Michael Wessels, MD
Senior Physician in Pediatrics, Division of Infectious Diseases
John F. Enders Professor of Pediatrics and Professor of Medicine (Microbiology), Harvard Medical School
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Michael Wessels, MD
Senior Physician in Pediatrics, Division of Infectious Diseases
John F. Enders Professor of Pediatrics and Professor of Medicine (Microbiology), Harvard Medical School
Medical Services
Languages
English
Education
Medical School
Duke University
1979
Durham
Internship
Internal Medicine
Beth Israel Deaconess Medical Center
1980
Boston
MA
Residency
Internal Medicine
Beth Israel Deaconess Medical Center
1982
Boston
MA
Fellowship
Beth Israel Deaconess Medical Center
1982
Boston
MA
Fellowship
Infectious Diseases
Brigham & Women's Hospital/Beth Israel Deaconess Medical Center
1985
Boston
MA
Certifications
American Board of Internal Medicine (General)
American Board of Internal Medicine (Infectious Diseases)
Professional History
Michael Wessels, MD, is a Senior Physician in Medicine of the Division of Infectious Diseases at Boston Children’s Hospital, John F. Enders Professor of Pediatrics, and Professor of Medicine (Microbiology) at Harvard Medical School. Dr. Wessels served as Chief of the Division of Infectious Diseases at Boston Children's Hospital from 2000 through 2018 and is a member of the clinical and research faculty.
He received his undergraduate education at Oberlin College, attended medical school at Duke University, and completed clinical training in medicine and Infectious Diseases in Harvard-affiliated programs. As a postdoctoral fellow with Dr. Dennis Kasper, Wessels characterized antigenic properties of group B streptococcal polysaccharides and described the synthesis and immunogenicity of polysaccharide-protein conjugate vaccines against this important neonatal pathogen.
His more recent work has identified novel virulence functions for a number of group A streptococcal products, notably the hyaluronic acid capsular polysaccharide and the bacterial toxins streptolysin O and NAD-glycohydrolase, and regulation of these and other virulence determinants by the CsrRS two component system. Wessels is a member of the American Society for Clinical Investigation, the Association of American Physicians, and the American Pediatric Society. He is a fellow of the Infectious Diseases Society of America and the American Academy of Microbiology.
Approach to Care
I began my career as a physician-scientist in internal medicine and infectious diseases at Beth Israel and Brigham and Women’s Hospitals. In addition to my clinical practice, I directed a research program focused on streptococcal infections at the Channing Laboratory, a research division of Brigham and Women’s Hospital. From 2000 through 2018, I served as the Chief of the Division of Infectious Diseases at Boston Children’s Hospital, where I have had the privilege of participating in patient care, recruiting talented faculty and trainees, and continuing research on the molecular basis of streptococcal infections.
Publications
SLO co-opts host cell glycosphingolipids to access cholesterol-rich lipid rafts for enhanced pore formation and cytotoxicity. View Abstract
Bacterial Sphingolipids Exacerbate Colitis by Inhibiting ILC3-derived IL-22 Production. View Abstract
Interplay between human STING genotype and bacterial NADase activity regulates inter-individual disease variability. View Abstract
Streptococcus pyogenes Pharyngitis and Scarlet Fever View Abstract
Cell Wall and Surface Molecules of Streptococcus pyogenes: Capsule View Abstract
Streptococcus pyogenes can support or inhibit growth of Haemophilus influenzae by supplying or restricting extracellular NAD. View Abstract
Simultaneous Late, Late-Onset Group B Streptococcal Meningitis in Identical Twins. View Abstract
Structure of the Streptococcus pyogenes NAD+ Glycohydrolase Translocation Domain and Its Essential Role in Toxin Binding to Oropharyngeal Keratinocytes. View Abstract
Identification of Group A Streptococcus Genes Directly Regulated by CsrRS and Novel Intermediate Regulators. View Abstract
Improved transformation efficiency of group A Streptococcus by inactivation of a type I restriction modification system. View Abstract
RocA Binds CsrS To Modulate CsrRS-Mediated Gene Regulation in Group A Streptococcus. View Abstract
Streptolysin O Induces the Ubiquitination and Degradation of Pro-IL-1ß. View Abstract
Capsular Polysaccharide of Group A Streptococcus. View Abstract
Blocking Neuronal Signaling to Immune Cells Treats Streptococcal Invasive Infection. View Abstract
