About

Julie Parsonnet is a professor in the Department of Medicine specializing in Infectious Diseases at Stanford University. Her work focuses on infectious diseases, contributing to the understanding and treatment of various infectious conditions. As a faculty member within the Stanford Program in Human Biology, she is involved in interdisciplinary research and education related to health and disease. Her role includes advancing knowledge in infectious diseases through research and teaching, supporting the interdepartmental undergraduate Program in Human Biology.

Research topics

• Medicine
• Internal medicine
• Immunology
• Pathology
• Biology
• Environmental health
• Microbiology
• Virology
• Demography
• Pediatrics
• Genetics
• Endocrinology
• Biochemistry
• Bioinformatics
• Obstetrics
• Physiology

Selected publications

• P-1746. Use of Intrathecal Amphotericin for Coccidioidal Meningitis

  Open Forum Infectious Diseases · 2026-01-01

  articleOpen accessSenior author

  Abstract Background Cases of coccidioidomycosis are increasing dramatically in the U.S. The utility of intrathecal (IT) amphotericin in treating coccidioidal meningitis (CM) in the era of azole therapy is unknown. We sought to understand how IT therapy is associated with mortality.1A:Patients Receiving IT Amphotericin, by Quarter, From Time of Diagnosis1B:Patients NOT Receiving IT Amphotericin, By Quarter, from Time of Diagnosis Methods We conducted a retrospective chart review of adult patients with laboratory-proven CM seen at Stanford Hospital and Clinics by an Infectious Diseases physician from 2008-2023.Table 1:Baseline demographics and CM treatmentsTable 2:Cox Proportional Hazard Model for Mortality Results 57 patients met inclusion criteria. All patients received azole therapy. Twenty-seven of those patients (47.4%) additionally received IT amphotericin. Patients receiving IT therapy had higher rates of IV amphotericin use (88.9% vs. 56.7%, p = 0.02) and corticosteroid use (51.9% vs. 26.7%, p = 0.09), and higher median therapeutic switches per year (0.84 vs. 0.44, p = 0.01). An unadjusted Kaplan-Meier curve demonstrated a five-year mortality rate of 26.7% in the IT amphotericin group, compared to 6.7% in non-receiver group, p = 0.28. A Cox regression revealed that older age at diagnosis (HR 1.07, 95% CI 1.03-1.11), receipt of IT amphotericin (HR 13.9, 95% CI 1.93-100.48), and corticosteroid use (HR 8.3, 95% CI 1.92-35.4) were significantly associated with mortality, with a significant interaction between IT amphotericin and corticosteroids (interaction HR 0.14, 95% CI 0.02-0.97). Conclusion Patients who received IT amphotericin had higher mortality rates than those who did not, likely reflecting disease refractory to treatment. More therapies are needed for those who have disease progression on azole therapy. Disclosures All Authors: No reported disclosures

  PublisherDOI

• <i>Helicobacter pylori</i> Screen-and-Treat Programs for Gastric Cancer Prevention — IARC Working Group Report

  New England Journal of Medicine · 2026-03-11 · 1 citations

  article
  PublisherDOI

• Flush with data: harnessing emergency department wastewater as an innovative approach for surveillance of infectious diseases

  American Journal of Epidemiology · 2026-01-27 · 1 citations

  article

  Wastewater surveillance was widely adopted during the COVID-19 pandemic, where it proved useful in providing timely, actionable public health information. However, reliance on data from large wastewater treatment plants can be inadequate when rapid, local insights are needed. In this article, we propose integrating routine wastewater surveillance for transmissible infectious diseases within United States emergency department settings. Monitoring wastewater from the emergency department is a promising innovation which could allow for more rapid generation of actionable data, deepen our understanding of community-level infectious disease burden, and better inform public health efforts.

  PublisherDOI

• Pelayo Correa, MD, FAACR: In Memoriam (1927–2025)

