Coccidioidomycosis: Factors Affecting the Host-Parasite Interaction
The inhaled arthroconidia of Coccidioides immitis mature to form large (30–80 µm) endosporulating spherules. Each spherule releases hundreds of endospores, taxing immunologic reserves. Polymorphonuclear neutrophils (PMNs) are prominent in the lesions of coccidioidomycosis, but their effectiveness is...
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| Veröffentlicht in: | Journal of Infectious Diseases 1983-03, Vol.147 (3), p.372-390 |
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| creator | Drutz, David J. Huppert, Milton |
| description | The inhaled arthroconidia of Coccidioides immitis mature to form large (30–80 µm) endosporulating spherules. Each spherule releases hundreds of endospores, taxing immunologic reserves. Polymorphonuclear neutrophils (PMNs) are prominent in the lesions of coccidioidomycosis, but their effectiveness is questionable. Arthroconidia possess an antiphagocytic surface derived from the original hyphal outer wall layer. Only 20%–30% of arthroconidia or endospores that are ingested by PMNs are killed. PMNs can digest the outer wall layer of spherules but may not induce lethal injury. Cell-mediated immunity is central to host defense. Macrophages ingest arthroconidia and endospores but may be unable to kill them unless lymphokines stimulate phagolysosomal fusion. Whether spherules can be killed by macrophages is unclear. C. immitis is stimulated directly by serum levels of estradiol and progesterone achieved in pregnant women. This, together with the depressed cell-mediated immunity of pregnancy, may account for the virulent nature of coccidioidomycosis in pregnant women. |
| doi_str_mv | 10.1093/infdis/147.3.372 |
| format | Article |
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Each spherule releases hundreds of endospores, taxing immunologic reserves. Polymorphonuclear neutrophils (PMNs) are prominent in the lesions of coccidioidomycosis, but their effectiveness is questionable. Arthroconidia possess an antiphagocytic surface derived from the original hyphal outer wall layer. Only 20%–30% of arthroconidia or endospores that are ingested by PMNs are killed. PMNs can digest the outer wall layer of spherules but may not induce lethal injury. Cell-mediated immunity is central to host defense. Macrophages ingest arthroconidia and endospores but may be unable to kill them unless lymphokines stimulate phagolysosomal fusion. Whether spherules can be killed by macrophages is unclear. C. immitis is stimulated directly by serum levels of estradiol and progesterone achieved in pregnant women. This, together with the depressed cell-mediated immunity of pregnancy, may account for the virulent nature of coccidioidomycosis in pregnant women.</description><identifier>ISSN: 0022-1899</identifier><identifier>EISSN: 1537-6613</identifier><identifier>DOI: 10.1093/infdis/147.3.372</identifier><identifier>PMID: 6300253</identifier><language>eng</language><publisher>United States: The University of Chicago Press</publisher><subject>Age Factors ; Animals ; Cell Wall - physiology ; Cell walls ; Child, Preschool ; Coccidioides ; Coccidioides - drug effects ; Coccidioides - growth & development ; Coccidioides - physiology ; Coccidioides immitis ; Coccidioidomycosis ; Coccidioidomycosis - immunology ; Coccidioidomycosis - microbiology ; Coccidioidomycosis - prevention & control ; Continental Population Groups ; Endospores ; Estradiol - pharmacology ; Female ; Fungi ; Humans ; Infections ; Infectious Diseases Society of America ; Macaca mulatta ; Macrophages - physiology ; Male ; Mice ; Middle Aged ; Neutrophils ; Neutrophils - physiology ; Phagocytosis ; Pregnancy ; Pregnancy Complications, Infectious - immunology ; Receptors, Cell Surface - physiology ; Sex Factors ; Sex hormones ; Spores, Fungal ; Yeasts</subject><ispartof>Journal of Infectious Diseases, 1983-03, Vol.147 (3), p.372-390</ispartof><rights>Copyright 1983 The University of Chicago</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c385t-b54123f48cecaeeab7ec20c3f2fc480dd702e8f628463175700ab7d7d6a1cb1e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/30119428$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/30119428$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>309,310,314,780,784,789,790,803,23930,23931,25140,27924,27925,58017,58250</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6300253$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Drutz, David J.