Binding of NAD+-Glycohydrolase to Streptolysin O Stabilizes Both Toxins and Promotes Virulence of Group A Streptococcus. View Abstract
Inhibition of Inflammasome-Dependent Interleukin 1ß Production by Streptococcal NAD+-Glycohydrolase: Evidence for Extracellular Activity. View Abstract
NAD+-Glycohydrolase Promotes Intracellular Survival of Group A Streptococcus. View Abstract
Pharyngitis and Scarlet Fever View Abstract
Cell Wall and Surface Molecules: Capsule View Abstract
Group A streptococcal bacteremia without a source is associated with less severe disease in children. View Abstract
Choosing an antibiotic for skin infections. View Abstract
Case records of the Massachusetts General Hospital. Case 6-2015. A 16-year-old boy with coughing spells. View Abstract
The human antimicrobial peptide LL-37 binds directly to CsrS, a sensor histidine kinase of group A Streptococcus, to activate expression of virulence factors. View Abstract
Streptolysin O and NAD-glycohydrolase prevent phagolysosome acidification and promote group A Streptococcus survival in macrophages. View Abstract
BsaB, a novel adherence factor of group B Streptococcus. View Abstract
Streptolysin O and its co-toxin NAD-glycohydrolase protect group A Streptococcus from Xenophagic killing. View Abstract
Vitamin D and the human antimicrobial peptide LL-37 enhance group a streptococcus resistance to killing by human cells. View Abstract
CsrRS and environmental pH regulate group B streptococcus adherence to human epithelial cells and extracellular matrix. View Abstract
Regulation and function of pilus island 1 in group B streptococcus. View Abstract
Signal transduction through CsrRS confers an invasive phenotype in group A Streptococcus. View Abstract
Clinical practice. Streptococcal pharyngitis. View Abstract
Streptolysin O inhibits clathrin-dependent internalization of group A Streptococcus. View Abstract
Inhibition of dendritic cell maturation by group A Streptococcus. View Abstract
CsrRS regulates group B Streptococcus virulence gene expression in response to environmental pH: a new perspective on vaccine development. View Abstract
Case records of the Massachusetts General Hospital. Case 2-2009. A 25-year-old man with pain and swelling of the right hand and hypotension. View Abstract
Induction of group A Streptococcus virulence by a human antimicrobial peptide. View Abstract
PerR confers phagocytic killing resistance and allows pharyngeal colonization by group A Streptococcus. View Abstract
Burden and economic cost of group A streptococcal pharyngitis. View Abstract
Variation in the group B Streptococcus CsrRS regulon and effects on pathogenicity. View Abstract
Mg(2+) signalling defines the group A streptococcal CsrRS (CovRS) regulon. View Abstract
The adenosine system selectively inhibits TLR-mediated TNF-alpha production in the human newborn. View Abstract
Innate immunity of the human newborn is polarized toward a high ratio of IL-6/TNF-alpha production in vitro and in vivo. View Abstract
Unique efficacy of Toll-like receptor 8 agonists in activating human neonatal antigen-presenting cells. View Abstract
Enhancement of streptolysin O activity and intrinsic cytotoxic effects of the group A streptococcal toxin, NAD-glycohydrolase. View Abstract
Changing epidemiology of acute rheumatic fever in the United States. View Abstract
The apoptotic response to pneumolysin is Toll-like receptor 4 dependent and protects against pneumococcal disease. View Abstract
Role of NADase in virulence in experimental invasive group A streptococcal infection. View Abstract
Genome analysis of multiple pathogenic isolates of Streptococcus agalactiae: implications for the microbial "pan-genome". View Abstract
Extracellular group A Streptococcus induces keratinocyte apoptosis by dysregulating calcium signalling. View Abstract
Streptolysin S. View Abstract
Structural and genetic diversity of group B streptococcus capsular polysaccharides. View Abstract
Cytolysin-dependent evasion of lysosomal killing. View Abstract
Regulation of virulence by a two-component system in group B streptococcus. View Abstract
Interaction between complement regulators and Streptococcus pyogenes: binding of C4b-binding protein and factor H/factor H-like protein 1 to M18 strains involves two different cell surface molecules. View Abstract
Selective impairment of TLR-mediated innate immunity in human newborns: neonatal blood plasma reduces monocyte TNF-alpha induction by bacterial lipopeptides, lipopolysaccharide, and imiquimod, but preserves the response to R-848. View Abstract
Critical role of the complement system in group B streptococcus-induced tumor necrosis factor alpha release. View Abstract
