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The cytolethal distending toxin of Haemophilus ducreyi aggravates dermal lesions in a rabbit model of chancroid

Journal article
Authors Catharina Wising
Lena Mölne
Ing-Marie Jonsson
Karin Ahlman
Teresa Lagergård
Published in Microbes Infect
Volume 7
Issue 5-6
Pages 867-74
Publication year 2005
Published at Institute of Selected Clinical Sciences, Department of Dermatology and Venereology
Institute of Internal Medicine, Dept of Rheumatology and Inflammation Research
Institute of Medical Microbiology/Immunology
Pages 867-74
Language en
Links dx.doi.org/10.1016/j.micinf.2005.02...
Keywords Animals, Bacterial Toxins/*toxicity, Chancroid/*pathology, Comparative Study, Haemophilus Infections/pathology, Haemophilus ducreyi/*pathogenicity, Haemophilus influenzae, Rabbits, Research Support, Non-U.S. Gov't, Skin/pathology
Subject categories Microbiology in the medical area

Abstract

Haemophilus ducreyi, the etiologic agent of the sexually transmitted disease chancroid, produces a cytolethal distending toxin (HdCDT) that inhibits cultured cell proliferation, leading to cell death. A rabbit model of dermal infection was used to investigate the roles of H. ducreyi bacteria and HdCDT in the development, clinical appearance, and persistence of infection. A non-toxin producing H. ducreyi strain, and for comparison purposes a non-capsulated Haemophilus influenzae strain, were inoculated intradermally, with and without co-administration of purified HdCDT. Co-administration of HdCDT resulted in significant aggravation of H. ducreyi-induced inflammatory lesions, and development of ulcers in rabbit skin. Less pronounced inflammatory lesions and lack of epithelial eruption were observed after inoculation with H. influenzae. Histopathological sections of the H. ducreyi-induced lesions, in both the presence and absence of HdCDT, showed dense infiltrates of the same type inflammatory cells, with the exception of a prominent endothelial cell proliferation noted in sections from lesions caused by H. ducreyi and toxin. Signs of chronic inflammation with involvement of T cells, macrophages, eosinophils, and granuloma formation were observed after H. ducreyi inoculation both with and without toxin. In conclusion, H. ducreyi causes a pronounced, chronic inflammation with involvement of T cells and macrophages, and in combination with HdCDT production of ulcers in the rabbit model. These pathogenic mechanisms may promote the development and persistence of chancroid ulcers.

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