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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The importance of fecal colonization with P-fimbriated Escherichia coli for the later development of pyelonephritis was studied among infants before the age of 11 months. In contrast to previous studies, the fecal colonization with a P-fimbriated E. coli strain did not increase the incidence of acute pyelonephritis.
Infection
PMID:Fecal colonization with P-fimbriated Escherichia coli as a predictor of acute pyelonephritis in infancy--a prospective study. 290 94

During the clinical development of ciprofloxacin 1,519 treatments of UTI were documented. The most frequent specific diagnoses were uncomplicated UTI (46.6%), followed by non-specified UTI (21.7%), complicated UTI (19.4%), acute pyelonephritis (7.6%) and chronic pyelonephritis (4.1%). 70% of the causative organisms isolated were Enterobacteriaceae (Escherichia coli 38%, Proteus spp. 10% and Klebsiella pneumoniae 10%). Pseudomonas aeruginosa occurred in approximately 20% of the cases and the remaining 10% were gram-positive aerobes. Clinical resolution was achieved in about 90% in all specific diagnoses. The eradication rate for gram-negative Enterobacteriaceae was 93.8%, for P. aeruginosa 81.8% and for gram-positive aerobes 90.2%. Studies comparing ciprofloxacin and standard treatment have shown the high efficacy of ciprofloxacin making it a preferred agent particularly for infections caused by pathogens less susceptible to conventional drugs. According to the experience of clinical trials the recommended ciprofloxacin dose varies between 100 and 500 mg b.i.d. orally depending on the severity of clinical status and the susceptibility of the pathogen.
Infection 1988
PMID:Clinical experience with ciprofloxacin in the treatment of urinary tract infections: a review. 306 43

Infections of the urinary tract belong to the most frequent bacterially caused diseases. Strains of bacteria which are able to evoke an infection of the urinary tract distinguish themselves by particular properties. Hereby the existence of O- and K-antigens, the demonstration of adhesins (F-antigens), the ability of the formation of haemolysin and production of colicin V (aerobactin), the serum resistance as well the plasmid profile an important role is ascribed. The ability of uropathogenic bacteria to the adhesion to the epithelial cells of the urinary tract is significant for the development and the course of a disease. A connection is to be established between the rate of bacterial attachment of the epithelial cells and the activity of a pyelonephritis. The defence of an infection of the urinary tract takes place above all in the local area, in which cases among others the phenomenon of the antibody coated bacteria and disturbances of the formation of the secretory IgA are of interest. Various pathogenetic aspects of chronic infections of the urinary tract are discussed on the basis of reports from literature and findings of own investigations.
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PMID:[Pathogenetic aspects of chronic urinary tract infections]. 331 80

Experimental pyelonephritis was induced by intravenous inoculation of Staphylococcus aureus in homozygous Brattleboro diabetes insipidus (Hom Brattleboro DI), heterozygous Brattleboro (Het Brattleboro) and Wistar rats. One group of rats from each strain was implanted with morphine-containing pellet three days before inoculation. Another series of groups received D-aspartic acid (D-ASP) intraperitoneally, starting three days before inoculation throughout the experiments. Owing to the inhibition by morphine or D-ASP of food intake, another control group from each strain was subjected to food restriction. Pyelonephritis development on the tenth day of inoculation was evaluated by the determination of viable bacteria in urine and total kidney tissue, and pathomorphological lesions in kidney. Hom Brattleboro DI rats appeared more resistant. Morphine or D-ASP significantly increased the findings in three strains of rat.
Infection 1988
PMID:Aggravation by morphine and D-aspartic acid of pyelonephritis induced by i.v. inoculation of Staphylococcus aureus in rats. 336 Apr 96

Infection persists for long periods in chronic pyelonephritis, but the cellular basis of the host-parasite relationship is poorly understood. We have obtained quantitative data on the relationship between the pathogen (E. coli) and cellular defence mechanisms. Depletion of cellular components was carried out using whole body irradiation, methylprednisolone, cyclophosphamide or carrageenan and silica particles. A system of administering cyclophosphamide and methylprednisolone through the use of a slow release carrier, as well as graded doses of irradiation, was then developed to allow the controlled reduction of cellular competence. Quantitative studies in a host with chronic pyelonephritis and normal cellular defence reserves showed that severe depletion of granulocytic cells is necessary before host defence mechanisms are adversely affected. This finding conflicts with the observation that microorganisms survive and persist in the kidney for extended periods. Additionally, noncellular factors may also limit bacterial growth.
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PMID:Cellular basis of host defence in pyelonephritis. I. Chronic infection. 351 38

The antibacterial activity of ofloxacin, a new gyrase inhibitor, was tested in experimental acute occlusive pyelonephritis in rats caused by Escherichia coli O4:H5 and Pseudomonas aeruginosa A 9532. Therapy was performed using increasing concentrations of the substance during three days. Effectiveness of therapy was investigated by determination of the bacterial counts in the tissue of kidneys and in the urine obtained by puncture of the bladder. As little as 3 X 3.75 mg/kg/day of the substance was effective and reduced the E. coli counts. The dosage of 3 X 7.5 mg/kg/day was effective in pseudomonas infections.
Infection 1986
PMID:[Results of ofloxacin treatment of experimental urinary tract infections]. 351 71

