Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to determine the pathogenic responsibility of Escherichia coli adhesins (ADHs) in urinary infections (UI), 2,000 different patients suffering different clinical urinary and male sexual gland infections were monitored. The ADHs were determined by agglutination techniques with human and guinea-pig red blood cells, Candida albicans and Saccharomyces cerevisiae cells and latex sensitized with GAL-GAL. In uncomplicated UIs, the possession of ADH is the main invasion mechanism for E. coli. The rate of E. coli ADH strains is very high (89%) in acute cases (727 of 818 cases: 310 of 362 cystitis; 104 of 113 recidivant cystitis; 120 of 126 pyelonephritis; 158 of 173 prostatitis, and 34 of 43 orchiepididymitis) and rare (10%) in asymptomatic or chronic cases (24 of 235 cases: 14 of 148 bacteriurias; 8 of 74 prostatitis, and 2 of 13 orchiepididymitis). A close relation is established between the presence of ADH and clinical symptoms. 90% (218 of 242) of acute cases with systemic symptoms are due to MR-type ADH strains, especially the P subtype. 71% (409 of 576) of acute cases with local symptoms are due to MS-type ADH strains. In complicated UIs the expression of ADH is not an essential condition for the invasion of the urinary apparatus. It has been strongly suggested that males are significantly more resistant to UI, both in the tract and parenchyma, than women. It can be deduced that the underlying disease is more liable to UI the lower the adherence level shown by isolated strains. Thus catheters, reflux and neurogenic bladder are, by far, more aggressive alterations than the prostatic adenoma, vesical tumor or lithiasis.
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PMID:Frequency and distribution of uropathogenic Escherichia coli adhesins: a clinical correlation over 2,000 cases. 168 Jun 92

One thousand five hundred strains obtained from patients suffering from different clinical forms of urinary infections (UI) and dependent glands have been studied with the aim of establishing the pathogenic responsibility of E. coli adhesion protein (ADH) in urinary infections (UI). ADH were determined using agglutination techniques with guinea pig and human red cells, C. albicans and S. cerevisiae spores and GAL-GAL sensitized latex. In non complicated UI, the presence of ADH is the main invasion mechanism for E. coli. The frequency of adherent strains is very high (569/648) in acute cases (207/247 cystitis + 69/98 recurrent cystitis + 108/114 pyelonephritis + 140/154 prostatitis + 28/35 orchyepidimitis and scarce (14/184) in asymptomatic or chronic cases (6/107 bacteriurias + 7/67 prostatitis + 1/10 orchyepidimitis). A close relationship is established between the presence of ADH and clinical symptoms. The acute cases with general symptoms are caused in 85% of cases (188/216) by strains with ADH type MR specially subtype P. The acute cases with local symptoms (only urinary syndrome) are caused in 77% of cases (297/387) by strains with ADH type Ms. In complicated UI the expression of adhesion proteins does not constitute and essential requisite in order to invade the urinary tract. It is suggested that males are significantly more resistant the females to UI both parenchymal and urinary tract. It is deduced that underlying factors are more predisposing to UI the smaller the adherence rate of isolated strains is. Thus, reflux and neurogenic bladder probes are by far more aggressive alterations than prostatic adenoma, bladder tumor and lithiasis.
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PMID:[The role of E. coli adhesins in the pathogenesis of urinary infection]. 168 74

E. coli cause greater than 90% of urinary tract infections (UTI) in childhood. The capacity to adhere to urinary tract epithelial cells characterizes E. coli strains that cause acute pyelonephritis. Galactose alpha 1-4Galactose beta is the minimal receptor for adhering uropathogenic E. coli. Gal alpha 1-4Gal beta-binding bacteria caused significantly higher body temperature, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), pyuria, and lower renal concentrating capacity than E. coli lacking this specificity. The binding bacteria thus appeared to be more potent inducers of acute inflammation. Since inflammation may lead to tissue damage, we examined the relationship of infection with Gal alpha 1-4Gal beta-positive bacteria to renal scarring. The frequency of renal scarring was 5% in boys with Gal alpha 1-4Gal beta-positive and 40% in boys with Gal alpha 1-4Gal beta-negative E. coli. Analysis of binding capacity with the help of a newly developed latex agglutination assay can thus be used as an effective predictor of risk for renal scarring.
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PMID:Bacterial attachment, inflammation and renal scarring in urinary tract infection. 181 92

Escherichia coli (E. coli) causes greater than 90% of urinary tract infections, UTI, in childhood. The capacity to adhere to urinary tract epithelial cells characterizes E. coli strains that cause acute pyelonephritis. Adherence of uropathogenic E. coli is the result of a specific interaction between bacterial adhesins and glycolipid receptors on the host cells, especially the globoseries of glycolipids which share the Galactose alpha 1-greater than 4Galactose beta disaccharide (Gal alpha 1-greater than 4Gal beta). In childhood UTI, Gal alpha 1-greater than 4Gal beta-binding bacteria caused significantly higher body temperature, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and pyuria, and lower renal concentrating capacity, than E. coli lacking this specificity. The Gal alpha 1-greater than 4Gal beta-binding bacteria thus appeared to be more potent inducers of inflammation than other strains. Since inflammation may lead to tissue damage we examined the relationship of infection with Gal alpha 1-greater than 4Gal beta-positive bacteria to renal scarring. The frequency of renal scarring was 5% in boys with Gal alpha 1-greater than 4Gal beta-positive and 40% in boys with Gal alpha 1-greater than 4Gal beta-negative E. coli. Bacterial binding to Gal alpha 1-greater than 4Gal beta can be detected with a commercially available test reagent. This reagent can thus be used as an effective predictor of risk for renal scarring. Interleukin-6 (IL-6) is a pyrogen and inducer of the acute phase reactants. It was shown to be produced locally in the urinary tract, in response to UTI, and to spread systemically. Mucosal challenge with dead bacteria was sufficient to induce the IL-6 response. Circulating IL-6, and/or IL-1 and tumor necrosis factor could explain the fever, as well as increased ESR and CRP found in association with acute symptomatic UTI.
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PMID:Bacterial adherence as a virulence factor in urinary tract infection. 228 1