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  • 1
    Online Resource
    Online Resource
    Variability in DPA and Calcium Content in the Spores of Clostridium Species
    Frontiers Media SA ; 2016
    In:  Frontiers in Microbiology Vol. 7 ( 2016-11-11)
    Details
    In: Frontiers in Microbiology, Frontiers Media SA, Vol. 7 ( 2016-11-11)
    Type of Medium: Online Resource
    ISSN: 1664-302X
    URL: Article
    DOI: 10.3389/fmicb.2016.01791
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2016
    detail.hit.zdb_id: 2587354-4
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  • 2
    Online Resource
    Online Resource
    Impact of iron reduction on the metabolism of Clostridium acetobutylicum
    Wiley ; 2019
    In:  Environmental Microbiology Vol. 21, No. 10 ( 2019-10), p. 3548-3563
    Details
    In: Environmental Microbiology, Wiley, Vol. 21, No. 10 ( 2019-10), p. 3548-3563
    Abstract: Iron is essential for most living organisms. In addition, its biogeochemical cycling influences important processes in the geosphere (e.g., the mobilization or immobilization of trace elements and contaminants). The reduction of Fe(III) to Fe(II) can be catalysed microbially, particularly by metal‐respiring bacteria utilizing Fe(III) as a terminal electron acceptor. Furthermore, Gram‐positive fermentative iron reducers are known to reduce Fe(III) by using it as a sink for excess reducing equivalents, as a form of enhanced fermentation. Here, we use the Gram‐positive fermentative bacterium Clostridium acetobutylicum as a model system due to its ability to reduce heavy metals. We investigated the reduction of soluble and solid iron during fermentation. We found that exogenous (resazurin, resorufin, anthraquinone‐2,6‐disulfonate) as well as endogenous (riboflavin) electron mediators enhance solid iron reduction. In addition, iron reduction buffers the pH, and elicits a shift in the carbon and electron flow to less reduced products relative to fermentation. This study underscores the role fermentative bacteria can play in iron cycling and provides insights into the metabolic profile of coupled fermentation and iron reduction with laboratory experiments and metabolic network modelling.
    Type of Medium: Online Resource
    ISSN: 1462-2912 , 1462-2920
    URL: Issue
    URL: Article
    DOI: 10.1111/emi.v21.10
    DOI: 10.1111/1462-2920.14640
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2020213-1
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Evaluation of SARS‐CoV‐2 antibody levels on hospital admission as a correlate of protection against mortality
    Wiley ; 2023
    In:  Journal of Internal Medicine Vol. 293, No. 6 ( 2023-06), p. 694-703
    Details
    In: Journal of Internal Medicine, Wiley, Vol. 293, No. 6 ( 2023-06), p. 694-703
    Abstract: Millions of people have now been vaccinated against severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). However, it is still unclear which antibody levels provide protection against mortality. It is further unknown whether measuring antibody concentrations on hospital admission allows for identifying patients with a high risk of mortality. Objectives To evaluate whether anti‐SARS‐CoV2‐spike antibodies on hospital admission predict in‐hospital mortality in patients with coronavirus disease 2019. Methods We conducted a prospective, multicentre cohort study on 1152 hospitalized patients who tested positive for SARS‐CoV‐2 with a polymerase chain reaction–based assay. Patients were classified by vaccination status. Anti‐SARS‐CoV‐2 spike antibodies were determined on hospital admission. The investigated end point was in‐hospital mortality for any cause. Results Spike antibodies on hospital admission were significantly lower in non‐survivors in both non‐vaccinated (73 U/ml, 95%CI 0–164 vs. 175 U/ml, 95%CI 124–235, p  = 0.002) and vaccinated patients (1056 U/ml, 95%CI 701–1411 vs. 1668 U/ml, 95%CI 1580–1757, p   〈  0.001). Further, spike antibodies were significantly lower in fully vaccinated and boostered patients who died compared to those who survived (mean 883 U/ml, 95%CI 406–1359 vs. 1292 U/ml, 95%CI 1152–1431, p  = 0.017 and 1485 U/ml, 95%CI 836–2133 vs. 2050 U/ml, 95%CI 1952–2149, p  = 0.036). Patients infected with the currently prevailing Omicron variant were three times more likely to die if spike antibodies were 〈 1200 U/ml (OR 3.458, 95%CI 1.562–7.656, p  = 0.001). After adjusting for potential confounders, this value increased to an aOR of 4.079 (95%CI 1.809–9.198, p   〈  0.001). Conclusion Anti‐SARS‐CoV2 spike‐antibody levels on hospital admission are inversely associated with in‐hospital mortality. Hospitalized patients with lower antibody levels have a higher risk of mortality.
