.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Efficacy of erythromycin lactobionate for treating Pseudomonas aeruginosa bacteremia in mice.

We induced endogenous Pseudomonas aeruginosa bacteremia by administering cyclophosphamide and ampicillin to specific pathogen-free mice fed P. aeruginosa. Using this model, we evaluated the efficacy of erythromycin lactobionate (EML) in treating P. aeruginosa bacteremia. Treatment with EML at 50 and 100 mg/kg of body weight per day twice a day for 14 days significantly increased the survival rate. The most effective dose was 100 mg/kg/day, with a survival rate of 80% compared with a 20% survival rate in the control. However, the administration of EML at 500 mg/kg/day rather decreased the survival rate. In a model of intravenous infection, treatment with EML at 100 mg/kg/day twice a day for 7 days before the bacterial challenge also enhanced the survival rate. EML levels in serum, liver, and stool were apparently lower than the MIC (512 micrograms/ml). These observations suggest that EML is effective against P. aeruginosa bacteremia despite a lack of specific activity for this pathogen. Although the protective mechanism is still unclear, it is possible that a subinhibitory level of EML may affect the virulence of P. aeruginosa and enhance the host defense system.

Animals↗

Potential effects of erythromycin on host defense systems and virulence of Pseudomonas aeruginosa.

We evaluated several potential effects of erythromycin (EM) on host defense systems and the virulence of Pseudomonas aeruginosa. Peritoneal macrophages obtained from mice given 250 mg of EM per kg of body weight for 7 days by the intraperitoneal, intravenous, subcutaneous, or oral route produced significantly greater amounts of thymocyte-activating factors. These data suggest that EM enhances the in vivo production of cytokines, such as interleukins 1 and 6. Treatment of P. aeruginosa D4 with subinhibitory concentrations of EM enhanced the association of bacteria with murine Kupffer cells in vitro and increased bacterial clearance from the blood in mice. EM suppressed the in vitro production of exotoxin A, total protease, elastase, and phospholipase C by P. aeruginosa D4; exotoxin A production by P. aeruginosa PA-103; and total protease production by P. aeruginosa B16 and PAO1 in a generally dose-dependent manner. These data demonstrate that EM produces various effects in addition to its direct antimicrobial activity, suggesting that it has potential as an immunomodulator or bacterial virulence-suppressing agent against P. aeruginosa and other infections.

Adjuvants, Immunologic↗

Spontaneous coronary artery dissection after a natural course for 10 years--a case report.

We encountered a patient with spontaneous coronary artery dissection complicated by acute inferior myocardial infarction. A 58-year-old male was admitted to our hospital due to acute inferior myocardial infarction in 1979. Coronary angiography performed 4 weeks after the onset showed a double lumen divided by a linear intimal flap in the right coronary artery, suggesting coronary artery dissection, but no apparent occlusion. Subsequently, he had been medicated with nitrates without any recurrent infarction. In February, 1989, 10 years after the first examination, coronary angiography was again performed and showed that the dissection had remained unchanged. Acetylcholine infusion into the right coronary artery induced coronary spasm. The prognosis of this condition seems to be better than has been generally considered, particularly in patients such as ours in whom the involvement of coronary spasm in the development of coronary artery dissection and myocardial infarction is suggested. When coronary spasm in controlled by treatment with nitrates or calcium antagonists, an uneventful course may be expected.

Acetylcholine↗

[Effect of macrolide antibiotics on human serum-bactericidal sensitivity of Pseudomonas aeruginosa S-6].

It is well known that long-term administration of erythromycin (EM) at a small dose is effective for persistent infections with Pseudomonas aeruginosa in diffuse panbronchiolitis or chronic bronchitis patients. Since EM is less active against P. aeruginosa in vitro, we have been interested in the mechanisms of clinical efficacy of EM in these patients. This study examines the effect of macrolide antibiotics on human serum-bactericidal sensitivity of P. aeruginosa S-6, clinically isolated from the patient with respiratory tract infection. A significant increase in serum-bactericidal sensitivity of P. aeruginosa S-6 was observed on agar containing EM of 10 micrograms/ml after incubation for 36-60 hours (p less than 0.05). The enhancement of serum sensitivity of P. aeruginosa S-6 was apparently observed even at a concentration of EM 1.5 micrograms/ml after the 48 hours incubation (p less than 0.01). Of other macrolide antibiotics used, clarithromycin (CAM) also increased the serum-bactericidal sensitivity of P. aeruginosa S-6 as well as EM, however no change in the sensitivity was found with kitasamycin, josamycin, rokitamycin and oleandomycin. The results suggest that the change of serum-bactericidal sensitivity of P. aeruginosa induced by EM or CAM may, in part, contribute to the clinical efficacy of these antibiotics against persistent pulmonary P. aeruginosa infections.

Anti-Bacterial Agents↗

Role of bacterial association with Kupffer cells in occurrence of endogenous systemic bacteremia.

Bacteremia in immunocompromised hosts often arises from their endogenous intestinal flora. We produced experimental endogenous bacteremia by administering cyclophosphamide and ampicillin to conventional and specific-pathogen-free mice. The frequencies of bacteremia and mortality in the conventional mice were significantly higher than for the specific-pathogen-free mice. Pseudomonas aeruginosa was the major pathogen causing systemic bacteremia in conventional mice and was associated with a high mortality rate. Morganella morganii caused systemic bacteremia in both conventional and specific-pathogen-free mice. In contrast, Escherichia coli, enterococci, or other species most often caused portal bacteremia only. To determine the mechanism of occurrence of systemic bacteremia, we investigated bacterial blood clearance in mice and association with murine Kupffer cells, using several bacterial strains isolated from mice with bacteremia. Blood clearance rates and the abilities of isolated Kupffer cells to associate with bacteria were significantly greater for the organisms causing portal bacteremia than for those causing systemic bacteremia. There were no significant differences between the blood clearance rates in carrageenan-treated mice and that in normal mice. Moreover, association at 4 degrees C was not different from that at 37 degrees C. The results suggest that blood clearance of bacteria reflects bacterial adherence to Kupffer cells and that the resistance of bacteria to association with Kupffer cells plays an important role in the occurrence of overwhelming systemic bacteremia in this animal model.

Agglutination↗

[Investigation on the etiology of sepsis by using experimental mouse model with leukocytopenia. 3. The role of Kupffer cells in the etiology of bacteremia].

In the previous report, we showed that the reticuloendothelial system (RES), especially the liver, played an important role in the etiology of bacteremia or sepsis as the major protective system. In this study, to investigate the role of Kupffer cells in the etiology of bacteremia, we isolated and cultured murine Kupffer cells using a technique involving perfusion with collagenase and DNase. We compared the adherence and phagocytosis rate of two groups of isolated bacteria from bacteremic mice by these cells. One group was bacteria causing systemic bacteremia consisted of P. aeruginosa and M. morganii, and the other was bacteria causing portal bacteremia consisted of E. coli, E. cloacae, K. pneumoniae and Enterococci. As a consequence, the following facts were revealed. 1. The bacterial phagocytosis and adherence rate by Kupffer cells were significantly higher in bacteria causing portal bacteremia than in bacteria causing systemic bacteremia. These data were correlated to each blood clearance rate from mice. 2. Blood clearance rate reflected mainly adherence of Kupffer cells to bacteria, and it was suggested that these adherence were one of the most important factor to protect the hosts from the advance of bacteremia from the portal to the systemic. 3. In the case of using peritoneal macrophage, we couldn't find the same correlation, so the possibility was suggested that the above phenomenon was specific to Kupffer cells.

Animals↗