Evaluation of an Isogenic Hemolysin-Deficient Mutant in the Human Model of Haemophilus ducreyi Infection

• Published in: The Journal of infectious diseases Vol. 178; no. 1; pp. 191 - 199
• Main Authors: Palmer, K. L., Thornton, A. C., Fortney, K. R., Hood, A. F., Munson, R. S., Spinola, S. M.
• Format: Journal Article
• Language: English
• Published: Chicago, IL The University of Chicago Press 01.07.1998; University of Chicago Press; Oxford University Press
• Subjects: Adult; Bacteria; Bacterial diseases; Biological and medical sciences; Biopsies; Chancroid; Chancroid - microbiology; Chancroid - pathology; Dosage; Dose response relationship; Double-Blind Method; Experimental bacterial diseases and models; Female; Haemophilus ducreyi; Haemophilus ducreyi - classification; Haemophilus ducreyi - genetics; Haemophilus ducreyi - pathogenicity; Hemolysin proteins; Hemolysin Proteins - genetics; Hemolysin Proteins - physiology; Humans; Infections; Infectious diseases; Lesions; Major Articles; Male; Medical sciences; Mutagenesis; Phenotype; Toxins; Virulence; Human; Pathogenesis; Infection; Pasteurellaceae; Experimental disease; Sexually transmitted disease; Chancroid; Bacteriosis; Double blind study; Bacteria; Subcutaneous administration; Mutation; Hemolysin; Haemophilus ducreyi
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1086/515617

Haemophilus ducreyi causes the genital ulcerative disease chancroid. One putative virulence factor of H. ducreyi is a pore-forming hemolysin that displays toxicity against human fibroblasts and keratinocytes. In order to test the role of the hemolysin in pathogenesis, an isogenic hemolysin-deficient mutant was constructed, designated 35000HP-RSM1. The lipooligosaccharide, outer membrane protein patterns, and growth attributes of 35000HP-RSM1 were identical to its parent, 35000HP. Human subjects were challenged on the upper arm with the isogenic isolates in a double-blinded, randomized, escalating dose-response study. Pustules developed at a similar rate at sites inoculated with the mutant or parent. The cellular infiltrate and bacterial load in lesions were also similar. These results indicate the hemolysin does not play a role in pustule formation. Due to the limitations of this model, the role of the hemolysin at later stages of infection could not be determined.