{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,5,2]],"date-time":"2025-05-02T17:33:38Z","timestamp":1746207218419,"version":"3.37.3"},"reference-count":33,"publisher":"Springer Science and Business Media LLC","issue":"6","license":[{"start":{"date-parts":[[2022,6,2]],"date-time":"2022-06-02T00:00:00Z","timestamp":1654128000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2022,6,2]],"date-time":"2022-06-02T00:00:00Z","timestamp":1654128000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"funder":[{"name":"Universit\u00e4tsklinikum M\u00fcnster"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["J Clin Immunol"],"published-print":{"date-parts":[[2022,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Hyper-IgE syndromes (HIES) are a group of inborn errors of immunity (IEI) caused by monogenic defects such as in the gene <jats:italic>STAT3<\/jats:italic> (STAT3-HIES). Patients suffering from HIES show an increased susceptibility to <jats:italic>Staphylococcus aureus<\/jats:italic> (<jats:italic>S. aureus<\/jats:italic>) including skin abscesses and pulmonary infections. To assess if the underlying immune defect of STAT3-HIES patients influences the resistance patterns, pathogenicity factors or strain types of <jats:italic>S. aureus<\/jats:italic>. We characterized eleven <jats:italic>S. aureus<\/jats:italic> strains isolated from STAT3-HIES patients (<jats:italic>n<\/jats:italic>\u2009=\u20094) by whole genome sequencing (WGS) to determine presence of resistance and virulence genes. Additionally, we used multi-locus sequence typing (MLST) and protein A (<jats:italic>spa<\/jats:italic>) typing to classify these isolates. Bacterial isolates collected from this cohort of STAT3-HIES patients were identified as common <jats:italic>spa<\/jats:italic> types in Germany. Only one of the isolates was classified as methicillin-resistant <jats:italic>S. aureus<\/jats:italic> (MRSA). For one STAT3 patient WGS illustrated that infection and colonization occurred with different <jats:italic>S. aureus<\/jats:italic> isolates rather than one particular clone. The identified <jats:italic>S. aureus<\/jats:italic> carriage profile on a molecular level suggests that <jats:italic>S. aureus<\/jats:italic> strain type in STAT3-HIES patients is determined by local epidemiology rather than the underlying immune defect highlighting the importance of microbiological assessment prior to antibiotic treatment.<\/jats:p>","DOI":"10.1007\/s10875-022-01293-7","type":"journal-article","created":{"date-parts":[[2022,6,2]],"date-time":"2022-06-02T18:03:01Z","timestamp":1654192981000},"page":"1301-1309","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Molecular Assessment of Staphylococcus Aureus Strains in STAT3 Hyper-IgE Syndrome Patients"],"prefix":"10.1007","volume":"42","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4254-3700","authenticated-orcid":false,"given":"Vera","family":"Schwierzeck","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Renate","family":"Effner","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Felicitas","family":"Abel","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matthias","family":"Reiger","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gundula","family":"Notheis","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J\u00fcrgen","family":"Held","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Valeska","family":"Simon","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sebastian","family":"Dintner","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Reinhard","family":"Hoffmann","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Beate","family":"Hagl","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Johannes","family":"Huebner","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alexander","family":"Mellmann","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ellen D.","family":"Renner","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2022,6,2]]},"reference":[{"issue":"11","key":"1293_CR1","doi-asserted-by":"publisher","first-page":"675","DOI":"10.1038\/nrmicro.2017.104","volume":"15","author":"B Krismer","year":"2017","unstructured":"Krismer B, Weidenmaier C, Zipperer A, Peschel A. The commensal lifestyle of Staphylococcus aureus and its interactions with the nasal microbiota. Nat Rev Microbiol. 