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James M. Musser, MD, PhD

Chair, Department of Pathology & Genomic Medicine
Fondren Presidential Distinguished Chair, Research Institute
Professor of Pathology and Genomic Medicine, Institute for Academic Medicine
Director, Center for Molecular & Translational Human Infectious Diseases Research
Houston Methodist
Weill Cornell Medical College

Research Lab


Following postdoctoral research at the Institute of Molecular Evolutionary Genetics, Pennsylvania State University, and residency training in laboratory medicine at the Hospital of the University of Pennsylvania, Dr. Musser joined the pathology department, Baylor College of Medicine in Houston, Texas. He advanced through the academic ranks from 1991 to 1998, when he was promoted to professor. Dr. Musser served as the chief of the Laboratory of Human Bacterial Pathogenesis at the National Institute of Allergy and Infectious Diseases from 1999-2003. He joined Houston Methodist Research Institute in 2005 and served as co-director and executive vice president until 2010. In addition to holding the Fondren Presidential Distinguished Chair, Dr. Musser is also the chair of the Department of Pathology and Genomic Medicine and the director of the Center for Molecular and Translational Human Infectious Diseases Research. His research focuses on the molecular basis of host-pathogen interactions in group A Streptococcus and Mycobacterium tuberculosis. He serves on several editorial boards, has received many national and international honors and awards, and has published more than 300 research articles and book chapters.

Description of Research

The goal of Dr. Musser's research is to advance our understanding of pathogen-host interactions, broadly defined. His laboratory uses a highly integrated interdisciplinary research strategy that employs state-of-the-art techniques such as genome sequencing, expression microarray analysis, molecular population genetic analysis, relevant in vivo model systems, and analysis of host factors to gain new information about the molecular basis of infections caused by the human pathogenic bacterium group A Streptococcus (GAS) and Mycobacterium tuberculosis. All of the laboratory's work involves extensive collaboration with local, national, and international investigators with diverse areas of expertise.

One project is to identify key vaccine candidates against group A Streptococcus. This work is performed in collaboration with investigators in the private sector. GAS causes >700 million cases of human disease each year globally, yet no licensed vaccine is available, despite decades of study. Dr. Musser's goal is to use a multi-modality experimental strategy involving molecular dissection of the pathogen and host immunologic response, in vivo disease models, and analysis of clinical material to identify one or more protein antigens that protect humans against GAS pharyngitis and invasive disease.

A second project is designed to elucidate the molecular genetic events contributing to epidemics of GAS infection. This work is done in collaboration with several groups of investigators. The team uses a comprehensive, population-based sample of serotype M3 strains recovered over 16 years from patients with invasive infections as a model system. The project involves extensive (“deep”) comparative genome resequencing and genetic polymorphisms analysis using GAS strains from patients with well-defined clinical phenotype. The goal of this line of research is to understand precise temporal and geographic patterns of strain spread. In addition, the team seeks to define genetic polymorphisms and virulence regulatory circuits in the pathogen that influence clinical phenotype. Recent work has identified a novel virulence circuit involved in the pathogenesis of necrotizing fasciitis, also known as the “flesh-eating” disease. The research also has vaccine and public health implications.

Finally, Dr. Musser has a longstanding interest in the genetic epidemiology of human susceptibility to tuberculosis disease. Using a cohort of extensively defined human tuberculosis patients and controls, his team seeks to define human genetic factors that help to determine why some individuals get tuberculosis disease whereas others who have been exposed to the organism do not. A combination of single nucleotide polymorphism analysis and deep candidate gene resequencing is used, as well as other contemporary human genetic analysis methods.

Areas Of Expertise

Group A Streptococcus Mycobacterium tuberculosis
Education & Training

, University of Pennsylvania Health System
, University of Rochester

Intergenic variable-number tandem-repeat polymorphism upstream of rocA alters toxin production and enhances virulence in Streptococcus pyogenes
Zhu, L, Olsen, RJ, Horstmann, N, Shelburne, SA, Fan, J, Hu, T & Musser, JM 2016, Infection and Immunity, vol 84, no. 7, pp. 2086-2093. DOI:

Integrating rapid diagnostics and antimicrobial stewardship in two community hospitals improved process measures and antibiotic adjustment time
Lockwood, AM, Perez, KK, Musick, WL, Ikwuagwu, JO, Attia, E, Fasoranti, OO, Cernoch, PL, Olsen, RJ & Musser, JM 2016, Infection Control and Hospital Epidemiology, vol 37, no. 4, pp. 425-432. DOI:

Structural and functional analysis of RopB: A major virulence regulator in Streptococcus pyogenes
Makthal, N, Gavagan, M, Do, H, Olsen, RJ, Musser, JM & Kumaraswami, M 2016, Molecular Microbiology, vol 99, no. 6, pp. 1119-1133. DOI:

Intergenic variable-number tandem-repeat polymorphism upstream of rocA alters toxin production and enhances virulence in Streptococcus pyogenes
Zhu, L, Olsen, RJ, Horstmann, N, Shelburne, SA, Fan, J, Hu, Y & Musser, JM 2016, Infection and Immunity, vol 84, no. 7, pp. 2086-2093.

