Stanley M. Spinola, MD
Professor Emeritus of Microbiology & Immunology
Professor Emeritus of Medicine
Professor Emeritus of Pathology & Laboratory Medicine
Chair, Department of Microbiology and Immunology 2010-2019
Director Division of Infectious Diseases 1995-2010
David H. Jacobs Professor of Medicine 1999-2010
- Phone
- (317) 274-0506
- Address
-
MS 420
635 Barnhill Dr.
Indianapolis , IN 46202-5120 - PubMed:
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Bio
Dr. Spinola received a B.A. from Brown University in 1974 (Biology) and a M.D. from Georgetown University in 1978. He completed a residency in Internal Medicine and Pediatrics at the University of North Carolina at Chapel Hill in 1982 and served in the National Health Service Corps from 1982-1984. He completed a fellowship in Adult and Pediatric Infectious Diseases at the University of North Carolina in 1987, where he trained in Janne Cannon's laboratory on microbial pathogenesis. From 1987 to 1993, Dr. Spinola was at the State University of New York at Buffalo as an Assistant and then Associate Professor in the Department of Medicine. He came to Indiana University in 1993 to join the Division of Infectious Diseases in the Department of Medicine and was named the Division Director in 1995. In 1999, Dr. Spinola was named the first David H. Jacobs Professor of Infectious Diseases; he served as Chair of the Department of Microbiology and Immunology from 2010-2019. He retired in 2026 and is currently a Professor Emeritus of Microbiology and Immunology, Medicine, and Pathology and Laboratory Medicine. Dr. Spinola is a member of the American Society for Clinical Investigation and a Fellow in the American Academy of Microbiology and in the Infectious Diseases Society of America. He served for 2 terms as a Member and Chair of the Microbiology and Infectious Diseases Review Committee, a standing study section of NIAID. He has served as primary mentor for 7 graduate students, 7 ID fellows, 7 PhD postdoctoral fellows, 20 short term trainees, and 5 faculty members for Developmental Awards, K08 or K22 awards. He was the recipient of the Indiana University School of Medicine 2017 Basic Science Excellence in Faculty Mentoring Award.
Key Publications
Recent publications (since 2021)
- Griesenauer B, González-Beiras C, Fortney KR, Lin H, Gao X, Godornes C, Nelson DE, Katz BP, Lukehart SA, Mitjà O, Dong Q, Spinola SM. Streptococcus pyogenes is Associated with Idiopathic Cutaneous Ulcers in Children on a Yaws-Endemic Island. MBio. 2021 Jan 12;12(1):e03162-20. doi: 10.1128/mBio.03162-20. PMID: 33436440; PMCID: PMC7844543
- Brothwell JA, Griesenauer B, Chen L, Spinola SM. Interactions of the Skin Pathogen Haemophilus ducreyi with the Human Host. Frontiers in Immunology 03 February 2021 doi: 10.3389/fimmu.2020.615402. PMID: 33613541; PMCID: PMC7886810
- Fortney KR*, Smith SN*, van Rensburg JJ, Brothwell JA, Gardner JJ, Katz BP, Ahsan N, Duerfeldt AS, Mobley HLT, Spinola SM. A CpxA Phosphatase Inhibitor Activates CpxRA and is a Potential Treatment for Uropathogenic Escherichia coli in a Murine Model of Infection. Microbiology Spectrum 2022 Apr 27;10(2):e0243021. doi: 10.1128/spectrum.02430-21.Epub 2022 Mar 17. PMID: 35297652; PMCID: PMC9045377; * equal contribution
- *Brothwell JA and Spinola SM. Genes differentially expressed by Haemophilus ducreyi during anaerobic growth significantly overlap with those differentially expressed during experimental infection of human volunteers. J. Bacteriology 2022 May 17;204(5):e0000522. doi: 10.1128/jb.00005-22. Epub 2022 Apr 4. PMID: 35377183; PMCID: PMC9112927 *Editor’s Pick
- Brothwell JA, Fortney KR, Batteiger T, Katz BP, Spinola SM. Dispensability of Ascorbic Acid Uptake and Utilization Encoded by ulaABCD for the Virulence of Haemophilus ducreyi in Humans. J. Infect. Dis. 2022, Jul 25;jiac314. doi: 10.1093/infdis/jiac314. PMID: 35876728; PMCID: PMC10169391
- Brothwell JA, Fortney KR, Gao H, Wilson LS, Andrews CF, Tran TM, Hu X, Batteiger TA, Barnes S, Liu Y, Spinola SM. Haemophilus ducreyi infection induces oxidative stress, central metabolic changes, and a mixed pro- and anti-inflammatory environment in the human host. mBio. 2022 Dec 1;13(6):e0312522. doi: 10.1128/mbio.03125-22. PMID: 36453940; PMCID: PMC9765465; Erratum, 2023 Feb 28;14(1):e0352222. doi:10.1128/mbio.03522-22.Epub 2023 Feb 6; PMID: 36744942; PMCID: PMC9972968
- Griesenauer B, Ying X, Fortney KR, Gao X, González-Beiras C, Nelson DE, Ren J, Mitja O, Dong Q, Spinola SM. Two Streptococcus pyogenes emm types and several anaerobic bacterial species are associated with idiopathic cutaneous ulcers in children after community-based mass treatment with azithromycin. PLoS Negl Trop Dis. 2022 Dec 19;16(12):e0011009.doi:10.1371/journal.pntd.0011009.PMID: 36534698; PMCID: PMC9810193