  Cancer Epidemiology Biomarkers & Prevention · 2026-01-12

  article

  Pelayo Correa, distinguished pathologist-epidemiologist, visionary cancer researcher, and magnanimous teacher, is one of the most influential figures in modern cancer epidemiology and gastrointestinal pathology. Over a career spanning more than five decades, he transformed global understanding of gastric carcinogenesis, pioneered population-based cancer surveillance in Latin America, and helped shape epidemiology as an integrative, etiology-driven science. Dr. Correa was the founding editor-in-chief of Cancer Epidemiology, Biomarkers & Prevention (CEBP). As Dr. Fredrick Li acknowledged (1), Dr. Correa labored tirelessly to establish CEBP as a premier cancer subspecialty journal.Fifty years ago, Dr. Correa described in The Lancet (2) the multistep progression from chronic gastritis to intestinal-type gastric cancer, universally known as the Correa cascade. Helicobacter pylori’s link to chronic gastritis and peptic ulcer disease (3) and the early epidemiologic associations between the bacterium and gastric cancer (4) provided strong pathogenic support for the Correa cascade. This model revealed gastric cancer as the outcome of a gradual process, guiding population screening and linking pathology with epidemiology. Half a century later, it remains a cornerstone of gastric cancer research.Dr. Correa grew up in Sonsón, Colombia, earning his MD from the Universidad de Antioquia in Medellin. More interested in disease causation than in individual patient care, he pursued pathology, studying regional cancer patterns. His pathology residency at Emory University solidified his lifelong focus on understanding cancer pathogenesis.Upon returning to Colombia, Dr. Correa joined the Universidad del Valle in Cali, where the city’s pathology laboratory enabled the study of population-level cancer patterns. In 1961, his data attracted the attention of Dr. William Haenszel, director of the Biometry Branch of the US National Cancer Institute (NCI), National Institutes of Health (NIH). Drs. Correa and Haenszel started a fruitful collaboration that led to the foundation of the Cali Cancer Registry, the longest-running population-based registry in Latin America.In 1970, Dr. Correa joined the NCI Intramural Program as a visiting scientist and, in 1974, began a long tenure at Louisiana State University (LSU) Medical Center. Throughout, he continued his collaborations in Colombia. His landmark 1975 article (2) describing the stepwise progression to gastric adenocarcinoma redefined the field. This work documented a decades-long progression of the gastric mucosa from normal through atrophic gastritis, intestinal metaplasia, dysplasia, and ultimately intestinal-type gastric cancer. Based on his observation of geographic differences in rates of gastric cancer in Colombia, Dr. Correa initially posited that diet, specifically high intake of nitrates and salt and low intake of dietary antioxidants, precipitated gastric preneoplastic changes. These important findings led to the NCI Program Project on gastric cancer etiology that was continuously funded beginning in 1980. Part of this NIH grant funded the Chemoprevention Trial, which provides strong, long-term evidence that H. pylori eradication can meaningfully slow or reverse the progression of precancerous gastric lesions (5).Dr. Correa served as a professor of pathology at LSU for over 40 years, earning the distinguished rank of Boyd Professor in 1996. After Hurricane Katrina caused irreparable damage to his laboratory, Dr. Correa’s group joined the Department of Gastroenterology led by Dr. Richard Peek at Vanderbilt University Medical Center, where he was able to rebuild and expand his important work. At Vanderbilt, Dr. Correa was named the first holder of the Anne Potter Wilson Endowed Chair in Cancer Research.Dr. Correa authored more than 600 publications. His many honors include the International Agency for Research on Cancer Medal of Honor, the American Association for Cancer Research (AACR)–American Cancer Society Award for Research Excellence in Cancer Epidemiology and Prevention, the AACR Jane Cooke Wright Lectureship, the American Gastroenterological Association Distinguished Achievement Award, the Marshall and Warren Medal by the European Helicobacter and Microbiota Study Group, and the Distinguished Achievement Award from the American Society of Preventive Oncology. In 1994, Dr. Correa became a Fellow of the American Association for the Advancement of Science. In October 2006, Dr. Correa presented at the NIH Director’s Wednesday Afternoon Lecture Series. He was elected a Fellow of the AACR Academy in 2025. In addition, he served on the US President’s Cancer Panel and the National Cancer Advisory Board, highlighting his leadership in national cancer research policy.Dr. Correa valued intellectual honesty, inculcated by his mentor Dr. Alfredo Correa-Henao, and credited Dr. Haenszel as his greatest professional influence. He admired Dr. (Sir) Richard Doll and acknowledged the influence of leading US epidemiologists, including Drs. Joseph Fraumeni, Jr.; Abraham Lilienfeld; and Brian MacMahon. As a collaborative “etiologist,” he worked across disciplines to understand why diseases occur. Although Dr. Correa celebrated epidemiology’s achievements, he also warned against its fragmentation into overly mathematical or political branches. He viewed etiologic research as inherently team-based, valuing the contributions of individuals from different disciplines. He urged the field to remain etiology-driven and practical, advising future researchers to follow their curiosity while upholding rigor and independent thinking. Until his last days, he maintained a keen interest in the societal and historical determinants of health, always seeking to understand the root causes of disease.Despite the numerous recognitions and distinctions earned throughout his career, Dr. Correa remained modest and unassuming. He was known for his warmth, selfless nature, work ethic, and rigorous inquiry. Dr. Correa described himself as a workaholic. Nevertheless, his greatest joy remained his family. He enjoyed listening to tango music and singing along with it. Those left to cherish Dr. Correa’s memory are his daughter, sons, daughters-in-law, son-in-law, grandchildren, and great-grandchildren.Dr. Correa’s contributions have indelibly shaped cancer epidemiology, pathology, and global cancer control. Through foundational concepts, pioneering population-based cancer registries, and decades of etiologic research, he transformed the understanding of gastric cancer and inspired generations of scientists worldwide.His legacy endures in the multitude of students and colleagues he mentored and the scientific advances rooted in his curiosity and unwavering commitment to understanding the causes of cancer.This obituary is partially based on Dr. Correa’s own words during an interview with Dr. Elizabeth Fontham (6). Along with her, we are a group of female scientists who received invaluable mentorship, support, and guidance from Dr. Correa at different stages of our careers. It is remarkable to note that when many scientific fields have been characterized by male-dominated cultures, Dr. Correa actively welcomed many female mentees and collaborators. He will be profoundly missed by us and all those who had the privilege of knowing and working with him.

