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Craig E. Rubens, MD, PhD

Craig E. Rubens, MD, PhD

Infectious Disease

On staff since July 1984

Children's Title: Executive Director, Global Alliance to Prevent Prematurity and Stillbirth (GAPPS)

Academic Title: Affiliate Professor of Global Health, Affiliate Professor of Pediatrics, University of Washington School of Medicine

Research Center(s): Center for Global Infectious Disease Research, Center for Developmental Therapeutics

"When I had just started my pediatric residency, my first clinical rotation was in the neonatal intensive care unit. This was the same month my second child, Brandon, was born. I witnessed infants dying in their fathers' arms, due to infections and premature birth, and couldn’t help relate to the sense of loss and what it would mean to those families forever. I devoted my career at that point to understanding why infections during pregnancy and the first few months of life happened, how they led to disease like preterm birth and stillbirths, and set out to find out how best to stop these terrible outcomes from happening. Over the years, I have learned that the best solutions to provide outstanding patient care come from better knowledge generated by research and that answers to complex health issues rely on teamwork and collaboration at several levels to make an impact. "

Making a Difference


Board Certification(s)
Medical/Professional School
University of South Carolina School of Medicine, Columbia, Immunology and Microbiology
University of Washington, Seattle
Pediatrics, Children's Hospital and Regional Medical Center, Seattle
Clinical Interests

Prevention of Prematurity

Research Description

I have a long-standing research program on the molecular pathogenesis of bacterial perinatal infections. Group B streptococci (GBS) are a major cause of perinatal infections, including intrauterine infections, and pneumonia, sepsis and meningitis in newborn infants. Using this organism, I have explored how this pathogen causes disease using molecular techniques, cell, and animal models that emulate human reproductive infections during pregnancy and infection of the neonate during parturition. Molecular approaches are used to identify the genetic and biochemical basis of specific bacterial virulence traits?such as epithelial/endothelial cell entry and transcytosis, evasion of innate immune mechanisms by inhibiting complement activation and phagocytic uptake, and microbial survival in various host environments (bloodstream, reproductive system, and neonatal lung).

My laboratory pioneered genetic techniques to identify the genes and biosynthetic mechanisms important for the production of capsular polysaccharide and other virulence traits by GBS. Projects also include characterizing the early stages of bacterial pneumonia by investigating the host/pathogen interactions using genomic and proteomic techniques. This project characterizes the bacterial response to the lung airway, specific traits critical for microbial persistence in the face of lung innate immunity, and has begun to characterize the host airway proteome for the proteins and other factors that contribute to innate immune mechanisms.

Recently, my laboratory is developing a model to understand the mechanisms of infection-induced preterm labor and premature birth. This model explores how bacteria ascend in the female reproductive track to incite inflammation during pregnancy that leads to preterm labor and intra-amniotic infection. Insights from the above studies have begun to identify new means of preventing or treating pneumonia, preterm labor, perinatal bacterial infections, and improving reproductive outcomes.


Research Focus Area

Host: Pathogen Interaction

Awards and Honors

Award NameAward DescriptionAwarded ByAward Date
U.S. News Top DoctorU.S. News and World Report 2012