2017;15(11):675\u201387.","journal-title":"Nat Rev Microbiol"},{"issue":"13","key":"1293_CR2","doi-asserted-by":"publisher","first-page":"1198","DOI":"10.1056\/NEJMoa1306801","volume":"370","author":"SS Magill","year":"2014","unstructured":"Magill SS, Edwards JR, Bamberg W, Beldavs ZG, Dumyati G, Kainer MA, et al. Multistate point-prevalence survey of health care-associated infections. N Engl J Med. 2014;370(13):1198\u2013208.","journal-title":"N Engl J Med"},{"issue":"16","key":"1293_CR3","doi-asserted-by":"publisher","first-page":"1608","DOI":"10.1056\/NEJMoa073687","volume":"357","author":"SM Holland","year":"2007","unstructured":"Holland SM, DeLeo FR, Elloumi HZ, Hsu AP, Uzel G, Brodsky N, et al. STAT3 mutations in the hyper-IgE syndrome. N Engl J Med. 2007;357(16):1608\u201319.","journal-title":"N Engl J Med"},{"issue":"7157","key":"1293_CR4","doi-asserted-by":"publisher","first-page":"1058","DOI":"10.1038\/nature06096","volume":"448","author":"Y Minegishi","year":"2007","unstructured":"Minegishi Y, Saito M, Tsuchiya S, Tsuge I, Takada H, Hara T, et al. Dominant-negative mutations in the DNA-binding domain of STAT3 cause hyper-IgE syndrome. Nature. 2007;448(7157):1058\u201362.","journal-title":"Nature"},{"issue":"16","key":"1293_CR5","doi-asserted-by":"publisher","first-page":"1667","DOI":"10.1056\/NEJMc076367","volume":"357","author":"ED Renner","year":"2007","unstructured":"Renner ED, Torgerson TR, Rylaarsdam S, A\u00f1over-Sombke S, Golob K, LaFlam T, et al. STAT3 mutation in the original patient with Job\u2019s syndrome. N Engl J Med. 2007;357(16):1667\u20138.","journal-title":"N Engl J Med"},{"issue":"5","key":"1293_CR6","doi-asserted-by":"publisher","first-page":"1234","DOI":"10.1016\/j.jaci.2006.12.666","volume":"119","author":"AF Freeman","year":"2007","unstructured":"Freeman AF, Kleiner DE, Nadiminti H, Davis J, Quezado M, Anderson V, et al. Causes of death in hyper-IgE syndrome. J Allergy Clin Immunol. 2007;119(5):1234\u201340.","journal-title":"J Allergy Clin Immunol"},{"issue":"6","key":"1293_CR7","doi-asserted-by":"publisher","first-page":"1291","DOI":"10.1084\/jem.20082767","volume":"206","author":"Y Minegishi","year":"2009","unstructured":"Minegishi Y, Saito M, Nagasawa M, Takada H, Hara T, Tsuchiya S, et al. Molecular explanation for the contradiction between systemic Th17 defect and localized bacterial infection in hyper-IgE syndrome. J Exp Med. 2009;206(6):1291\u2013301.","journal-title":"J Exp Med"},{"issue":"9","key":"1293_CR8","doi-asserted-by":"publisher","first-page":"1691","DOI":"10.1111\/all.13753","volume":"74","author":"C Kr\u00f6ner","year":"2019","unstructured":"Kr\u00f6ner C, Neumann J, Ley-Zaporozhan J, Hagl B, Meixner I, Spielberger BD, et al. Lung disease in STAT3 hyper-IgE syndrome requires intense therapy. Allergy. 2019;74(9):1691\u2013702.","journal-title":"Allergy"},{"issue":"2","key":"1293_CR9","doi-asserted-by":"publisher","first-page":"177","DOI":"10.1111\/pai.12512","volume":"27","author":"B Hagl","year":"2016","unstructured":"Hagl B, Heinz V, Schlesinger A, Spielberger BD, Sawalle-Belohradsky J, Senn-Rauh M, et al. Key findings to expedite the diagnosis of hyper-IgE syndromes in infants and young children. Pediatr Allergy Immunol. 2016;27(2):177\u201384.","journal-title":"Pediatr Allergy Immunol"},{"issue":"7188","key":"1293_CR10","doi-asserted-by":"publisher","first-page":"773","DOI":"10.1038\/nature06764","volume":"452","author":"JD Milner","year":"2008","unstructured":"Milner JD, Brenchley JM, Laurence A, Freeman AF, Hill BJ, Elias KM, et al. Impaired T(H)17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome. Nature. 