A strain of C. difficile that was resistant to fluoroquinolones and had binary toxin and a partial deletion of the tcdC gene was responsible for this outbreak of C. difficile-associated diarrhea. Exposure to fluoroquinolones or cephalosporins was a risk factor.

In this study, health care-associated C. difficile infection and colonization were differentially associated with defined host and pathogen variables. The NAP1 strain was predominant among patients with C. difficile infection, whereas asymptomatic patients were more likely to be colonized with other strains. (Funded by the Consortium de Recherche sur le Clostridium difficile.).

This study helped to quantify the impact of strain NAP1 on the incidence and severity of C. difficile-associated disease in Québec in 2005. The identification of the geographic dissemination of this predominant strain may help to focus regional infection-control efforts.

Résumé Les auteurs exposent les composantes d'un modèle de recherche collaborative lié à une certaine façon de faire de la recherche «avec» plutôt que «sur» les praticiens. C'est sous l'angle de la double fonction de recherche et de formation, à concilier dans la démarche collaborative, que leur modèle est abordé. Le texte situe historiquement l'émergence de l'idée de collaboration de recherche en éducation et présente les trois facettes complémentaires du modèle: a) une définition conceptuelle du modèle conduit à préciser le sens donné aux notions de recherche et de formation; b) le modèle est illustré par une description de cinq projets différents basés sur une démarche collaborative commune; c) une lecture transversale des cinq projets conduit à discuter des composantes du modèle.

Since 2002, an epidemic of Clostridium difficile infections has occurred in southern Quebec, Canada. At Hôpital Maisonneuve-Rosemont, Montreal, Quebec, Canada, the incidence of C. difficile infections increased from 11/1,000 admissions (1999 to 2002) to 27/1,000 admissions (2003 to 2005). We compared the exposures and outcomes for patients infected with strains with different ribopatterns isolated before (n ‫؍‬ 55) and during (n ‫؍‬ 175) the epidemic, as well as the in vitro activities of antibiotics against those isolates. During the preepidemic period, 46 isolates (84%) were of ribotype 001, 1 was of ribotype 027, and 8 were of other ribopattern types. During the epidemic period, ribotype 027 strains accounted for 140 (80%) isolates; 26 (15%) were of ribotype 001, and 7 were of other ribopattern types. Ribotype 027 strains were highly resistant to fluoroquinolones (FQs) but were susceptible to clindamycin. A pattern of prior specific antibiotic exposure that selected for antibiotic-resistant ribotype C. difficile infections was observed for FQs (ribotype 027) and clindamycin (ribotype 001). The rate of mortality was higher among older patients, those with a high Charlson comorbidity index, and those with longer previous hospitalizations. By multivariate analysis, patients infected with ribotype 027 were twice as likely to die within 30 days of diagnosis than patients infected with other ribotypes (adjusted odds ratio, 2.06; 95% confidence interval, 1.00 to 4.22). The observations from this study support the notion that continued selective antibiotic pressure resulted in the superimposition of the hypertoxigenic ribotype 027 clone on top of the prior dominant ribotype 001 clone in a setting of preexisting high endemicity, thus leading to the high rates of morbidity and mortality seen in the Quebec outbreak. Stringent antibiotic stewardship measures, combined with aggressive infection control, are required to curtail the epidemic of C. difficile infections.

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The levels of S-adenosylmethionine (AdoMet) and of S-adenosylhomocysteine (AdoHcy) as well as the ratio of AdoMet/AdoHcy were determined in the liver, lungs, testes and kidneys of weanling male rats fed a commercial chow diet or 5 different amino acid-defined diets for 1-5 weeks. The amino acid-defined diets used were as follows: diet 1, supplemented with methionine, choline, folic acid and vitamin B12; diet 2, deficient in methionine and choline; diet 3, deficient in methionine alone; diet 4, deficient in choline alone; diet 5, deficient in methionine, choline, folic acid and vitamin B12. All methionine-deficient diets were supplemented with an equimolar dose of its metabolic precursor, homocystine. The animals were sacrificed after 1, 3 and 5 weeks of treatment. In animals fed either the chow diet or diet 1, liver was the organ found to contain the highest levels of AdoMet and AdoHcy. Similarly, in animals fed diet 1 or chow, the testes and lungs contained the lowest level of AdoMet, while the lungs contained the lowest levels of AdoHcy. In general, the tissue levels of AdoHcy and AdoMet in rats fed diet 1 were very similar to the corresponding values found in chow-fed rats. Diet 1 feeding, however, led to higher hepatic levels of AdoMet than did the administration of the chow diet. The administration of the methyl-deficient diets generally led to decreased hepatic AdoMet contents at 3 and 5 weeks; the methyl-deficient diets also led to increased AdoHcy contents and decreased AdoMet:AdoHcy ratios when compared with diet 1. Linear regression analysis showed a significant direct correlation between the observed hepatic AdoMet levels and the methyl content of the diet as well as an inverse correlation between hepatic AdoHcy levels and dietary methyl contents. Unlike liver, the lung and testes did not show any decrease in AdoMet content following feeding of the methyl-deficient diets. These tissues did show, however, early significant increases in AdoHcy contents and corresponding decreases in the ratios of AdoMet:AdoHcy. These changes were found to be proportional to the dietary methyl content. The renal contents of AdoMet, AdoHcy and the ratio of AdoMet/AdoHcy were unaffected by any of the diets administered except for diet 5. The administration of diet 5 to rats for 5 weeks led to a significant increase in renal AdoHcy. These results provide evidence indicating that dietary methyl insufficiency may exert its role in carcinogenesis through a decreased availability of AdoMet in vivo.

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