The oral cavity harbors hundreds of microbial species that are present either as planktonic cells, or incorporated into biofilms. The majority of the oral microbes are commensal organisms. Those that are pathogenic microbes can result in oral infections, and at times initiate systemic diseases. Biofilms that contain pathogens have been challenging to control. Many conventional antimicrobials have proven to be ineffective. Recent advances in science and technology are providing new approaches for pathogen control and containment and methods to characterize biofilms. This perspective provides: 1) A general understanding of biofilm development; 2) A description of emerging chemical and biological methods to control oral biofilms; 3) An overview of high-throughput analytical approaches to analyze biofilms.

Biofilm formation on catheters is thought to contribute to persistence of catheter-associated urinary tract infections (CAUTI), which represent the most frequent nosocomial infections. Knowledge of genetic factors for catheter colonization is limited, since their role has not been assessed using physicochemical conditions prevailing in a catheterized human bladder. The current study aimed to combine data from a dynamic catheterized bladder model in vitro with in vivo expression analysis for understanding molecular factors relevant for CAUTI caused by Escherichia coli. By application of the in vitro model that mirrors the physicochemical environment during human infection, we found that an E. coli K-12 mutant defective in type 1 fimbriae, but not isogenic mutants lacking flagella or antigen 43, was outcompeted by the wild-type strain during prolonged catheter colonization. The importance of type 1 fimbriae for catheter colonization was verified using a fimA mutant of uropathogenic E. coli strain CFT073 with human and artificial urine. Orientation of the invertible element (IE) controlling type 1 fimbrial expression in bacterial populations harvested from the colonized catheterized bladder in vitro suggested that the vast majority of catheter-colonizing cells (up to 88%) express type 1 fimbriae. Analysis of IE orientation in E. coli populations harvested from patient catheters revealed that a median level of ϳ73% of cells from nine samples have switched on type 1 fimbrial expression. This study supports the utility of the dynamic catheterized bladder model for analyzing catheter colonization factors and highlights a role for type 1 fimbriae during CAUTI.

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The role played by hemostasis in the pathogenesis of ischemic stroke is still controversial. In the present study, we looked for a possible association of ischemic stroke and high clotting activity of factor II (FII:C), factor V (FV:C), factor VII (FVII:C), factor X (FX:C) and fibrinogen. We investigated 157 non-anti-coagulated patients (86 males, 71 females; median age 41 y, range 16-73 ), who had survived ischemic stroke for at least 2 months, and 193 healthy controls with similar age and sex distribution (104 males, 89 females; median age 39 y, range 19-74). Patients showed significantly higher body mass index, as well as significantly higher prevalence of arterial hypertension, smoking and hyperlipidemia. FV:C (p = 0.05), FX:C (p = 0.04) and fibrinogen (p = 0.05) were higher in patients as compared to controls. In a univariate risk analysis FX:C and FV:C were associated with the relative risk for ischemic stroke showing an odds ratio (OR) of up to 2.8 (95% CI: 1.05-7.6) and 3.4 (95%CI: 1.4-7.9), respectively, for levels above 130%. In a multivariate analysis using a logistic regression model including age, sex, arterial hypertension, smoking habit, diabetes, hyperlipidemia, BMI and the coagulation factors, FV:C was still found to significantly (p=0.03) add to the risk of ischemic stroke. An increase of factor FV:C by 10% was associated with an increase in the relative risk of 19% (95% CI.: 2%-38%). In conclusion, we found a high plasma level of FV:C to be a prevalent (FV:C > 130% in 20/157 patients) and independent risk factor for ischemic stroke.