Global report on preterm birth and stillbirth (7 of 7): mobilizing resources to accelerate innovative solutions (Global Action Agenda).
BMC pregnancy and childbirth , 2010 Feb 23: S7
Global report on preterm birth and stillbirth (6 of 7): ethical considerations.
BMC pregnancy and childbirth , 2010 Feb 23: S6
Global report on preterm birth and stillbirth (5 of 7): advocacy barriers and opportunities.
BMC pregnancy and childbirth , 2010 Feb 23: S5
Global report on preterm birth and stillbirth (4 of 7): delivery of interventions.
BMC pregnancy and childbirth , 2010 Feb 23: S4
Global report on preterm birth and stillbirth (3 of 7): evidence for effectiveness of interventions.
BMC pregnancy and childbirth , 2010 Feb 23: S3
Global report on preterm birth and stillbirth (2 of 7): discovery science.
BMC pregnancy and childbirth , 2010 Feb 23: S2
Global report on preterm birth and stillbirth (1 of 7): definitions, description of the burden and opportunities to improve data.
BMC pregnancy and childbirth , 2010 Feb 23: S1
Staphylococcus aureus elicits marked alterations in the airway proteome during early pneumonia.
Infection and immunity , 2008 Dec: 5862-72
Characterization of the accessory Sec system of Staphylococcus aureus.
Journal of bacteriology , 2008 Sep: 6188-96
Host airway proteins interact with Staphylococcus aureus during early pneumonia.
Infection and immunity , 2008 Mar: 888-98
A streptococcal penicillin-binding protein is critical for resisting innate airway defenses in the neonatal lung.
Journal of immunology (Baltimore, Md. : 1950) , 2007 Sep 1: 3196-202
Structure of Streptococcus agalactiae serine/threonine phosphatase. The subdomain conformation is coupled to the binding of a third metal ion.
The FEBS journal , 2007 Jun: 3128-37
Structure of the Streptococcus agalactiae family II inorganic pyrophosphatase at 2.80 A resolution.
Acta crystallographica. Section D, Biological crystallography , 2007 Jun: 738-43
Staphylococcus aureus exploits cathelicidin antimicrobial peptides produced during early pneumonia to promote staphylokinase-dependent fibrinolysis.
The Journal of infectious diseases , 2007 May 1: 1365-72
Regulation of cytotoxin expression by converging eukaryotic-type and two-component signalling mechanisms in Streptococcus agalactiae.
Molecular microbiology , 2006 Nov: 941-57
Crystallization and preliminary crystallographic analysis of two Streptococcus agalactiae proteins: the family II inorganic pyrophosphatase and the serine/threonine phosphatase.
Acta crystallographica. Section F, Structural biology and crystallization communications , 2006 Sep 1: 891-4
Evidence for siderophore-dependent iron acquisition in group B streptococcus.
Molecular microbiology , 2006 Jan: 707-21
Genome analysis of multiple pathogenic isolates of Streptococcus agalactiae: implications for the microbial "pan-genome".
Proceedings of the National Academy of Sciences of the United States of America , 2005 Sep 27: 13950-5
Structural and genetic diversity of group B streptococcus capsular polysaccharides.
Infection and immunity , 2005 May: 3096-103
Construction and characterization of transposon TnphoZ for the identification of genes encoding exported proteins in Streptococcus agalactiae.
FEMS microbiology letters , 2004 Dec 15: 257-64
The NeuC protein of Escherichia coli K1 is a UDP N-acetylglucosamine 2-epimerase.
Journal of bacteriology , 2004 Feb: 706-12
Comparison of DNA dot blot hybridization and lancefield capillary precipitin methods for group B streptococcal capsular typing.
Journal of clinical microbiology , 2004 Jan: 146-50
MtaR, a regulator of methionine transport, is critical for survival of group B streptococcus in vivo.
Journal of bacteriology , 2003 Nov: 6592-9
The Delta subunit of RNA polymerase is required for virulence of Streptococcus agalactiae.
Infection and immunity , 2003 Jul: 4011-7
A eukaryotic type serine/threonine kinase and phosphatase in Streptococcus agalactiae reversibly phosphorylate an inorganic pyrophosphatase and affect growth, cell segregation, and virulence.
The Journal of biological chemistry , 2003 Apr 18: 14429-41
A novel streptococcal surface protease promotes virulence, resistance to opsonophagocytosis, and cleavage of human fibrinogen.
The Journal of clinical investigation , 2003 Jan: 61-70
Penicillin-binding proteins in Streptococcus agalactiae: a novel mechanism for evasion of immune clearance.
Molecular microbiology , 2003 Jan: 247-56
CpsK of Streptococcus agalactiae exhibits alpha2,3-sialyltransferase activity in Haemophilus ducreyi.
Molecular microbiology , 2002 Jul: 109-22
Identification of novel adhesins from Group B streptococci by use of phage display reveals that C5a peptidase mediates fibronectin binding.
Infection and immunity , 2002 Jun: 2869-76

Primary Office

Seattle Children's Met Park West
MPW 10 - GAPPS Program
1100 Olive Way - Suite 1000
Seattle, WA 98101

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