Evaluation of an Isogenic Hemolysin-Deficient Mutant in the Human Model of Haemophilus ducreyi Infection
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...
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| Veröffentlicht in: | The Journal of infectious diseases 1998-07, Vol.178 (1), p.191-199 |
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| creator | Palmer, K. L. Thornton, A. C. Fortney, K. R. Hood, A. F. Munson, R. S. Spinola, S. M. |
| description | 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. |
| doi_str_mv | 10.1086/515617 |
| format | Article |
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L. ; Thornton, A. C. ; Fortney, K. R. ; Hood, A. F. ; Munson, R. S. ; Spinola, S. M.</creator><creatorcontrib>Palmer, K. L. ; Thornton, A. C. ; Fortney, K. R. ; Hood, A. F. ; Munson, R. S. ; Spinola, S. M.</creatorcontrib><description>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.</description><identifier>ISSN: 0022-1899</identifier><identifier>EISSN: 1537-6613</identifier><identifier>DOI: 10.1086/515617</identifier><identifier>PMID: 9652440</identifier><identifier>CODEN: JIDIAQ</identifier><language>eng</language><publisher>Chicago, IL: The University of Chicago Press</publisher><subject>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</subject><ispartof>The Journal of infectious diseases, 1998-07, Vol.178 (1), p.191-199</ispartof><rights>Copyright 1998 Infectious Diseases Society of America</rights><rights>1998 INIST-CNRS</rights><rights>Copyright University of Chicago, acting through its Press Jul 1998</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c453t-13e7be078b5240cd893f6734f54f99d2a17eb6dc062541cd3a6b30caad2101e53</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/30114134$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/30114134$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,780,784,803,27924,27925,58017,58250</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2353463$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9652440$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Palmer, K. L.</creatorcontrib><creatorcontrib>Thornton, A. C.</creatorcontrib><creatorcontrib>Fortney, K. R.</creatorcontrib><creatorcontrib>Hood, A. F.</creatorcontrib><creatorcontrib>Munson, R. S.</creatorcontrib><creatorcontrib>Spinola, S. M.</creatorcontrib><title>Evaluation of an Isogenic Hemolysin-Deficient Mutant in the Human Model of Haemophilus ducreyi Infection</title><title>The Journal of infectious diseases</title><addtitle>J Infect Dis</addtitle><description>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.</description><subject>Adult</subject><subject>Bacteria</subject><subject>Bacterial diseases</subject><subject>Biological and medical sciences</subject><subject>Biopsies</subject><subject>Chancroid</subject><subject>Chancroid - microbiology</subject><subject>Chancroid - pathology</subject><subject>Dosage</subject><subject>Dose response relationship</subject><subject>Double-Blind Method</subject><subject>Experimental bacterial diseases and models</subject><subject>Female</subject><subject>Haemophilus ducreyi</subject><subject>Haemophilus ducreyi - classification</subject><subject>Haemophilus ducreyi - genetics</subject><subject>Haemophilus ducreyi - pathogenicity</subject><subject>Hemolysin proteins</subject><subject>Hemolysin Proteins - genetics</subject><subject>Hemolysin Proteins - physiology</subject><subject>Humans</subject><subject>Infections</subject><subject>Infectious diseases</subject><subject>Lesions</subject><subject>Major Articles</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mutagenesis</subject><subject>Phenotype</subject><subject>Toxins</subject><subject>Virulence</subject><issn>0022-1899</issn><issn>1537-6613</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkN-LEzEcxIMoZz31PxCCiG-r-b3dR-883crdKagg9xKy2W9s6m5Sk43Y_94tLT3waR4-M8MwCD2n5A0lS_VWUqlo_QAtqOR1pRTlD9GCEMYqumyax-hJzhtCiOCqPkNnjZJMCLJA66s_Zihm8jHg6LAJeJXjTwje4hbGOOyyD9V7cN56CBO-KZOZxQc8rQG3ZZwDN7GHYR9uzZzYrv1QMu6LTbDzeBUc2H37U_TImSHDs6Oeo-8frr5dttX154-ry3fXlRWSTxXlUHdA6mU3DyS2XzbcqZoLJ4Vrmp4ZWkOneksUk4LanhvVcWKN6RklFCQ_R68PvdsUfxfIkx59tjAMJkAsWVMlFVFCzMaX_xk3saQwb9OM8YY0vG7u22yKOSdwepv8aNJOU6L3v-vD77PxxbGtdCP0J9vx6Jm_OnKTrRlcMsH6fLIxLrlQ_L5mk6eYTpgTSgXl-9HVgfs8wd8TN-mXnl-qpW5_3Om72y9fLz5dKH3L_wF_9KE1</recordid><startdate>19980701</startdate><enddate>19980701</enddate><creator>Palmer, K. L.</creator><creator>Thornton, A. C.</creator><creator>Fortney, K. R.</creator><creator>Hood, A. F.</creator><creator>Munson, R. S.</creator><creator>Spinola, S. M.</creator><general>The University of Chicago Press</general><general>University of Chicago Press</general><general>Oxford University Press</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7QL</scope><scope>C1K</scope></search><sort><creationdate>19980701</creationdate><title>Evaluation of an Isogenic Hemolysin-Deficient Mutant in the Human Model of Haemophilus ducreyi Infection</title><author>Palmer, K. L. ; Thornton, A. C. ; Fortney, K. R. ; Hood, A. F. ; Munson, R. S. ; Spinola, S. 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L.</creatorcontrib><creatorcontrib>Thornton, A. C.</creatorcontrib><creatorcontrib>Fortney, K. R.</creatorcontrib><creatorcontrib>Hood, A. F.</creatorcontrib><creatorcontrib>Munson, R. S.</creatorcontrib><creatorcontrib>Spinola, S. M.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>The Journal of infectious diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Palmer, K. L.</au><au>Thornton, A. C.</au><au>Fortney, K. R.</au><au>Hood, A. F.</au><au>Munson, R. S.</au><au>Spinola, S. M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evaluation of an Isogenic Hemolysin-Deficient Mutant in the Human Model of Haemophilus ducreyi Infection</atitle><jtitle>The Journal of infectious diseases</jtitle><addtitle>J Infect Dis</addtitle><date>1998-07-01</date><risdate>1998</risdate><volume>178</volume><issue>1</issue><spage>191</spage><epage>199</epage><pages>191-199</pages><issn>0022-1899</issn><eissn>1537-6613</eissn><coden>JIDIAQ</coden><abstract>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.</abstract><cop>Chicago, IL</cop><pub>The University of Chicago Press</pub><pmid>9652440</pmid><doi>10.1086/515617</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of infectious diseases, 1998-07, Vol.178 (1), p.191-199 |
| issn | 0022-1899 1537-6613 |
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| source | MEDLINE; JSTOR Archive Collection A-Z Listing; Oxford University Press Journals All Titles (1996-Current) |
| 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 |
| title | Evaluation of an Isogenic Hemolysin-Deficient Mutant in the Human Model of Haemophilus ducreyi Infection |
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