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Accurate exposure assessments are needed to evaluate health hazards caused by airborne microorganisms and require air samplers that efficiently capture representative samples. This highlights the need for samplers with well-defined performance characteristics. While generic aerosol performance measurements are fundamental to evaluate/compare samplers, the added complexity caused by the diversity of microorganisms, especially in combination with cultivation-based analysis methods, may render such measurements inadequate to assess suitability for bioaerosols. Specific performance measurements that take into account the end-toend sampling process, targeted bioaerosol and analysis method could help guide selection of air samplers.Nine different samplers (impactors/impingers/cyclones/ electrostatic precipitators/filtration samplers) were subjected to comparative performance testing in this work. Their end-to-end cultivation-based biological sampling efficiencies (BSEs) and PCR-/microscopy-based physical sampling efficiencies (PSEs) relative to a reference sampler (BioSampler) were determined for gram-negative and gram-positive vegetative bacteria, bacterial spores, and viruses.Significant differences were revealed among the samplers and shown to depend on the bioaerosol's stress-sensitivity and particle size. Samplers employing dry collection had lower BSEs for stresssensitive bioaerosols than wet collection methods, while nonfilterbased samplers showed reduced PSEs for 1 μm compared to 4 μm bioaerosols. Several samplers were shown to underestimate bioaerosol concentration levels relative to the BioSampler due to having lower sampling efficiencies, although they generally obtained samples that were more concentrated due to having higher concentration factors.Our work may help increase user awareness about important performance criteria for bioaerosol sampling, which could contribute to methodological harmonization/standardization and result in more reliable exposure assessments for airborne pathogens and other bioaerosols of interest.

Recently, it was shown that a cellulose-negative mutant (Cell) ofAcetobacterxylinum ATCC 23769 carried an insertion of an indigenous transposable element (IS1031A) about 500 bp upstream of the bcs operon, required for cellulose synthesis. Here we show that Cell can be complemented by wild-type DNA covering the insertion point. Nucleotide sequencing of this region revealed the presence of two open reading frames, ORF1 and ORF2. ORF2, which is disrupted by the IS1031A insertion in Cell, potentially encodes the complementing function. ORF1 encodes a protein (CMCax) with significant homology to previously described endoglucanases. A cloned DNA fragment containing ORF1 expressed a carboxymethyl cellulose-hydrolyzing activity in Escherichia coli. In A. xylinum, CMCax is secreted into the culture growth medium. The CMCax mature protein consists of 322 amino acids and has a molecular mass of 35.6 kDa.

X-linked neutropenia (XLN, OMIM #300299) is a rare form of severe congenital neutropenia. It was originally described in a three-generation family with 5 affected members and with an L270P mutation in the GTP-ase binding domain (GBD) of the Wiskott-Aldrich-syndrome protein (WASP) (Devriendt, et al 2001). Here, we report and describe a large three-generation family with XLN, with 10 affected males and 8 female carriers. A c.882T>C WAS gene mutation was identified, resulting in an I294T mutation. The infectious course is variable and mild in view of the deep neutropenia. In addition to the original description, low-normal IgA levels, low to low-normal platelet counts and reduced NK-cell counts also appear as consistent XLN features. However, inverted CD4/CD8 ratios were not found in this family, nor were cases identified with myelodysplastic syndrome or acute myeloid leukaemia. Female carriers exhibited a variable attenuated phenotype. Like L270P WASP, I294T WASP is constitutively active towards actin polymerisation In conclusion, this largest XLN kindred identified to date provides new independent genetic evidence that mutations disrupting the auto-inhibitory GBD of WASP are the cause of XLN. Reduced NK cells, low to low normal platelet counts and low to low-normal IgA levels are also features of XLN.