2008;452(7188):773\u20136.","journal-title":"Nature"},{"issue":"12","key":"1293_CR11","doi-asserted-by":"publisher","first-page":"2394","DOI":"10.1111\/all.13969","volume":"74","author":"W van de Veen","year":"2019","unstructured":"van de Veen W, Kr\u00e4tz CE, McKenzie CI, Aui PM, Neumann J, van Noesel CJM, et al. Impaired memory B-cell development and antibody maturation with a skewing toward IgE in patients with STAT3 hyper-IgE syndrome. Allergy. 2019;74(12):2394\u2013405.","journal-title":"Allergy"},{"issue":"1","key":"1293_CR12","doi-asserted-by":"publisher","first-page":"181","DOI":"10.1016\/j.jaci.2008.04.037","volume":"122","author":"ED Renner","year":"2008","unstructured":"Renner ED, Rylaarsdam S, Anover-Sombke S, Rack AL, Reichenbach J, Carey JC, et al. Novel signal transducer and activator of transcription 3 (STAT3) mutations, reduced T(H)17 cell numbers, and variably defective STAT3 phosphorylation in hyper-IgE syndrome. J Allergy Clin Immunol. 2008;122(1):181\u20137.","journal-title":"J Allergy Clin Immunol"},{"issue":"2","key":"1293_CR13","doi-asserted-by":"publisher","first-page":"559","DOI":"10.1016\/j.jaci.2011.09.017","volume":"129","author":"A Meyer-Bahlburg","year":"2012","unstructured":"Meyer-Bahlburg A, Renner ED, Rylaarsdam S, Reichenbach J, Schimke LF, Marks A, et al. Heterozygous signal transducer and activator of transcription 3 mutations in hyper-IgE syndrome result in altered B-cell maturation. J Allergy Clin Immunol. 2012;129(2):559\u201362, 562.e1-2.","journal-title":"J Allergy Clin Immunol"},{"issue":"9","key":"1293_CR14","doi-asserted-by":"publisher","first-page":"1279","DOI":"10.1093\/cid\/cix140","volume":"64","author":"S Stentzel","year":"2017","unstructured":"Stentzel S, Hagl B, Abel F, Kahl BC, Rack-Hoch A, Br\u00f6ker BM, et al. Reduced Immunoglobulin (Ig) G Response to Staphylococcus aureus in STAT3 Hyper-IgE Syndrome. Clin Infect Dis. 2017;64(9):1279\u201382.","journal-title":"Clin Infect Dis"},{"issue":"8","key":"1293_CR15","doi-asserted-by":"publisher","first-page":"3595","DOI":"10.1172\/JCI121486","volume":"128","author":"IA Myles","year":"2018","unstructured":"Myles IA, Anderson ED, Earland NJ, Zarember KA, Sastalla I, Williams KW, et al. TNF overproduction impairs epithelial staphylococcal response in hyper IgE syndrome. J Clin Invest. 2018;128(8):3595\u2013604.","journal-title":"J Clin Invest"},{"issue":"3","key":"1293_CR16","doi-asserted-by":"publisher","first-page":"771","DOI":"10.1016\/S0091-6749(95)70185-0","volume":"95","author":"H Kimata","year":"1995","unstructured":"Kimata H. High-dose intravenous gamma-globulin treatment for hyperimmunoglobulinemia E syndrome. J Allergy Clin Immunol. 1995;95(3):771\u20134.","journal-title":"J Allergy Clin Immunol"},{"issue":"4","key":"1293_CR17","doi-asserted-by":"publisher","first-page":"e1","DOI":"10.1097\/MD.0b013e31825f95b9","volume":"91","author":"M-O Chandesris","year":"2012","unstructured":"Chandesris M-O, Melki I, Natividad A, Puel A, Fieschi C, Yun L, et al. Autosomal dominant STAT3 deficiency and hyper-IgE syndrome: molecular, cellular, and clinical features from a French national survey. Medicine (Baltimore). 2012;91(4):e1-19.","journal-title":"Medicine (Baltimore)"},{"issue":"2","key":"1293_CR18","doi-asserted-by":"publisher","first-page":"23","DOI":"10.3390\/pathogens6020023","volume":"6","author":"I Sastalla","year":"2017","unstructured":"Sastalla I, Williams KW, Anderson ED, Myles IA, Reckhow JD, Espinoza-Moraga M, et al. Molecular typing of staphylococcus aureus isolated from patients with autosomal dominant hyper IgE syndrome. Pathogens. 2017;6(2):23. https:\/\/doi.org\/10.3390\/pathogens6020023.","journal-title":"Pathogens"},{"issue":"1","key":"1293_CR19","doi-asserted-by":"publisher","first-page":"121","DOI":"10.1007\/s004390100505","volume":"109","author":"JT den Dunnen","year":"2001","unstructured":"den Dunnen JT, Antonarakis SE. Nomenclature for the description of human sequence variations. Hum Genet. 