    Type of Medium: Online Resource
    ISSN: 0954-6820 , 1365-2796
    URL: Issue
    URL: Article
    DOI: 10.1111/joim.v293.6
    DOI: 10.1111/joim.13606
    RVK:
    XA 54380
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2006883-9
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  • 4
    Online Resource
    Online Resource
    Genes Activated by Vibrio cholerae upon Exposure to Caenorhabditis elegans Reveal the Mannose-Sensitive Hemagglutinin To Be Essential for Colonization
    American Society for Microbiology ; 2018
    In:  mSphere Vol. 3, No. 3 ( 2018-06-27)
    Details
    In: mSphere, American Society for Microbiology, Vol. 3, No. 3 ( 2018-06-27)
    Abstract: During its life cycle, the facultative human pathogen Vibrio cholerae , which is the causative agent of the diarrheal disease cholera, needs to adapt to a variety of different conditions, such as the human host or the aquatic environment. Importantly, cholera infections originate from the aquatic reservoir where V. cholerae persists between the outbreaks. In the aquatic environment, bacteria are constantly threatened by predatory protozoa and nematodes, but our knowledge of the response pathways and adaptation strategies of V. cholerae to such stressors is limited. Using a temporally controlled reporter system of transcription, we identified more than 100 genes of V. cholerae induced upon exposure to the nematode Caenorhabditis elegans , which emerged recently as a valuable model for environmental predation during the aquatic lifestyle of V. cholerae . Besides others, we identified and validated the genes encoding the mannose-sensitive hemagglutinin (MSHA) type IV pilus to be significantly induced upon exposure to the nematode. Subsequent analyses demonstrated that the mannose-sensitive hemagglutinin is crucial for attachment of V. cholerae in the pharynx of the worm and initiation of colonization, which results in growth retardation and developmental delay of C. elegans . Thus, the surface adhesion factor MSHA could be linked to a fitness advantage of V. cholerae upon contact with bacterium-grazing nematodes. IMPORTANCE The waterborne diarrheal disease cholera is caused by the bacterium Vibrio cholerae . The facultative human pathogen persists as a natural inhabitant in the aquatic ecosystem between outbreaks. In contrast to the human host, V. cholerae requires a different set of genes to survive in this hostile environment. For example, predatory micrograzers are commonly found in the aquatic environment and use bacteria as a nutrient source, but knowledge of the interaction between bacterivorous grazers and V. cholerae is limited. In this study, we successfully adapted a genetic reporter technology and identified more than 100 genes activated by V. cholerae upon exposure to the bacterium-grazing nematode Caenorhabditis elegans . This screen provides a first glimpse into responses and adaptational strategies of the bacterial pathogen against such natural predators. Subsequent phenotypic characterization revealed the mannose-sensitive hemagglutinin to be crucial for colonization of the worm, which causes developmental delay and growth retardation.
    Type of Medium: Online Resource
    ISSN: 2379-5042
    URL: Article
    DOI: 10.1128/mSphereDirect.00238-18
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2018
    detail.hit.zdb_id: 2844248-9
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