  PublisherDOI

• Pilot ED Wastewater Surveillance During the 2024-2025 Respiratory Virus Season

  JAMA Network Open · 2026-01-22

  articleOpen access

  This cross-sectional study compares emergency department (ED) wastewater surveillance for prevalence of respiratory viral pathogens with clinical testing trends at 2 urban US hospitals during the 2024-2025 respiratory virus season.

  PublisherOA PDFDOI

• Dialysis Facility Closures in the US From 2018 to 2024: A Serial Cross-Sectional Study

  American Journal of Kidney Diseases · 2026-03-21 · 1 citations

  article
  PublisherDOI

• Time of Day of Sars-Cov-2 Vaccination and Antibody Response in Patients Receiving Dialysis

  SSRN Electronic Journal · 2025-01-01

  preprintOpen access
  PublisherDOI

• P-492. Quantification of HIV Shedding in Viremic Patients

  Open Forum Infectious Diseases · 2025-01-29

  articleOpen accessSenior author

  Abstract Background Identifying pockets of undiagnosed HIV is a critical step in the U.S. Ending the HIV Epidemic (EHE). Wastewater-based epidemiology represents a novel way to build agnostic population-level data about disease distribution. We detected HIV virus in two sewersheds in Northern California. We are now conducting a study to measure how much HIV virus is shed into urine and stool, to better estimate cases represented by wastewater detection. HIV-1 RNA Detected in Concentrated Urine Methods We are recruiting participants from HIV clinics in San Mateo and Santa Clara Counties. Patients must be 18 years or older with HIV-1 viral load of &amp;gt;10,000 copies/ml at the time of recruitment. Subjects are asked to provide 5 weekly self-collected blood (Tasso), urine, and stool samples. The plasma is analyzed by established HIV-1 RNA quantitative PCR techniques. Nucleic acids from urine, concentrated (centrifuged) urine, and stool are suspended in DNA/RNA Shield, then extracted using the ZymoBIOMICS DNA/RNA Miniprep Kit (ZymoBIOMICS #R2002). HIV genome-specific primers target the Long Terminal Repeat (LTR) region of the HIV-1 genome. Droplets for digital droplet PCR are generated using the AutoDG Automated Droplet Generator. Reverse transcriptase PCR, which quantifies RNA and DNA combined, and direct PCR, which quantifies DNA, is then carried out with the Mastercycler Pro. Thresholding is performed using QX Manager Software. HIV-1 RNA Detected in Stool Results Two patients have been enrolled to date. Patient 1 was started on antiretroviral therapy after the first sample was obtained; Patient 2 was started on antiretroviral therapy 10 days before the first sample was collected. HIV-1 RNA was found in 87.5% (7/8) of concentrated urine samples, including 85.7% (6/7) of samples obtained while on ART (Table 1). Among stool samples, 25.0% (2/8) yielded HIV RNA, but only 14.3% (1/7) of those obtained on ART (Table 2). Nucleic acids were not detected in unconcentrated urine. Plasma viral load testing is pending, so only the initial clinical HIV-1 viral loads at enrollment are shown. Conclusion HIV-1 RNA is present in concentrated urine but also in stool samples of viremic patients, even up to five weeks after initiation of ART. When the study is complete, our results will bolster how to interpret HIV-1 detected in wastewater. Disclosures All Authors: No reported disclosures

  PublisherOA PDFDOI

• Flagellin in the human gut microbiome is a diet-adjustable adjuvant for vaccination