2001;109(1):121\u20134.","journal-title":"Hum Genet"},{"issue":"1","key":"1293_CR20","doi-asserted-by":"publisher","first-page":"153","DOI":"10.1186\/s13059-018-1540-z","volume":"19","author":"A Souvorov","year":"2018","unstructured":"Souvorov A, Agarwala R, Lipman DJ. SKESA: strategic k-mer extension for scrupulous assemblies. Genome Biol. 2018;19(1):153.","journal-title":"Genome Biol"},{"issue":"7","key":"1293_CR21","doi-asserted-by":"publisher","first-page":"2365","DOI":"10.1128\/JCM.00262-14","volume":"52","author":"SR Leopold","year":"2014","unstructured":"Leopold SR, Goering RV, Witten A, Harmsen D, Mellmann A. Bacterial whole-genome sequencing revisited: portable, scalable, and standardized analysis for typing and detection of virulence and antibiotic resistance genes. J Clin Microbiol. 2014;52(7):2365\u201370.","journal-title":"J Clin Microbiol"},{"key":"1293_CR22","doi-asserted-by":"publisher","first-page":"1662","DOI":"10.3389\/fmicb.2017.01662","volume":"8","author":"M Lebughe","year":"2017","unstructured":"Lebughe M, Phaku P, Niemann S, Mumba D, Peters G, Muyembe-Tamfum J-J, et al. The impact of the staphylococcus aureus virulome on infection in a developing country: a cohort study. Front Microbiol. 2017;8:1662.","journal-title":"Front Microbiol"},{"issue":"2","key":"1293_CR23","doi-asserted-by":"publisher","first-page":"191","DOI":"10.1016\/j.femsle.2005.04.007","volume":"246","author":"K Omoe","year":"2005","unstructured":"Omoe K, Hu D-L, Takahashi-Omoe H, Nakane A, Shinagawa K. Comprehensive analysis of classical and newly described staphylococcal superantigenic toxin genes in Staphylococcus aureus isolates. FEMS Microbiol Lett. 2005;246(2):191\u20138.","journal-title":"FEMS Microbiol Lett"},{"issue":"1","key":"1293_CR24","doi-asserted-by":"publisher","first-page":"21","DOI":"10.1016\/j.ijmm.2016.11.007","volume":"307","author":"K Becker","year":"2017","unstructured":"Becker K, Schaumburg F, Fegeler C, Friedrich AW, K\u00f6ck R. Staphylococcus aureus from the German general population is highly diverse. Int J Med Microbiol. 2017;307(1):21\u20137.","journal-title":"Int J Med Microbiol"},{"issue":"4","key":"1293_CR25","doi-asserted-by":"publisher","first-page":"350","DOI":"10.1016\/j.cmi.2017.12.016","volume":"24","author":"AC Sch\u00fcrch","year":"2018","unstructured":"Sch\u00fcrch AC, Arredondo-Alonso S, Willems RJL, Goering RV. Whole genome sequencing options for bacterial strain typing and epidemiologic analysis based on single nucleotide polymorphism versus gene-by-gene-based approaches. Clin Microbiol Infect. 2018;24(4):350\u20134.","journal-title":"Clin Microbiol Infect"},{"issue":"12","key":"1293_CR26","doi-asserted-by":"publisher","first-page":"2874","DOI":"10.1128\/JCM.00790-16","volume":"54","author":"A Mellmann","year":"2016","unstructured":"Mellmann A, Bletz S, B\u00f6king T, Kipp F, Becker K, Schultes A, et al. Real-time genome sequencing of resistant bacteria provides precision infection control in an institutional setting. J Clin Microbiol. 2016;54(12):2874\u201381.","journal-title":"J Clin Microbiol"},{"issue":"19","key":"1293_CR27","first-page":"331","volume":"111","author":"E Meyer","year":"2014","unstructured":"Meyer E, Schr\u00f6der C, Gastmeier P, Geffers C. The reduction of nosocomial MRSA infection in Germany: an analysis of data from the Hospital Infection Surveillance System (KISS) between 2007 and 2012. Dtsch Arztebl Int. 2014;111(19):331\u20136.","journal-title":"Dtsch Arztebl Int"},{"issue":"3","key":"1293_CR28","doi-asserted-by":"publisher","first-page":"215","DOI":"10.1016\/j.jinf.2018.12.005","volume":"78","author":"TS Kramer","year":"2019","unstructured":"Kramer TS, Schr\u00f6der C, Behnke M, Aghdassi SJ, Geffers C, Gastmeier P, et al. Decrease of methicillin resistance in Staphylococcus aureus in nosocomial infections in Germany-a prospective analysis over 10 years. J Infect. 