ArticleInfection and immunity2006
A DltA mutant of Haemophilus ducreyi Is partially attenuated in its ability to cause pustules in human volunteers.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Molecular pathogenesis ofMicrobiology and molecular biology reviews : MMBR · 2025Review
- Article
- Interactions of the Skin PathogenFrontiers in immunology · 2020Review
- Article
- Outer membrane protein P4 is not required for virulence in the human challenge model of Haemophilus ducreyi infection.BMC microbiology · 2014Article
- Sialylation of lipooligosaccharides is dispensable for the virulence of Haemophilus ducreyi in humans.Infection and immunity · 2012Article
- Characterization of the CpxRA regulon in Haemophilus ducreyi.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
- Inactivation of the Haemophilus ducreyi luxS gene affects the virulence of this pathogen in human subjects.The Journal of infectious diseases · 2009Article
- Experimental infection of human volunteers with Haemophilus ducreyi: fifteen years of clinical data and experience.The Journal of infectious diseases · 2009Article
- A fibrinogen-binding lipoprotein contributes to the virulence of Haemophilus ducreyi in humans.The Journal of infectious diseases · 2009Article
- Haemophilus ducreyi LspA proteins are tyrosine phosphorylated by macrophage-encoded protein tyrosine kinases.Infection and immunity · 2008Article
- Outer membrane protein DsrA is the major fibronectin-binding determinant of Haemophilus ducreyi.Infection and immunity · 2008Article
- Identification of Haemophilus ducreyi genes expressed during human infection.Microbiology (Reading, England) · 2008Article
- Dysregulated immune profiles for skin and dendritic cells are associated with increased host susceptibility to Haemophilus ducreyi infection in human volunteers.Infection and immunity · 2007Article
- Haemophilus ducreyi partially activates human myeloid dendritic cells.Infection and immunity · 2007Article
- Experimental infection with Haemophilus ducreyi in persons who are infected with HIV does not cause local or augment systemic viral replication.The Journal of infectious diseases · 2007Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Haemophilus ducreyi produces two outer membrane proteins, called DltA (H. ducreyi lectin A) and DsrA (H. ducreyi serum resistance A), that contribute to the ability of the organism to evade complement-mediated serum killing. In contrast to their isogenic parent strain, 35000HP, the DsrA mutant FX517 exhibits 0% survival in 50% normal human serum and the DltA mutant FX533 exhibits 23% survival. Compared to 35000HP, FX517 does not cause pustule formation in human volunteers. To test whether DltA was required for virulence in humans, seven volunteers were experimentally infected with 35000HP and FX533. Four subjects were inoculated with fixed doses of 35000HP (101 CFU or 130 CFU) at three sites on one arm and escalating doses of FX533 (range, 46 CFU to 915 CFU) at three sites on the other arm. Pustules only developed at mutant-injected sites at doses nearly twofold higher than that of the parent, suggesting that FX533 was partially attenuated. Three subjects were inoculated with similar doses of the parent (67 CFU) and mutant (104 CFU) at three sites. Pustules formed at five of nine parent sites and one of nine mutant sites. Overall, the papule and pustule formation rates for 35000HP and FX533 were similar for the trial. However, for the five subjects who received similar doses of the parent and mutant, pustules developed at 7 of 15 sites (46.7%; 95% confidence interval [CI], 16.9% to 76.5%) inoculated with the parent and at 1 of 15 (6.7%; 95% CI, 0.1% to 18.4%) sites inoculated with the mutant (P = 0.043). We concluded that the DltA mutant was attenuated in its ability to cause disease at doses similar to that of the parent.
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