- Brothwell JA, Fortney KR, Williams JS, Batteiger TA, Duplantier R, Grounds D, Jannasch AS, Katz BP, Spinola SM. Formate production is dispensable for Haemophilus ducreyi virulence in human volunteers. Infection and Immunity 2023 Sep 14;91(9):e0017623. doi:10.1128/iai.00176-23. Epub 2023 Aug 18; PMID: 37594273; PMCID: PMC10501210
- Fortney KR, Brothwell JA, Batteiger TA, Duplantier R, Katz BP, Spinola SM. A Haemophilus ducreyi strain lacking the yfeABCD iron transport system is virulent in human volunteers. Infection and Immunity, 2024 Jun 11;92(6):e0005824. doi: 10.1128/iai.00058-24. Epub 2024 May 23; PMID 38780215; PMCID: PMC11237573
- Al-Tawfiq JA and Spinola SM. Infections caused by Haemophilus ducreyi: one organism, two stories. Clinical Microbiology Reviews, 2024 Sep 17:e0013524. doi: 10.1128/cmr.00135-24. PMID: 39287406; PMCID: PMC11629627
- Brothwell JA, Wei Y, Wang J, Guo T, Zhang C, Fortney KR, Duplantier R, Chen L, Batteiger TA, Kaplan MH, Spinola SM* and Cao S*. A high-resolution view of the immune and stromal cell response to Haemophilus ducreyiinfection in human volunteers. mBio, 2025 Mar 12;16(3):e0388524. doi: 10.1128/mbio.03885-24. PMID: 39882906; PMCID: PMC11898715 *Co-corresponding authors
- Fortney KR, Brothwell JA, Batteiger TA, Duplantier R, Katz BP, Spinola SM. The protein degradation system encoded by hslUV (clpYQ) is dispensable for the virulence of Haemophilus ducreyi in human volunteers. Infection and Immunity 2025, Apr 10:e0057724. doi: 10.1128/iai.00577-24. PMID: 40208051
- Elsener T.A, Cehovin A, Philp C, Fortney KR, Spinola SM, Maiden MJ, Tang CM. Origin, evolution, and success of pbla, the gonococcal beta-lactamase plasmid, and implications for public health. PLOS Pathogens 2025, May 6;21(5): e1013151.doi:10.1371/journal.ppat.1013151. PMID: 40327678; PMCID: PMC1208092
- Spinola SM, Fortney KR, Ofner S, Gebregziabher N, Brothwell JA, Katz BP. The molecular pathogenesis of Haemophilus ducreyi infection in human volunteers Microbiol Mol Biol Rev. 2025 Sep 25;89(3):e0005524. doi: 10.1128/mmbr.00055-24.PMID: 40844291; PMCID: PMC12462288
- Brothwell JA*, Toh E*, Ying X*,Dong Q, Xu LH, Giacani L, González-Beiras C, Mitjà O, Gao X#, Spinola SM#. The etiology of exudative cutaneous ulcers in a yaws-endemic community prior to receipt of antimicrobials is similar to that found in communities after mass treatment with azithromycin. mSphere, in press. #Co-corresponding authors.
| Year | Degree | Institution |
|---|---|---|
| 1982 | Residency | University of North Carolina, Chapel Hill |
| 1978 | MD | Georgetown University |
| 1974 | BA | Brown University |
The Spinola laboratory focuses on the pathogenesis of and host response to the bacterium Haemophilus ducreyi in an experimental model of human infection and the etiology of cutaneous ulcers in children who live in the tropics.
H. ducreyi causes painful cutaneous leg ulcers in children in the tropics and the genital ulcer disease chancroid in adults, which facilitates the transmission of HIV-1. The laboratory developed a model in which human volunteers are infected on the skin of the arm with the bacterium that is relevant to both syndromes. Features of the model include a low dose required for infection (1 to 100 CFU) and a clinical course and a cutaneous immune response that mimics naturally occurring disease. In both experimental and natural infection, H. ducreyi resides in an abscess, and the primary mechanism by which the organism causes disease is evasion of phagocytosis. One major project in the laboratory is to determine a molecular interaction network between H. ducreyi and the host on a transcriptional level using RNA-sequencing and the metabolomic consequences of this interaction. Preliminary data indicate that H. ducreyi is exploiting the metabolic environment shaped by the host immune response by utiizing alternative carbon sources such as vitamin C and adapting to anaerobiosis in vivo. Another major project is to try to understand how H. ducreyi causes leg ulcers in children and by microbiome analysis discover other agents that cause this syndrome. There are currently 1 technician and 2 post doctoral fellows in the laboratory. New trainees will be exposed to molecular biology, immunology, cell biology, microbiome research, and the methods and ethics of human research.
Gangaiah D; Marinov GK; Roberts SA; Robson J; Spinola SM; Genome announcements 2016 Feb 4
Singer M; Li W; Morré SA; Ouburg S; Spinola SM; The Journal of infectious diseases 2016 Apr 27
Gangaiah D; Zhang X; Baker B; Fortney KR; Gao H; Holley CL; Munson RS Jr; Liu Y; Spinola SM; Infection and immunity 2016 Apr 22
Infectious Diseases; Sexually Transmitted Infections; Skin ulcers in children; Human Subjects Research Ethics
Desc: Excellence in Faculty Mentoring Award- Basic Science
Scope: School
Date: 2017-09-01
Desc: Trustees' Teaching Award
Scope: University
Date: 2007-05-01
Desc: Elected Member
Scope: National
Date: 1905-06-21