Transcriptome remodeling contributes to epidemic disease caused by the human pathogen Streptococcus pyogenes
Beres, SB, Kachroo, P, Nasser, W, Olsen, RJ, Zhu, L, Flores, AR, de la Riva, I, Paez-Mayorga, J, Jimenez, FE, Cantu, C, Vuopio, J, Jalava, J, Kristinsson, KG, Gottfredsson, M, Corander, J, Fittipaldi, N, Di Luca, MC, Petrelli, D, Vitali, LA, Raiford, A, Jenkins, L & Musser, JM 2016, mBio, vol 7, no. 3, e00403-16. DOI:

Musser et al. Reply to “emergence of the same successful clade among distinct populations of emm89 streptococcus pyogenes in multiple geographic regions”
Musser, JM, Zhu, L, Olsen, RJ & Nasser, W 2015, mBio, vol 6, no. 6, e01838-15. DOI:

Adhesin competence repressor (AdcR) from Streptococcus pyogenes controls adaptive responses to zinc limitation and contributes to virulence
Sanson, M, Makthal, N, Flores, AR, Olsen, RJ, Musser, JM & Kumaraswami, M 2015, Nucleic Acids Research, vol 43, no. 1, pp. 418-432. DOI:

A molecular trigger for intercontinental epidemics of group A Streptococcus
Zhu, L, Olsen, RJ, Nasser, W, Beres, SB, Vuopio, J, Kristinsson, KG, Gottfredsson, M, Porter, AR, DeLeo, FR & Musser, JM 2015, The Journal of clinical investigation, vol 125, no. 9, pp. 3545-3559. DOI:

Molecular pathogenesis lessons from the world of infectious diseases research
Musser, JM & Deleo, FR 2015, American Journal of Pathology, vol 185, no. 6, pp. 1502-1504. DOI:

Comparative whole genome sequencing of community-associated methicillin-resistant Staphylococcus aureus sequence type 8 from primary care clinics in a Texas community
Lee, GC, Long, SW, Musser, JM, Beres, SB, Olsen, RJ, Dallas, SD, Nunez, YO & Frei, CR 2015, Pharmacotherapy, vol 35, no. 2, pp. 220-228. DOI:

Improving positive blood culture removal time significantly decreases total processing time
Salazar, E, Divatia, M, Cernoch, PL, Olsen, RJ, Long, SW, Land, GA, Davis, JR & Musser, JM 2015, Archives of Pathology and Laboratory Medicine, vol 139, no. 2, pp. 199-203. DOI:

The majority of 9,729 group A streptococcus strains causing disease secrete SpeB cysteine protease: Pathogenesis implications
Olsen, RJ, Raghuram, A, Cantu, C, Hartman, MH, Jimenez, FE, Lee, S, Ngo, A, Rice, KA, Saddington, D, Spillman, H, Valson, C, Flores, AR, Beres, SB, Wesley Long, S, Nasser, W & Musser, JM 2015, Infection and Immunity, vol 83, no. 12, pp. 4750-4758. DOI:

A single amino acid replacement in the sensor kinase lias contributes to a carrier phenotype in group a streptococcus
Flores, AR, Jewell, BE, Yelamanchili, D, Olsen, RJ & Musser, JM 2015, Infection and Immunity, vol 83, no. 11, pp. 4237-4246. DOI:

Phosphorylation events in the multiple gene regulator of group A Streptococcus significantly influence global gene expression and virulence
Sanson, M, Makthal, N, Gavagan, M, Cantu, C, Olsen, RJ, Musser, JM & Kumaraswami, M 2015, Infection and Immunity, vol 83, no. 6, pp. 2382-2395. DOI:

Haemagglutinin mutations and glycosylation changes shaped the 2012/13 influenza A(H3N2) epidemic, Houston, Texas
Stucker, KM, Schobel, SA, Olsen, RJ, Hodges, HL, Lin, X, Halpin, RA, Fedorova, N, Stockwell, TB, Tovchigrechko, A, Das, SR, Wentworth, DE & Musser, JM 2015, Eurosurveillance, vol 20, no. 18.

Natural variant of collagen-like protein a in serotype M3 group a Streptococcus increases adherence and decreases invasive potential
Flores, AR, Jewell, BE, Versalovic, EM, Olsen, RJ, Bachert, BA, Lukomski, S & Musser, JM 2015, Infection and Immunity, vol 83, no. 3, pp. 1122-1129. DOI:

PBP2a mutations causing high-level ceftaroline resistance in clinical methicillin-resistant Staphylococcus aureus isolates
Long, SW , Olsen, RJ, Mehta, SC, Palzkill, T, Cernoch, PL, Perez, KK, Musick, WL, Rosato, AE & Musser, JM 2014, Antimicrobial Agents and Chemotherapy, vol 58, no. 11, pp. 6668-6674. DOI:

Precisely modulated pathogenicity island interference with late phage gene transcription
Ram, G, Chen, J, Ross, HF, Novick, RP & Musser, JM 2014, Proceedings of the National Academy of Sciences of the United States of America, vol 111, no. 40, pp. 14536-14541. DOI:

Absence of Patient-to-Patient intrahospital transmission of staphylococcus aureus as determined by Whole-Genome sequencing
Wesley Long, S , Beres, SB , Olsen, RJ & Musser, JM 2014, mBio, vol 5, no. 5, e01692-1. DOI:

Molecular characterization of an invasive phenotype of group a streptococcus arising during human infection using whole genome sequencing of multiple isolates from the same patient
Flores, AR, Sahasrabhojane, P, Saldaña, M, Galloway-Peña, J, Olsen, RJ, Musser, JM & Shelburne, SA 2014, Journal of Infectious Diseases, vol 209, no. 10, pp. 1520-1523. DOI: