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Aspergillus fumigatus is a major airborne nosocomial pathogen that is responsible for severe mycosis in immunocompromised patients. We studied the efficacy of an innovative mobile air-treatment device in eliminating A. fumigatus from the air following experimental massive contamination in a high-security room. Viable mycological particles were isolated from sequential air samples in order to evaluate the device's effectiveness in removing the fungus. The concentration of airborne conidia was reduced by 95% in 18 min. Contamination was reduced below the detection threshold in 29 min, even when the machine was at the lowest airflow setting. In contrast, during spontaneous settling with no air treatment, conidia remained airborne for more than 1 h. This indoor air contamination model provided consistent and reproducible results. Because the air purifier proved to be effective at eliminating a major contaminant, it may prove useful in preventing air-transmitted disease agents. In an experimental space mimicking a hospital room, the AirLyse air purifier, which uses a combination of germicidal ultraviolet C irradiation and titanium photocatalysis, effectively eliminated Aspergillus conidia. Such a mobile device may be useful in routine practice for lowering microbiological air contamination in the rooms of patients at risk.

We investigated human immunodeficiency virus (HIV) type 1 RNA, proviral DNA, and antiretroviral drug-resistant variants in cervicovaginal secretions of HIV-1-infected women receiving antiretroviral therapy. The prevalence of detectable HIV-1 RNA in genital secretions was inversely related to the number of antiretroviral drugs taken by the patients. Proviral DNA was detected in approximately half of all samples of cervicovaginal secretions from HIV-1-infected women, regardless of the presence or absence of HIV-1 RNA in cervicovaginal secretions and of the antiretroviral regimen. In cervicovaginal secretions of most women with persisting genital viral replication, HIV variants exhibiting mutations associated with drug resistance against protease and reverse-transcriptase pol genes were found. Our observations indicate that antiretroviral therapy is not effective in purging the female genital tract of cell-associated provirus and that antiretroviral drugs that penetrate the female genital tract at suboptimal concentrations exert a potent selective pressure on genital HIV variants when local replication of free HIV-1 RNA persists.

International audience; Care-related infections are a major public health concern. Their transmission can be associated with environmental factors. This study looks at air contamination around 45 patients colonized with multidrug-resistant organisms (MDROs). We found that 30 hospital rooms (67%) were contaminated with MDRO species and 10 rooms (22%) were contaminated with at least 1 MDRO.

Objective. We investigated the relationship between human immunodeficiency virus (HIV) phenotypic susceptibility to didanosine and the antiviral activity of didanosine (ddI) in the JAGUAR study. Methods. Baseline plasma HIV phenotypic susceptibility to ddI was assessed using a phenotype assay of patients randomized to receive ddI or placebo for 4 weeks in addition to their current regimen. Phenotypic susceptibility scores (PSSs) were then calculated for each sample. Associations between PSS and week 4 reductions in plasma HIV-1 RNA load or virologic response were assessed using linear regression and Jonckherre’s test and the Wilcoxon and Cochran-Armitage tests, respectively. Results. In the ddI arm, a significant association between reduction in viral load and continuous PSS was observed ( ). Using distinct categories, an increasing fold change (FC) in susceptibility to ddI was strongly P ! .0001 associated with smaller reductions in plasma HIV-1 RNA load ( ). The proportion of virologic responders P ! .0001 was 83% (15/18) for patients with a ddI FC 1.3, 50% (33/66) for patients with an FC of 1.3‐2.2, and 29% (4/ 14) for patients with an FC 2.2 ( ). After we determined these findings, 3 ddI FC categories were P p .0008 defined using 1.3 and 2.2 as thresholds. Conclusions. The relationship between phenotypic susceptibility to ddI and reduction in plasma HIV-1 RNA load describes a continuum. The establishment of a lower clinical cutoff at 1.3 and an upper clinical cutoff at 2.2 are clinically relevant.