</creatorcontrib><creatorcontrib>Huppert, Milton</creatorcontrib><title>Coccidioidomycosis: Factors Affecting the Host-Parasite Interaction</title><title>Journal of Infectious Diseases</title><addtitle>J Infect Dis</addtitle><description>The inhaled arthroconidia of Coccidioides immitis mature to form large (30–80 µm) endosporulating spherules. Each spherule releases hundreds of endospores, taxing immunologic reserves. Polymorphonuclear neutrophils (PMNs) are prominent in the lesions of coccidioidomycosis, but their effectiveness is questionable. Arthroconidia possess an antiphagocytic surface derived from the original hyphal outer wall layer. Only 20%–30% of arthroconidia or endospores that are ingested by PMNs are killed. PMNs can digest the outer wall layer of spherules but may not induce lethal injury. Cell-mediated immunity is central to host defense. Macrophages ingest arthroconidia and endospores but may be unable to kill them unless lymphokines stimulate phagolysosomal fusion. Whether spherules can be killed by macrophages is unclear. C. immitis is stimulated directly by serum levels of estradiol and progesterone achieved in pregnant women. This, together with the depressed cell-mediated immunity of pregnancy, may account for the virulent nature of coccidioidomycosis in pregnant women.</description><subject>Age Factors</subject><subject>Animals</subject><subject>Cell Wall - physiology</subject><subject>Cell walls</subject><subject>Child, Preschool</subject><subject>Coccidioides</subject><subject>Coccidioides - drug effects</subject><subject>Coccidioides - growth & development</subject><subject>Coccidioides - physiology</subject><subject>Coccidioides immitis</subject><subject>Coccidioidomycosis</subject><subject>Coccidioidomycosis - immunology</subject><subject>Coccidioidomycosis - microbiology</subject><subject>Coccidioidomycosis - prevention & control</subject><subject>Continental Population Groups</subject><subject>Endospores</subject><subject>Estradiol - pharmacology</subject><subject>Female</subject><subject>Fungi</subject><subject>Humans</subject><subject>Infections</subject><subject>Infectious Diseases Society of America</subject><subject>Macaca mulatta</subject><subject>Macrophages - physiology</subject><subject>Male</subject><subject>Mice</subject><subject>Middle Aged</subject><subject>Neutrophils</subject><subject>Neutrophils - physiology</subject><subject>Phagocytosis</subject><subject>Pregnancy</subject><subject>Pregnancy Complications, Infectious - immunology</subject><subject>Receptors, Cell Surface - physiology</subject><subject>Sex Factors</subject><subject>Sex hormones</subject><subject>Spores, Fungal</subject><subject>Yeasts</subject><issn>0022-1899</issn><issn>1537-6613</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1983</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM1LKzEUR4M80fqxdyPM6u2mJrnJZPp2UqxVBEVUxE1IMzcaXzvRJAX974201KWruzjndxeHkCNGh4yO4MT3rvPphAk1hCEovkUGTIKqm4bBHzKglPOataPRLtlL6ZVSKqBRO2SngYIkDMh4HKz1nQ--C4tPG5JP_6qJsTnEVJ06hzb7_rnKL1hNQ8r1jYkm-YzVRZ8xFs-H_oBsOzNPeLi---R-cnY3ntZX1-cX49Or2kIrcz2TgnFworVoDaKZKbScWnDcWdHSrlOUY-sa3ooGmJKK0uJ0qmsMszOGsE_-rv6-xfC-xJT1wieL87npMSyTbqkoUST8KjKQJZKQRaQr0caQUkSn36JfmPipGdXfgfUqsC6BNegSuEyO17-XswV2m8G66A9_TaXhBgNlbCR4W3i94j5l_NhwE__rRoGSevr4pC_Pbxl7EFw_whezKZDh</recordid><startdate>198303</startdate><enddate>198303</enddate><creator>Drutz, David J.</creator><creator>Huppert, Milton</creator><general>The University of Chicago Press</general><general>University of Chicago Press</general><scope>BSCLL</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>7T5</scope><scope>H94</scope><scope>M7N</scope><scope>7X8</scope></search><sort><creationdate>198303</creationdate><title>Coccidioidomycosis: Factors Affecting the Host-Parasite Interaction</title><author>Drutz, David J. ; Huppert, Milton</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c385t-b54123f48cecaeeab7ec20c3f2fc480dd702e8f628463175700ab7d7d6a1cb1e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1983</creationdate><topic>Age Factors</topic><topic>Animals</topic><topic>Cell