ArticleInfection and immunity2001
DsrA-deficient mutant of Haemophilus ducreyi is impaired in its ability to infect human volunteers.
Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
54 citing papers in PubMed, 72 citations in OpenAlex.
- A Class IInfection and immunity · 2019Trial
- Molecular pathogenesis ofMicrobiology and molecular biology reviews : MMBR · 2025Review
- Article
- Genes Differentially Expressed by Haemophilus ducreyi during Anaerobic Growth Significantly Overlap Those Differentially Expressed during Experimental Infection of Human Volunteers.Journal of bacteriology · 2022Article
- Interactions of the Skin PathogenFrontiers in immunology · 2020Review
- Article
- Defining Potential Vaccine Targets of Haemophilus ducreyi Trimeric Autotransporter Adhesin DsrA.Monoclonal antibodies in immunodiagnosis and immunotherapy · 2015Article
- Molecular phylogenetic analysis of non-sexually transmitted strains of Haemophilus ducreyi.PloS one · 2015Article
- Article
- Outer membrane protein P4 is not required for virulence in the human challenge model of Haemophilus ducreyi infection.BMC microbiology · 2014Article
- Trimeric autotransporter DsrA is a major mediator of fibrinogen binding in Haemophilus ducreyi.Infection and immunity · 2013Article
- The Haemophilus ducreyi Fis protein is involved in controlling expression of the lspB-lspA2 operon and other virulence factors.Infection and immunity · 2013Article
- Safety and immunological outcomes following human inoculation with nontypeable Haemophilus influenzae.The Journal of infectious diseases · 2013Article
- Sialylation of lipooligosaccharides is dispensable for the virulence of Haemophilus ducreyi in humans.Infection and immunity · 2012Article
- A Haemophilus ducreyi CpxR deletion mutant is virulent in human volunteers.The Journal of infectious diseases · 2011Article
- Characterization of the CpxRA regulon in Haemophilus ducreyi.Infection and immunity · 2010Article
- Activation of the CpxRA system by deletion of cpxA impairs the ability of Haemophilus ducreyi to infect humans.Infection and immunity · 2010Article
- Role played by CD4+FOXP3+ regulatory T Cells in suppression of host responses to Haemophilus ducreyi during experimental infection of human volunteers.The Journal of infectious diseases · 2010Article
- Host-pathogen interplay of Haemophilus ducreyi.Current opinion in infectious diseases · 2010Review
- Inactivation of the Haemophilus ducreyi luxS gene affects the virulence of this pathogen in human subjects.The Journal of infectious diseases · 2009Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Haemophilus ducreyi produces an outer membrane protein called DsrA, which is required for serum resistance. An isogenic dsrA mutant, FX517, was constructed previously in H. ducreyi 35000. Compared to its parent, FX517 cannot survive in normal human serum. When complemented in trans with a plasmid containing dsrA, FX517 is converted to a serum-resistant phenotype (C. Elkins, K. J. Morrow, Jr., and B. Olsen, Infect. Immun. 68:1608-1619, 2000). To test whether dsrA was transcribed in vivo, we successfully amplified transcripts in five biopsies obtained from four experimentally infected human subjects. To test whether DsrA was required for virulence, six volunteers were experimentally infected with 35000 and FX517 and observed for papule and pustule formation. Each subject was inoculated with two doses (70 to 80 CFU) of live 35000 and 1 dose of heat-killed bacteria on one arm and with three doses (ranging from 35 to 800 CFU) of live FX517 on the other arm. Papules developed at similar rates at sites inoculated with the mutant or parent. However, mutant papule surface areas were significantly smaller than parent papules. The pustule formation rate was 58% (95% confidence interval [CI] of 28 to 85%) at 12 parent sites, and 0% (95% CI of 0 to 15%) at 18 mutant sites (P = 0.0004). Although biosafety regulations precluded our testing the complemented mutant in humans, these results suggest that expression of DsrA facilitates the ability of H. ducreyi to progress to the pustular stage of disease.
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