Impairment of the bacterial biofilm stability by triclosan

The accumulation of the widely-used antibacterial and antifungal compound triclosan (TCS) in freshwaters raises concerns about the impact of this harmful chemical on the biofilms that are the dominant life style of microorganisms in aquatic systems. However, investigations to-date rarely go beyond effects at the cellular, physiological or morphological level. The present paper focuses on bacterial biofilms addressing the possible chemical impairment of their functionality, while also examining their substratum stabilization potential as one example of an important ecosystem service. The development of a bacterial assemblage of natural composition – isolated from sediments of the Eden Estuary (Scotland, UK) – on non-cohesive glass beads (<63 µm) and exposed to a range of triclosan concentrations (control, 2 – 100 µg L−1) was monitored over time by Magnetic Particle Induction (MagPI). In parallel, bacterial cell numbers, division rate, community composition (DGGE) and EPS (extracellular polymeric substances: carbohydrates and proteins) secretion were determined. While the triclosan exposure did not prevent bacterial settlement, biofilm development was increasingly inhibited by increasing TCS levels. The surface binding capacity (MagPI) of the assemblages was positively correlated to the microbial secreted EPS matrix. The EPS concentrations and composition (quantity and quality) were closely linked to bacterial growth, which was affected by enhanced TCS exposure. Furthermore, TCS induced significant changes in bacterial community composition as well as a significant decrease in bacterial diversity. The impairment of the stabilization potential of bacterial biofilm under even low, environmentally relevant TCS levels is of concern since the resistance of sediments to erosive forces has large implications for the dynamics of sediments and associated pollutant dispersal. In addition, the surface adhesive capacity of the biofilm acts as a sensitive measure of ecosystem effects.Publisher PDFPeer reviewe

Mycobacterial and nonbacterial pulmonary complications in hospitalized patients with human immunodeficiency virus infection: A prospective, cohort study

<p>Abstract</p> <p>Background</p> <p>A prospective observational study was done to describe nonbacterial pulmonary complications in hospitalized patients with human immunodeficiency virus (HIV) infection.</p> <p>Methods</p> <p>The study included 1,225 consecutive hospital admissions of 599 HIV-infected patients treated from April 1995 through March 1998. Data included demographics, risk factors for HIV infection, Acute Physiology and Chronic Health Evaluation (APACHE) II score, pulmonary complications, CD4⁺ lymphocyte count, hospital stay and case-fatality rate.</p> <p>Results</p> <p>Patient age (mean ± SD) was 38.2 ± 8.9 years, 62% were men, and 84% were African American. The median APACHE II score was 14, and median CD4⁺ lymphocyte count was 60/μL. Pulmonary complications were <it>Pneumocystis carinii</it> pneumonia (85) in 78 patients, <it>Mycobacterium avium</it> complex (51) in 38, <it>Mycobacterium tuberculosis</it> (40) in 35, <it>Mycobacterium gordonae</it> (11) in 11, <it>Mycobacterium kansasii</it> (10) in 9, <it>Cytomegalovirus</it> (10) in 10, <it>Nocardia asteroides</it> (3) in 3, fungus ball (2) in 2, respiratory syncytial virus (1), herpes simplex virus (1), <it>Histoplasma capsulatum</it> (1), lymphoma (3) in 3, bronchogenic carcinoma (2) in 2, and Kaposi sarcoma (1). The case-fatality rate of patients was 11% with <it>Pneumocystis carinii</it> pneumonia; 5%, <it>Mycobacterium tuberculosis</it>; 6%, <it>Mycobacterium avium</it> complex; and 7%, noninfectious pulmonary complications.</p> <p>Conclusion</p> <p>Most pulmonary complications in hospitalized patients with HIV are from <it>Pneumocystis</it> and mycobacterial infection.</p