A-56619 and A-56620 are two new aryl-fluoroquinolones which are as potent as or more potent than norfloxacin when administered orally and subcutaneously in mouse protection tests against Staphylococcus aureus, Streptococcus pyogenes, and Streptococcus pneumoniae. A-56619 and A-56620 were more potent than norfloxacin when administered orally against Escherichia coli, Proteus mirabilis, Serratia marcescens, and Pseudomonas aeruginosa. A-56620 was as potent or two- to threefold more potent than norfloxacin when administered subcutaneously against members of the family Enterobacteriaceae and Pseudomonas aeruginosa. Infection with Salmonella typhimurium was more effectively treated with A-56619 (50% effective dose [ED50], 1.4 mg/kg per day) than with norfloxacin (ED50, 62.8 mg/kg per day). E. coli or Pseudomonas pyelonephritis in mice was more effectively treated with A-56619 or A-56620 than with norfloxacin. After oral treatment, the ED50s of A-56619 and A-56620 were less than 12.5 mg/kg per day against E. coli and 62.9 and 38 mg/kg per day against P. aeruginosa pyelonephritis, respectively. Norfloxacin was ineffective at 200 mg/kg per day against E. coli or P. aeruginosa pyelonephritis. A-56619 and A-56620 were also more potent than norfloxacin in treatment of mixed bacterial pyelonephritis caused by E. coli and Streptococcus faecalis. A-56619 was at least 30 times more potent than norfloxacin and A-56620 was 4 to 11 times more potent than norfloxacin when administered against Klebsiella pneumonia in mice. A-56619 and A-56620 were at least 2 to 10 times more potent than norfloxacin against Staphylococcus aureus infections in immunosuppressed mice. A-56619 was equally potent in all in vivo tests when administered orally or subcutaneously, whereas A-56620 was similar to norfloxacin in being more potent when administered subcutaneously. The peak serum levels after subcutaneous and oral administration of A-56619 and A-56620 were higher than that of norfloxacin. The serum hal-lives of A-56619 and A-56620 after subcutaneous and oral administration were longer than the serum half-life of norfloxacin.
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PMID:In vivo evaluation of A-56619 (difloxacin) and A-56620: new aryl-fluoroquinolones. 352 73

Aminoglycosides have a low molecular weight and bind weakly to proteins. They are easily filtered through the glomeruli, bind to phospholipid receptors located on the brush border of proximal tubule cells, and penetrate within the cells by endocytosis. Aminoglycosides decrease lysosomal A and C phospholipase and sphingomyelinase activities. This impairs the degradation of phospholipids, with formation of abnormal intralysosomal structures called myeloid bodies as a result. These myeloid bodies are gradually eliminated from the cells into the lumen of the tubule and excreted in the urine. We studied the urinary excretion of phospholipids following 1, 3, 5 and 10 days of treatment with gentamicin (3 mg/kg/day) or tobramycin (3 mg/kg/day) in patients with acute pyelonephritis. Infection-free, non-treated subjects were used as controls. Patients with a urinary tract infection treated by a quinolone made up a third group. Urinary N-acetyl-beta-D-glucosaminidase (NAG), an indicator of epithelial necrosis, was also evaluated. Results were expressed per ml urine, per mg creatinine and per 24 hours. Only the results expressed per mg creatinine appeared valid. No significant increase in serum creatinine or urinary NAG was found in patients under gentamicin. In the patients with a urinary tract infection not treated with an aminoglycoside, urinary phospholipid excretion on D1 was decreased as compared to controls (p less than 0.01). Urinary phospholipid excretion was never found to be increased in patients under aminoglycosides. No significant difference was found between males and females. Mistaken interpretations occurred if urinary excretion of phospholipids or NAG was not expressed per mg creatinine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Urinary excretion of phospholipids: index of aminoglycoside nephrotoxicity]. 353 46

Lipid A is the toxic component of endotoxin in gram-negative bacteria. Antibodies to lipid A are not usually found in healthy persons (or only at a low titer) without a corresponding history of infection. Even gram-negative septicemia is found to be accompanied by only low titers. A completely different situation is seen in patients with chronic or recurrent infections due to Enterobacteriaceae and other gram-negative bacteria. Here it is notable that the antibody titer varies with the type of disorder (e.g. cystitis and pyelonephritis). A severe wound infection, e.g. due to Pseudomonas aeruginosa, also leads to measurable lipid A antibody titers. Varying antibody titers can be observed in cystic fibrosis, Crohn's disease, and severe surgical infections. One can conclude that a significantly elevated antibody titer develops during an extensive tissue involvement of long duration and indeed is caused by tissue inhibition by endotoxin. Based on clinical experience, it can be assumed that lipid A antibodies present in the body have a protective effect in septic shock.
Infection
PMID:[Lipoid A antibody titer in the human]. 359 12

Lipid A is the toxic component of endotoxin in gram-negative bacteria. Antibodies to lipid A are not usually found in healthy persons (or only at a low titer) without a corresponding history of infection. Even gram-negative septicemia is found to be accompanied by only low titers. A completely different situation is seen in patients with chronic or recurrent infections due to Enterobacteriaceae and other gram-negative bacteria. Here it is notable that the antibody titer varies with the type of disorder (e. g. cystitis and pyelonephritis). A severe would infection, e. g. due to Pseudomonas aeruginosa, also leads to measurable lipid A antibody titers. Varying antibody titers can be observed in cystic fibrosis, Crohn's disease, and severe surgical infections. One can conclude that a significantly elevated antibody titer develops during an extensive tissue involvement of long duration and indeed is caused by tissue inhibition by endotoxin. Based on clinical experience, it can be assumed that lipid A antibodies present in the body have a protective effect in septic shock.
Infection 1987
PMID:[Lipoid A antibody titer in humans]. 361 Mar 31


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