Wall - physiology</topic><topic>Cell walls</topic><topic>Child, Preschool</topic><topic>Coccidioides</topic><topic>Coccidioides - drug effects</topic><topic>Coccidioides - growth & development</topic><topic>Coccidioides - physiology</topic><topic>Coccidioides immitis</topic><topic>Coccidioidomycosis</topic><topic>Coccidioidomycosis - immunology</topic><topic>Coccidioidomycosis - microbiology</topic><topic>Coccidioidomycosis - prevention & control</topic><topic>Continental Population Groups</topic><topic>Endospores</topic><topic>Estradiol - pharmacology</topic><topic>Female</topic><topic>Fungi</topic><topic>Humans</topic><topic>Infections</topic><topic>Infectious Diseases Society of America</topic><topic>Macaca mulatta</topic><topic>Macrophages - physiology</topic><topic>Male</topic><topic>Mice</topic><topic>Middle Aged</topic><topic>Neutrophils</topic><topic>Neutrophils - physiology</topic><topic>Phagocytosis</topic><topic>Pregnancy</topic><topic>Pregnancy Complications, Infectious - immunology</topic><topic>Receptors, Cell Surface - physiology</topic><topic>Sex Factors</topic><topic>Sex hormones</topic><topic>Spores, Fungal</topic><topic>Yeasts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Drutz, David J.</creatorcontrib><creatorcontrib>Huppert, Milton</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of Infectious Diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Drutz, David J.</au><au>Huppert, Milton</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Coccidioidomycosis: Factors Affecting the Host-Parasite Interaction</atitle><jtitle>Journal of Infectious Diseases</jtitle><addtitle>J Infect Dis</addtitle><date>1983-03</date><risdate>1983</risdate><volume>147</volume><issue>3</issue><spage>372</spage><epage>390</epage><pages>372-390</pages><issn>0022-1899</issn><eissn>1537-6613</eissn><abstract>The inhaled arthroconidia of Coccidioides immitis mature to form large (30–80 µm) endosporulating spherules. Each spherule releases hundreds of endospores, taxing immunologic reserves. Polymorphonuclear neutrophils (PMNs) are prominent in the lesions of coccidioidomycosis, but their effectiveness is questionable. Arthroconidia possess an antiphagocytic surface derived from the original hyphal outer wall layer. Only 20%–30% of arthroconidia or endospores that are ingested by PMNs are killed. PMNs can digest the outer wall layer of spherules but may not induce lethal injury. Cell-mediated immunity is central to host defense. Macrophages ingest arthroconidia and endospores but may be unable to kill them unless lymphokines stimulate phagolysosomal fusion. Whether spherules can be killed by macrophages is unclear. C. immitis is stimulated directly by serum levels of estradiol and progesterone achieved in pregnant women. This, together with the depressed cell-mediated immunity of pregnancy, may account for the virulent nature of coccidioidomycosis in pregnant women.</abstract><cop>United States</cop><pub>The University of Chicago Press</pub><pmid>6300253</pmid><doi>10.1093/infdis/147.3.372</doi><tpages>19</tpages></addata></record> |
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| ispartof | Journal of Infectious Diseases, 1983-03, Vol.147 (3), p.372-390 |
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| language | eng |
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| source | MEDLINE; JSTOR Archive Collection A-Z Listing |
| subjects | Age Factors Animals Cell Wall - physiology Cell walls Child, Preschool Coccidioides Coccidioides - drug effects Coccidioides - growth & development Coccidioides - physiology Coccidioides immitis Coccidioidomycosis Coccidioidomycosis - immunology Coccidioidomycosis - microbiology Coccidioidomycosis - prevention & control Continental Population Groups Endospores Estradiol - pharmacology Female Fungi Humans Infections Infectious Diseases Society of America Macaca mulatta Macrophages - physiology Male Mice Middle Aged Neutrophils Neutrophils - physiology Phagocytosis Pregnancy Pregnancy Complications, Infectious - immunology Receptors, Cell Surface - physiology Sex Factors Sex hormones Spores, Fungal Yeasts |
| title | Coccidioidomycosis: Factors Affecting the Host-Parasite Interaction |
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