Disease relevance of Chancroid

• Most skin-infiltrating lymphocytes in allergic delayed-type hypersensitivity (DTH) and bacterial chancroid skin lesions express both CCR4 and CLA, but only about 10% express CCR10 [1].
• As part of our efforts to evaluate the role of sialic acid in the pathobiology of these organisms, we have initiated studies of the enzymes from Haemophilus ducreyi (the infectious agent of chancroid) responsible for the activation and attachment of sialic acid to the lipooligosaccharide [2].
• An investigation of genital ulcers in Jackson, Mississippi, with use of a multiplex polymerase chain reaction assay: high prevalence of chancroid and human immunodeficiency virus infection [3].
• Fleroxacin, as a single oral dose, is an effective treatment for culture-proven chancroid in patients who are HIV-1 seronegative [4].
• During the last 3 to 4 years, incidence rates of syphilis and chancroid have fallen in the United States, despite continued problems throughout the country with crack cocaine abuse [5].

High impact information on Chancroid

• We conducted a randomized double-blind trial comparing a single dose of trimethoprim-sulfametrole (640 to 3200 mg) with five-day regimens of either trimethoprim-sulfametrole (160 to 800 mg twice daily) or trimethoprim alone (200 mg twice daily) for the treatment of men with chancroid [6].
• We conclude that the sulfamethoxazole-trimethoprim combination is as efficacious as streptomycin and probably superior to sulfisoxazole and tetracycline in the treatment of chancroid [7].
• Thirty-five men with chancroid were randomly treated with oral sulfisoxazole, sulfisoxazole and tetracycline, sulfamethoxazole-trimethoprim, or intramuscular streptomycin [7].
• Single-dose thiamphenicol for chancroid [8].
• Fleroxacin is an acceptable alternative to existing treatment regimens for chancroid in men [9].

Chemical compound and disease context of Chancroid

• Treatment of chancroid with ciprofloxacin. A prospective, randomized clinical trial [10].
• If resistance to trimethoprim-sulfamethoxazole becomes widespread, ciprofloxacin may become a first-line therapy for chancroid [10].
• Antimicrobial therapy of chancroid: effectiveness of erythromycin [11].
• Single-dose ceftriaxone for chancroid [12].
• Azithromycin prevents experimental chancroid for nearly 2 months [13].

Biological context of Chancroid

• Neutropenia restores virulence to an attenuated Cu,Zn superoxide dismutase-deficient Haemophilus ducreyi strain in the swine model of chancroid [14].
• An outbreak of chancroid in Orange County, California: descriptive epidemiology and disease-control measures [15].
• Of the regimens recommended by the U.S. Public Health Service for the treatment of chancroid, our results support the use of erythromycin, ceftriaxone, and ciprofloxacin, and perhaps ofloxacin, but suggest that amoxicillin-clavulanic acid and sulfamethoxazole-trimethoprim should be used with caution [16].
• Failure of sulphonamides to eradicate H ducreyi in some patients with chancroid is associated with the presence of a sulphonamide resistant plasmid [17].

Anatomical context of Chancroid

• These data support the hypothesis that the H. ducreyi hemolysin is important in the pathogenesis of chancroid and may contribute to ulcer formation, invasion of epithelial cells, and evasion of the immune response [18].
• IL-8 produced in response to H. ducreyi infection may be involved in recruiting polymorphonuclear leukocytes and other inflammatory cells, thereby contributing to the tissue necrosis and ulcer formation characteristic of chancroid [19].
• Finally, we wanted to examine the importance of keratinocyte adhesion in chancroid pathogenesis so we tested the wild-type and dsrA mutant strains of H. ducreyi in our swine models of chancroid pathogenesis [20].

Gene context of Chancroid

• When evaluated in the temperature-dependent rabbit model for chancroid, the lspA1 lspA2 double mutant was substantially less virulent than the wild-type strain 35000HP [21].
• The dsrA mutant was less virulent than the wild type in both the normal and immune cell-depleted swine models of chancroid infection [20].
• Both the cdtA mutant and the cdtB mutant were found to be fully virulent in the temperature-dependent rabbit model for experimental chancroid [22].
• The isogenic H. ducreyi cdtC mutant was shown to be as virulent as its wild-type parent strain in the temperature-dependent rabbit model for experimental chancroid [23].
• An H. ducreyi mutant with an inactivated tadA gene exhibited a small decrease in virulence in the temperature-dependent rabbit model for experimental chancroid, whereas another H. ducreyi mutant with inactivated flp-1 and flp-2 genes was as virulent as the wild-type parent strain [24].

Analytical, diagnostic and therapeutic context of Chancroid

• A randomized, double-blind study of the efficacy of fleroxacin versus trimethoprim-sulfamethoxazole in men with culture-proven chancroid [4].
• Treatment failure rates for culture-proven chancroid were 19% for trimethoprim-sulfamethoxazole, 12.9% and 7.4%, respectively, for low- and high-dose erythromycin regimens, and 8.3% and 0, respectively, for low- and high-dose ciprofloxacin regimens [25].
• In contrast, one HincII and two HindIII ribotypes were observed among 28 isolates collected during the Orange County, Calif., chancroid epidemic that occurred in 1981 and 1982 [26].
• It may therefore be concluded from our study that the oral administration of ciprofloxacin to chancroid patients with or without buboes is highly effective and free from side effects [27].

References