2019;78(3):215\u20139.","journal-title":"J Infect"},{"key":"1293_CR29","doi-asserted-by":"publisher","unstructured":"Layer F, Strommenger B, Cuny C, Noll I, Eckmanns T, Werner G. Eigenschaften, H\u00e4ufigkeit und Verbreitung von MRSA in Deutschland. Epid Bull. 2019;42:437\u201342. https:\/\/doi.org\/10.25646\/6320.2.","DOI":"10.25646\/6320.2"},{"issue":"2","key":"1293_CR30","doi-asserted-by":"publisher","first-page":"336","DOI":"10.1016\/j.jid.2017.09.023","volume":"138","author":"CP Harkins","year":"2018","unstructured":"Harkins CP, Pettigrew KA, Oravcov\u00e1 K, Gardner J, Hearn RMR, Rice D, et al. The microevolution and epidemiology of staphylococcus aureus colonization during atopic eczema disease flare. J Invest Dermatol. 2018;138(2):336\u201343.","journal-title":"J Invest Dermatol"},{"issue":"357","key":"1293_CR31","doi-asserted-by":"publisher","first-page":"357ra124","DOI":"10.1126\/scitranslmed.aag1153","volume":"8","author":"BA Diep","year":"2016","unstructured":"Diep BA, Le VTM, Badiou C, Le HN, Pinheiro MG, Duong AH, et al. IVIG-mediated protection against necrotizing pneumonia caused by MRSA. Sci Transl Med. 2016;8(357):357ra124.","journal-title":"Sci Transl Med"},{"issue":"1","key":"1293_CR32","doi-asserted-by":"publisher","DOI":"10.1002\/cti2.1009","volume":"7","author":"A Ruzin","year":"2018","unstructured":"Ruzin A, Wu Y, Yu L, Yu X-Q, Tabor DE, Mok H, et al. Characterisation of anti-alpha toxin antibody levels and colonisation status after administration of an investigational human monoclonal antibody, MEDI4893, against Staphylococcus aureus alpha toxin. Clin Trans Immunol. 2018;7(1): e1009.","journal-title":"Clin Trans Immunol"},{"issue":"2","key":"1293_CR33","doi-asserted-by":"publisher","first-page":"1108","DOI":"10.1128\/AAC.02190-13","volume":"58","author":"L Hua","year":"2014","unstructured":"Hua L, Hilliard JJ, Shi Y, Tkaczyk C, Cheng LI, Yu X, et al. Assessment of an anti-alpha-toxin monoclonal antibody for prevention and treatment of Staphylococcus aureus-induced pneumonia. Antimicrob Agents Chemother. 2014;58(2):1108\u201317.","journal-title":"Antimicrob Agents Chemother"}],"container-title":["Journal of Clinical Immunology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/link.springer.com\/content\/pdf\/10.1007\/s10875-022-01293-7.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/link.springer.com\/article\/10.1007\/s10875-022-01293-7\/fulltext.html","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/link.springer.com\/content\/pdf\/10.1007\/s10875-022-01293-7.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,10,6]],"date-time":"2022-10-06T17:48:39Z","timestamp":1665078519000},"score":1,"resource":{"primary":{"URL":"https:\/\/link.springer.com\/10.1007\/s10875-022-01293-7"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2022,6,2]]},"references-count":33,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2022,8]]}},"alternative-id":["1293"],"URL":"https:\/\/doi.org\/10.1007\/s10875-022-01293-7","relation":{},"ISSN":["0271-9142","1573-2592"],"issn-type":[{"type":"print","value":"0271-9142"},{"type":"electronic","value":"1573-2592"}],"subject":[],"published":{"date-parts":[[2022,6,2]]},"assertion":[{"value":"7 January 2022","order":1,"name":"received","label":"Received","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"17 May 2022","order":2,"name":"accepted","label":"Accepted","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"2 June 2022","order":3,"name":"first_online","label":"First Online","group":{"name":"ArticleHistory","label":"Article History"}},{"order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Declarations"}},{"value":"The study was approved by the Institutional Review Board of the Medical School TUM (32\/20S-KH).","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethics Approval"}},{"value":"Written informed consent was obtained from all patients or their legal guardians.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent to Participate"}},{"value":"Patients signed informed consent regarding publishing their data.","order":4,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent for Publication"}},{"value":"The authors declare that they have no competing interests.","order":5,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing Interests"}}]}}