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-02-24 · 1 citations

  preprintOpen access

  ABSTRACT The intestinal microbiota is thought to modulate immune responsiveness to vaccines. Human studies on this topic, however, have yielded inconsistent results 1,2 . We hypothesized that the microbiome would influence innate immune responses, and thus vaccine reactogenicity, more directly than vaccine immunogenicity. To test this, we established the µHEAT (Microbial-Human Ecology And Temperature) study, which longitudinally profiled the fecal microbiota, oral body temperature and serum antibody responses of 171 healthy adults (18-40 years old) before and after vaccination for SARS-CoV-2. Increased temperature after vaccination (ΔT) was associated with habitual diet and with baseline metabolic and immune markers. The microbiomes of ΔT-high (ΔT hi ) participants were characterized by high expression of flagellin and an overabundance of the flagellated bacterium Waltera . Fecal samples from ΔT hi participants induced more inflammation in human cells and stronger post-vaccine temperature responses in mice compared to ΔT lo samples, suggesting a causal role for the microbiome. Moreover, Waltera flagellin replicated the inflammatory phenotypes in vitro and was modulable via a dietary additive. Overall, these data suggest that flagellin from the gut microbiome stimulates innate immunity and vaccine reactogenicity, and that this axis can be manipulated via diet. These findings have implications for improving human vaccine tolerance and immunogenicity.

  PublisherOA PDFDOI

• Influence of environmental exposures on T follicular helper cell function and implications on immunity: a comparison of Bangladeshi and American children

  mBio · 2025-03-10 · 1 citations

  articleOpen access

  ABSTRACT T follicular helper (Tfh) cells are crucial for B cell activation and subsequent antibody production. This functionality is influenced by surface markers such as CD40L, a costimulatory factor which promotes B cell activation, and CD57, which is a well-known marker of senescence. This study examined age-specific differences in Tfh cell function in Bangladeshi and American children. At age two, Bangladeshi children displayed impaired CD40L upregulation and significant CD57 downregulation upon stimulation. These patterns, not observed in American children of the same age, suggested an exhaustion-like phenotype potentially driven by environmental factors. Random forest and generalized estimating equations (GEE) modeling was used to analyze predictors of Tfh cell response to stimulation. Days since the last antibiotic treatment, total antibiotic treatments, diarrheal episodes, and malnutrition were identified as variables that significantly impacted the Tfh response to stimuli. To assess Tfh cell ability to promote antibody responses, we correlated Tfh functionality with antibody concentration post-vaccination and in response to infection with Cryptosporidium , an endemic apicomplexan parasite. Increased CD40L expression upon stimulation correlated positively with anti-Poliovirus type 2/3 neutralizing antibody and anti-Cp17 (a Cryptosporidium sporozoite antigen) IgA concentrations. In contrast, increased CD57 expression was significantly correlated with decreased anti-Cp17 IgA. This indicates that an activation-supportive phenotype (CD40L+) may be more effective in promoting immunity than a senescent phenotype (CD57+). Together, these findings suggest that early-life environmental exposures may program Tfh cell functionality, impacting immune response potential in settings with high pathogen exposure. IMPORTANCE T follicular helper (Tfh) cells are upstream mediators that shape the humoral immune response to specific antigens. The generation of an effective memory response to infection is vital to prevent subsequent reinfections. However, in areas with high burdens of exposure to infections, such as the urban community from Bangladesh studied here, children are consistently exposed to inflammatory pathogens. Specific environmental exposures significantly influenced Tfh cell activation and senescence phenotypes. Additionally, Tfh cell responses correlated with antibody concentrations following vaccination or infection, indicating that environmental factors may play a critical role in shaping effective immunity in early childhood.

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Recent grants

• NIH Grant R01CA055764

  NIH · $679k · 1995

• NIH Grant R01DK053689

  NIH · $1.8M · 2008

• Applied Genomics in Infectious Diseases

  NIH · $7.4M · 1995–2027

• NIH Grant R01CA095946

  NIH · $350k · 2007

• NIH Grant R03CA103492

  NIH · $158k · 2006

Frequent coauthors

• Catherine Ley

  Stanford University

  97 shared

• Jeannette Guarner

  Emory University

  68 shared

• Alejandro Mohar

  Instituto Nacional de Cancerología

  68 shared

• David Halperin

  National Patient Safety Foundation

  67 shared

• Roberto Herrera‐Goepfert

  Instituto Nacional de Cancerología

  65 shared

• Luz Helena Gutierrez Sanchez

  University of Alabama at Birmingham

  63 shared

• Philip A. Gruppuso

  Brown University

  37 shared

• Susan Pross

  University of South Florida

  36 shared

Education

• Ph.D., Microbiology and Immunology

  Stanford University

  1985

• M.S., Microbiology and Immunology

  Stanford University

  1981

• B.S., Microbiology

  University of California, Berkeley

  1977