Our Research

Streptococci are Gram-positive bacteria that commonly live as part of the human microbiota, especially in mucosal sites such as the gastrointestinal and urogenital tracts. In most people these organisms are commensals, but under certain conditions they can transition from commensal to pathogenic, causing invasive diseases.

A major clinical problem is mucosal colonization of the female reproductive and urinary tracts. Colonization can be asymptomatic, however this creates a reservoir for ascending infection, inflammation, and transmission. Importantly, Group B Streptococcus (Streptococcus agalactiae; GBS) can be transmitted from mother to infant during birth, placing neonates at risk for severe outcomes such as sepsis and meningitis. Group A Streptococcus (Streptococcus pyogenes; GAS) is more commonly known for pharyngitis and skin infections, but it can also cause severe gynecologic and postpartum infections, however, the  factors responsible for the bacteria persistence and disease progression are not well defined.

Our lab studies how streptococci interact with mucosal tissues and the immune system, with emphasis on how bacterial surface proteins drive adherence, persistence, and immune evasion. We use bacterial genetics, molecular microbiology, cell and tissue-based assays, and murine models to define mechanisms at the host–pathogen interface and to develop tract-relevant prevention strategies, including vaccines and non-antibiotic anti-colonization approaches.

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Group B Streptococcus infection of the female reproductive tract

GBS colonizes the urogenital tract in healthy men and women, however, maternal colonization is a key risk factor for vertical transmission and neonatal disease.

Our long-term goal is to identify conserved GBS virulence factors that can be leveraged for vaccine development and/or other anti-adhesive drugs to prevent maternal colonization and reduce neonatal morbidity associated with GBS.

Current Research Projects

Defining conserved surface proteins that promote vaginal colonization and immune evasion

We focus on highly conserved GBS proteins such as C5a peptidase (ScpB) and BvaP, which are present across sequenced strains but remain incompletely characterized. We test the hypothesis that specific domains within these proteins drive mucosal colonization and help GBS resist immune-mediated clearance.

Evaluating vaccine potential of conserved antigens

We assess whether immunization with ScpB provides protection during GBS infection in murine models, with the goal of identifying antigens that support broadly effective vaccine and anti-adhesin strategies.

Group A Streptococcus infection of the female reproductive tract and nasopharynx

GAS is widely known to be associated with pharyngitis and skin/soft tissue infections, however, the bacteria can also cause severe gynecologic and postpartum disease.

The bacterial and host factors that enable GAS persistence, ascending infection, and mucosal immune modulation in tract-specific environments are poorly defined. As such, we aim to identify and characterize the mechanistic parameters required for persistent infection in mucosal tissues.

Current Research Projects

Establish female reproductive system infection models and colonization maps

We develop and optimize murine models for vaginal ascending infection. We quantify GBS bacteria burden and spatial distribution across the vagina, cervix, and uterus.

Identifying GAS factors required for mucosal adherence and immune evasion

We test candidate GAS surface and secreted proteins for roles in persistence and dissemination, specifically, the mechanisms that alter neutrophil recruitment and function and modulate complement and antibody-dependent clearance under tract-relevant conditions. GAS infection of the female urinary tract and non-antibiotic prevention is an important cause of bacteriuria and urinary tract infection in healthy individuals, during pregnancy in addition to the elderly. Because antibiotic stewardship is especially important in maternal health, we are interested in non-antibiotic strategies that reduce urinary tract colonization and promote clearance.

Identifying active cranberry phytocompounds that inhibit GBS urinary colonization

With an increase prevalence and breadth of antibiotic resistance, there is an increased cry for remedial strategies against UTI other than antibiotics. Cranberry is widely used for UTI prevention, but the active components and their efficacy against GAS are not well defined. We fractionate cranberry preparations, identify candidate compounds using LC-MS, and test activity against GAS growth and colonization phenotypes.

Testing efficacy and mechanism in vivo

Using urinary tract colonization models, we evaluate whether identified compounds reduce adherence, invasion, and biofilm-associated persistence and whether they enhance immune-mediated killing. We also assess durability across diverse GAS isolates.

Group B Streptococcus (GBS) in the urinary tract and non-antibiotic prevention

GBS colonizes the female urinary tract asymptomatically, yet in some individuals it contributes to recurrent bacteriuria, symptomatic urinary tract infection, and complications during pregnancy.

Our long-term goal is to define the bacterial and host factors that permit GBS persistence in the urinary tract and to develop non-antibiotic strategies that reduce colonization, limit recurrence, and preserve the resident microbiota. Particularly, we are focused on dissecting the phytocompounds in Cranberry, to determine the antibacterial fraction for industrial and pharmaceutical drug development.

Current Research Projects

Defining conserved GBS factors that promote urinary tract colonization

We investigate conserved GBS surface-associated and secreted factors that support adhesion to uroepithelial cells, persistence in urine, and resistance to host immune response. We test the hypothesis that specific bacterial determinants enable GBS to establish and maintain urinary tract colonization under physiologically and biochemical relevant conditions.

Evaluating non-antibiotic approaches to prevent GBS persistence

We assess non-antibiotic prevention strategies, including anti-adhesive interventions, microbiota-informed approaches, and other methods that disrupt colonization without relying on conventional antibiotics. Our goal is to identify broadly effective prevention strategies that reduce urinary tract GBS burden while minimizing selective pressure for antimicrobial resistance.