The CsrR/CsrS two-component system of group A Streptococcus responds to environmental Mg2+. View Abstract
Recognition of pneumolysin by Toll-like receptor 4 confers resistance to pneumococcal infection. View Abstract
Cytotoxic effects of streptolysin o and streptolysin s enhance the virulence of poorly encapsulated group a streptococci. View Abstract
Complete genome sequence and comparative genomic analysis of an emerging human pathogen, serotype V Streptococcus agalactiae. View Abstract
NAD+-glycohydrolase acts as an intracellular toxin to enhance the extracellular survival of group A streptococci. View Abstract
Group A Streptococcus tissue invasion by CD44-mediated cell signalling. View Abstract
Absence of a cysteine protease effect on bacterial virulence in two murine models of human invasive group A streptococcal infection. View Abstract
Regulation of capsule gene expression by group A Streptococcus during pharyngeal colonization and invasive infection. View Abstract
Functional analysis in type Ia group B Streptococcus of a cluster of genes involved in extracellular polysaccharide production by diverse species of streptococci. View Abstract
Human granulocytic ehrlichiosis presenting as facial diplegia in a 42-year-old woman. View Abstract
CD44 as a receptor for colonization of the pharynx by group A Streptococcus. View Abstract
Bacterial determinants of persistent throat colonization and the associated immune response in a primate model of human group A streptococcal pharyngeal infection. View Abstract
Characterization of the linkage between the type III capsular polysaccharide and the bacterial cell wall of group B Streptococcus. View Abstract
Regulation of virulence factor expression in group A streptococcus. View Abstract
Role of complement component C1q in the IgG-independent opsonophagocytosis of group B streptococcus. View Abstract
Measurement of human antibodies to type III group B Streptococcus. View Abstract
Safety and immunogenicity of capsular polysaccharide-tetanus toxoid conjugate vaccines for group B streptococcal types Ia and Ib. View Abstract
Identification of csrR/csrS, a genetic locus that regulates hyaluronic acid capsule synthesis in group A Streptococcus. View Abstract
Molecular analysis of the capsule gene region of group A Streptococcus: the hasAB genes are sufficient for capsule expression. View Abstract
Molecular analysis of the role of the group A streptococcal cysteine protease, hyaluronic acid capsule, and M protein in a murine model of human invasive soft-tissue infection. View Abstract
Antibody responses in invasive group B streptococcal infection in adults. View Abstract
Structural properties of group B streptococcal type III polysaccharide conjugate vaccines that influence immunogenicity and efficacy. View Abstract
Hyaluronic acid capsule modulates M protein-mediated adherence and acts as a ligand for attachment of group A Streptococcus to CD44 on human keratinocytes. View Abstract
Structure of the has operon promoter and regulation of hyaluronic acid capsule expression in group A Streptococcus. View Abstract
Biology of streptococcal capsular polysaccharides. View Abstract
Relative contributions of hyaluronic acid capsule and M protein to virulence in a mucoid strain of the group A Streptococcus. View Abstract
Hyaluronic acid capsule modulates interactions of group A streptococci with human epidermal keratinocytes. View Abstract
Glycolipid intermediates in biosynthesis of group B streptococcal capsular polysaccharide. View Abstract
Role of complement and complement receptor C1qR in the antibody-independent killing of group B streptococcus. View Abstract
Regulation of hyaluronic acid capsule production by the has operon promoter in group A streptococci. View Abstract
Biology of streptococcal capsular polysaccharides. View Abstract
Immune response to type III group B streptococcal polysaccharide-tetanus toxoid conjugate vaccine. View Abstract
Hyaluronic acid capsule and the role of streptococcal entry into keratinocytes in invasive skin infection. View Abstract
Hyaluronate capsule and surface M protein in resistance to opsonization of group A streptococci. View Abstract
Characterization of cpsF and its product CMP-N-acetylneuraminic acid synthetase, a group B streptococcal enzyme that can function in K1 capsular polysaccharide biosynthesis in Escherichia coli. View Abstract
Studies of group B streptococcal infection in mice deficient in complement component C3 or C4 demonstrate an essential role for complement in both innate and acquired immunity. View Abstract
