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A six-month outbreak of Clostridium difficile infection among elderly residents of a middle-term-care facility was investigated. Pulsed-field gel electrophoresis was used to genotype 22 outbreak strains and 30 epidemiologically unrelated strains. A prospective case-control study was conducted to identify risk factors for epidemic Clostridium difficile-associated diarrhea. All epidemiologically unrelated Clostridium difficile strains of the same serogroup could be differentiated by their DNA patterns with two restriction enzymes ( Smal and Kspl). Among clustered strains, two epidemic serogroups (C and K) were identified. Two different DNA patterns were identified among serogroup C strains and three among serogroup K strains. Multivariate analysis showed that the risk of Clostridium difficile infection increased with antimicrobial chemotherapy (β-lactam agents and pristinamycin) and the presence of a feeding tube. This study confirms the high discriminative power of restriction fragment length polymorphism analysis by pulsed-field gel electrophoresis to describe Clostridium difficile epidemiology. The typing results confirm that infection was principally exogenous in this outbreak. Furthermore, they indicate the need to improve all measures limiting transmission of infection. [ABSTRACT FROM AUTHOR]

It is a well known fact that aminoglycosides increase urinary action of N-acetyl-beta-D-glucosaminidase (NAG) but the significance of this fact remains, as yet, nuclear. The aim of this study is firstly to attempt to form an explanation of the enzymatic effects of aminoglycosides by studying the excretion of A, B, I isoenzymes and by calculating the ratio A/B + I during gentamicin, tobramycin and amikacin therapy and secondly, by using this method, to try to propose a marker for evaluating nephrotoxicity. Our results indicate that all three antibiotics induce an increase in the excretion of the A-form, which is present freely in the lysosomes and in physiological urines, but that only gentamicin and tobramycin bring about an increase in the B-form associated with the lysosomal membrane. Since excretion of the B-form is associated with renal failure, it can be proposed as a good marker for evaluating nephrotoxicity. These observations allow us to advance the hypothesis that aminoglycosides determine an enzymatic inducing effect on the NAG synthesis with urinary excretion of the A-form by exocytosis whilst the excretion of the B-form, associated with the lysosomal membrane, would result from a rupture of this membrane. This lesion would bring about an excretion of toxic aminoside into the cytoplasm, causing damage to the mitochondrial apparatus. On the other hand isoenzymatic profiles, observed during cephalosporin treatment suggest a process of cellular necrosis.

88 patients (aged 55-96 years) with severe infections were treated during ten days with one of four different aminoglycosides: gentamicin, dibekacin, netilmicin (3 mg/kg/day) or amikacin (15 mg/kg/day). Creatinine clearance and urinary N-acetyl-glucosaminidase (NAG) activity were measured daily. In addition, NAG isoenzyme patterns were determined on the day of maximal urinary NAG excretion. Aminoglycoside-induced acute renal failure was more prevalent in the gentamicin group (42.8%) than in the dibekacin, netilmicin or amikacin groups (42.8%, 5.5% and 0% respectively). No relationship was found between total urinary NAG activity and nephrotoxic risk. Conversely, significantly elevated levels (p less than 0.001) of B isoenzyme were detected in the gentamicin group, whereas the highest A and I isoenzyme levels were found in the dibekacin and netilmicin groups. These results suggest that functional enzymuria with preferential urinary excretion of A and I isoenzymes should be distinguished from lesional enzymuria with preferential urinary excretion of the B isoenzyme. According to our data, the NAG-B isoenzyme may possibly be a specific marker of aminoglycoside nephrotoxicity.

A series of 9 cases of systemic affections associated with positive serology for yersinia pseudotuberculosis is reported. The clinical presentation of four cases was classical reactive arthritis with or without erythema nodosa; in two cases the patients had sacroileitis or Reiter's syndrome. The other three patients had unusual presentations: one Löfgren's syndrome, one cutaneous leukocytoclasis vasculitis with polyarthritis and glomerulonephritis, and one rhizomelic pseudopolyarthritis. Four patients (45 p. 100) had a positive HLA B27 antigen. In the absence of absolute bacteriological proof of cause and effect the authors discuss the relationship between these syndromes and Yersinia pseudotuberculosis infection. Although a Yersinia infection has not been formally established as the cause, there is some indirect evidence pointing to the reality of systemic Yersinia pseudotuberculosis infection.