{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T07:40:54Z","timestamp":1779176454985,"version":"3.51.4"},"reference-count":59,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2015,2,1]],"date-time":"2015-02-01T00:00:00Z","timestamp":1422748800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2015,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The clinical significance of polymicrobial interactions, particularly those between commensal species with high pathogenic potential, remains largely understudied. Although the dimorphic fungal species\n            <jats:named-content content-type=\"genus-species\">Candida albicans<\/jats:named-content>\n            and the bacterium\n            <jats:named-content content-type=\"genus-species\">Staphylococcus aureus<\/jats:named-content>\n            are common cocolonizers of humans, they are considered leading opportunistic pathogens. Oral candidiasis specifically, characterized by hyphal invasion of oral mucosal tissue, is the most common opportunistic infection in HIV\n            <jats:sup>+<\/jats:sup>\n            and immunocompromised individuals. In this study, building on our previous findings, a mouse model was developed to investigate whether the onset of oral candidiasis predisposes the host to secondary staphylococcal infection. The findings demonstrated that in mice with oral candidiasis, subsequent exposure to\n            <jats:named-content content-type=\"genus-species\">S. aureus<\/jats:named-content>\n            resulted in systemic bacterial infection with high morbidity and mortality. Histopathology and scanning electron microscopy of tongue tissue from moribund animals revealed massive\n            <jats:named-content content-type=\"genus-species\">C. albicans<\/jats:named-content>\n            hyphal invasion coupled with\n            <jats:named-content content-type=\"genus-species\">S. aureus<\/jats:named-content>\n            deep tissue infiltration. The crucial role of hyphae in the process was demonstrated using a non-hypha-producing and a noninvasive hypha-producing mutant strains of\n            <jats:named-content content-type=\"genus-species\">C. albicans<\/jats:named-content>\n            . Further, in contrast to previous findings,\n            <jats:named-content content-type=\"genus-species\">S. aureus<\/jats:named-content>\n            dissemination was aided but not contingent upon the presence of the Als3p hypha-specific adhesion. Importantly, impeding development of mucosal\n            <jats:named-content content-type=\"genus-species\">C. albicans<\/jats:named-content>\n            infection by administering antifungal fluconazole therapy protected the animals from systemic bacterial disease. The combined findings from this study demonstrate that oral candidiasis may constitute a risk factor for disseminated bacterial disease warranting awareness in terms of therapeutic management of immunocompromised individuals.\n          <\/jats:p>","DOI":"10.1128\/iai.02843-14","type":"journal-article","created":{"date-parts":[[2014,11,25]],"date-time":"2014-11-25T04:04:41Z","timestamp":1416888281000},"page":"604-613","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":77,"title":["Clinical Implications of Oral Candidiasis: Host Tissue Damage and Disseminated Bacterial Disease"],"prefix":"10.1128","volume":"83","author":[{"given":"Eric F.","family":"Kong","sequence":"first","affiliation":[{"name":"Department of Oncology and Diagnostic Sciences, Dental School, University of Maryland, Baltimore, Maryland, USA"},{"name":"Graduate Program in Life Sciences, Molecular Microbiology and Immunology Program, University of Maryland, Baltimore, Maryland, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sona","family":"Kuchar\u00edkov\u00e1","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology, VIB, KU Leuven, Belgium"},{"name":"Laboratory of Molecular Cell Biology, Institute of Botany and Microbiology, KU Leuven, Belgium"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1542-897X","authenticated-orcid":false,"given":"Patrick","family":"Van Dijck","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology, VIB, KU Leuven, Belgium"},{"name":"Laboratory of Molecular Cell Biology, Institute of Botany and Microbiology, KU Leuven, Belgium"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brian M.","family":"Peters","sequence":"additional","affiliation":[{"name":"Graduate Program in Life Sciences, Molecular Microbiology and Immunology Program, University of Maryland, Baltimore, Maryland, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark E.","family":"Shirtliff","sequence":"additional","affiliation":[{"name":"Department of Microbial Pathogenesis, Dental School, University of Maryland, Baltimore, Maryland, USA"},{"name":"Department of Microbiology and Immunology, School of Medicine, University of Maryland, Baltimore, Maryland, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mary Ann","family":"Jabra-Rizk","sequence":"additional","affiliation":[{"name":"Department of Oncology and Diagnostic Sciences, Dental School, University of Maryland, Baltimore, Maryland, USA"},{"name":"Department of Microbiology and Immunology, School of Medicine, University of Maryland, Baltimore, Maryland, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(05)17745-9"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.2174\/1874437001105010039"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/AEM.02474-05"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2672.2004.02213.x"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1111\/2049-632X.12123"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/CMR.00013-11"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/9781555817947"},{"key":"e_1_3_3_9_2","volume-title":"Polymicrobial diseases","author":"Jenkinson HF","year":"2002","unstructured":"Jenkinson HF, Douglas JL. 2002. 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