Cloning, sequence analysis and expression of the group A streptococcal guaB gene encoding inosine monophosphate dehydrogenase. View Abstract
Immunogenicity and protective activity in animals of a type V group B streptococcal polysaccharide-tetanus toxoid conjugate vaccine. View Abstract
Identification of a gene similar to ABC transporters near the capsule synthesis region of the group A streptococcal chromosome. View Abstract
Characterization of the capsular polysaccharide genes of group B streptococci. View Abstract
Critical role of the group A streptococcal capsule in pharyngeal colonization and infection in mice. View Abstract
Characterization of CMP-N-acetylneuraminic acid synthetase of group B streptococci. View Abstract
Neonatal mouse protection against infection with multiple group B streptococcal (GBS) serotypes by maternal immunization with a tetravalent GBS polysaccharide-tetanus toxoid conjugate vaccine. View Abstract
Functional activity of antibodies to the group B polysaccharide of group B streptococci elicited by a polysaccharide-protein conjugate vaccine. View Abstract
Effects on virulence of mutations in a locus essential for hyaluronic acid capsule expression in group A streptococci. View Abstract
Stimulation of protective antibodies against type Ia and Ib group B streptococci by a type Ia polysaccharide-tetanus toxoid conjugate vaccine. View Abstract
Capsular polysaccharide regulates neutrophil complement receptor interactions with type III group B streptococci. View Abstract
The changing spectrum of group B streptococcal disease. View Abstract
Improving choice of prescribed antibiotics through concurrent reminders in an educational order form. View Abstract
Identification of cpsD, a gene essential for type III capsule expression in group B streptococci. View Abstract
Prevention of C3 deposition by capsular polysaccharide is a virulence mechanism of type III group B streptococci. View Abstract
Group B Streptococcus type II polysaccharide-tetanus toxoid conjugate vaccine. View Abstract
Group B streptococcal opacity variants. View Abstract
Identification of a genetic locus essential for capsule sialylation in type III group B streptococci. View Abstract
Effects of chain length on the immunogenicity in rabbits of group B Streptococcus type III oligosaccharide-tetanus toxoid conjugates. View Abstract
Development of a vaccine against group B Streptococcus. View Abstract
Hyaluronic acid capsule is a virulence factor for mucoid group A streptococci. View Abstract
The alpha-L-(1----2)-trirhamnopyranoside epitope on the group-specific polysaccharide of group B streptococci. View Abstract
Structural determination and immunochemical characterization of the type V group B Streptococcus capsular polysaccharide. View Abstract
Correct structure of repeating unit of group B Streptococcus type III capsular polysaccharide. View Abstract
Immunogenicity in animals of a polysaccharide-protein conjugate vaccine against type III group B Streptococcus. View Abstract
Changing surgical antimicrobial prophylaxis practices through education targeted at senior department leaders. View Abstract
An oligosaccharide-tetanus toxoid conjugate vaccine against type III group B Streptococcus. View Abstract
Molecular analysis of two group B streptococcal virulence factors. View Abstract
Definition of a bacterial virulence factor: sialylation of the group B streptococcal capsule. View Abstract
Effect of hospitalwide change in clindamycin dosing schedule on clinical outcome. View Abstract
Antibody recognition of the type 14 pneumococcal capsule. Evidence for a conformational epitope in a neutral polysaccharide. View Abstract
Isolation and characterization of type IV group B Streptococcus capsular polysaccharide. View Abstract
Reduction of incorrect antibiotic dosing through a structured educational order form. View Abstract
A model of high-affinity antibody binding to type III group B Streptococcus capsular polysaccharide. View Abstract
Transposon mutagenesis of type III group B Streptococcus: correlation of capsule expression with virulence. View Abstract
Structure and immunochemistry of an oligosaccharide repeating unit of the capsular polysaccharide of type III group B Streptococcus. A revised structure for the type III group B streptococcal polysaccharide antigen. View Abstract
Immunochemical analysis of the types Ia and Ib group B streptococcal polysaccharides. View Abstract
Molecular size affects antigenicity of type III, group B Streptococcus capsular polysaccharide. View Abstract
Selective alteration in high affinity agonist binding: a mechanism of beta-adrenergic receptor desensitization. View Abstract