Dr. Dean Winslow specializes in infectious diseases and hospital-based internal medicine. He has practiced medicine for more than 40 years. Dr. Winslow has a special interest in bedside teaching of medical students, residents and fellows.

Clinical Focus

  • Infectious Disease
  • Hospital Medicine and Infectious Diseases

Academic Appointments

  • Professor - Med Center Line, Medicine

Administrative Appointments

  • Professoriate Appointment and Promotions Committee, Stanford University School of Medicine (2018 - Present)
  • Faculty, Bing Overseas Studies Program, University of Oxford, Stanford University (2017 - 2017)
  • Academic Physician-In-Chief, Stanford/ValleyCare, Stanford University School of Medicine (2015 - 2017)
  • Vice Chair, Department of Medicine, Stanford University School of Medicine (2015 - 2017)
  • Stanford Department of Medicine Core Faculty, Stanford University (2014 - Present)
  • Stanford Department of Medicine Professional Practice Evaluation Committee, Stanford University (2014 - Present)
  • Resident Fellow, Robinson House, Stanford University (2013 - 2017)
  • Clinician Educator Appointment and Promotions Committee, Stanford University (2004 - 2015)

Honors & Awards

  • Alwin C. Rambar-James B.D. Mark Award for Excellence in Patient Care, Stanford University School of Medicine (2019)
  • Society Citation, Infectious Diseases Society of America (2017)
  • Legion of Merit, Air Medal (3), Combat Action Medal, Afghanistan Campaign (2), Iraq Campaign (4), United States Air Force (2015)
  • David A. Rytand clinical teaching award, Department of Medicine, Stanford University (2014, 2015)
  • Award for Humanitarian Service to the People of Iraq, Iraqi Armed Forces (2008)
  • Humanitarian Service Award, American College of Physicians (2007)
  • George W. Bush Award- outstanding Air National Guard officer, Air Force Association (2006)
  • Malcom C.Grow Award - outstanding Air Force flight surgeon (ANG command), Society of USAF Flight Surgeons (1988)

Boards, Advisory Committees, Professional Organizations

  • Chair, Ethics and Conflict of Interest Committee, Infectious Diseases Society of America (2018 - Present)
  • Member, Sepsis Task Force, Infectious Diseases Society of America (2017 - Present)
  • Associate Editor, Diagnostic Microbiology and Infectious Disease (2014 - Present)
  • Chair, Standards and Practice Guidelines Committee, Infectious Diseases Society of America (2011 - 2017)
  • Associate Editor, Infectious Disease Alert (2005 - Present)
  • Editorial board, AIDS (London) (1993 - 2016)

Professional Education

  • Distinguished graduate, United States Air Force School of Aerospace Medicine, Flight surgeon (1983)
  • Graduate, United States Air Force, Air War College (2007)
  • Medical Education:Thomas Jefferson University (1976) PA
  • Fellowship:Oschner Foundation Hospital (1981) LA
  • Residency:Christiana Health Care Medical Center of Delaware (1979) DE
  • Board Certification: Infectious Disease, American Board of Internal Medicine (1982)
  • Board Certification: Internal Medicine, American Board of Internal Medicine (1979)

Community and International Work

  • Air National Guard, Afghanistan, Iraq


    Military Medicine

    Partnering Organization(s)


    Populations Served

    military and civilian



    Ongoing Project


    Opportunities for Student Involvement


  • The Eagle Fund, International


    Humanitarian aid

    Partnering Organization(s)

    Silicon Valley Community Foundation

    Populations Served

    currently focusing on Syrian and Iraqi refugees



    Ongoing Project


    Opportunities for Student Involvement


All Publications

  • Reply to Al-Hasan and Justo. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America Kalil, A. C., Gilbert, D. N., Winslow, D. L., Masur, H., Klompas, M. 2019; 68 (8): 1432

    View details for PubMedID 30102343

  • Acute Kidney Injury Due to Systemic Absorption of Antibiotics Impregnated in a Bone Cement Spacer: An Underrecognized Complication of a Common Intervention INFECTIOUS DISEASES IN CLINICAL PRACTICE Nakasone, T. S., Multani, A., Chary, A., Renault, C. A., Winslow, D. L. 2018; 26 (5): 291–93
  • Seroconversion on preexposure prophylaxis AIDS Rizzardini, G., Winslow, D. L. 2018; 32 (9): 1199–1200

    View details for PubMedID 29746319

  • Infectious Diseases Society of America (IDSA) POSITION STATEMENT: Why IDSA Did Not Endorse the Surviving Sepsis Campaign Guidelines CLINICAL INFECTIOUS DISEASES Kalil, A. C., Gilbert, D. N., Winslow, D. L., Masur, H., Klompas, M., IDSA Sepsis Task Force 2018; 66 (10): 1631–35


    IDSA did not endorse the 2016 Surviving Sepsis Campaign Guidelines despite being represented in the working group that drafted the guidelines document. Leadership from the IDSA, the Surviving Sepsis Campaign Guidelines, and the Society of Critical Care Medicine had numerous amicable discussions primarily regarding the bolded, rated guidelines recommendations. Our societies had different perspectives, however, regarding the interpretation of the major studies that informed the guidelines' recommendations, thus leading us to different conclusions and different perspectives on the recommendations. IDSA consequently elected not to endorse the guidelines. IDSA nonetheless hopes to be able to continue collaborating with the Surviving Sepsis Campaign and the Society of Critical Care Medicine to resolve our differences and to develop further strategies together to prevent sepsis and septic shock as well as reduce death and disability from these conditions both nationally and globally.

    View details for DOI 10.1093/cid/cix997

    View details for Web of Science ID 000432184200027

    View details for PubMedID 29182749

  • Treatment as prevention: some additional thoughts AIDS Detels, R., Winslow, D. L. 2012; 26 (4): 519-520

    View details for DOI 10.1097/QAD.0b013e32834fa17e

    View details for Web of Science ID 000300411500015

    View details for PubMedID 22156975

  • Efavirenz Plasma Concentrations and Cytochrome 2B6 Polymorphisms ANNALS OF PHARMACOTHERAPY Lindfelt, T., O'Brien, J., Song, J. C., Patel, R., Winslow, D. L. 2010; 44 (10): 1572-1578


    Interpatient variability in efavirenz concentrations may be due to CYP2B6 genetic polymorphisms. Efavirenz concentration and pharmacogenomic data are scarce in Latino patients.To evaluate the difference in trough and midpoint efavirenz plasma concentrations between HIV-positive Latino and white patients. In addition, this study evaluated the association between efavirenz concentrations and CYP2B6 polymorphisms in Latino and white HIV-positive subjects.This pilot study included 10 Latinos and 10 whites. Two efavirenz blood concentrations were determined: a trough and a midpoint. CYP2B6 genetic polymorphisms were analyzed at the 516 (G to T) and 785 (A to G) codons. The Mann-Whitney test was used to determine whether efavirenz concentrations varied with ethnicity. The Kruskal-Wallis test was used to determine whether efavirenz concentrations varied with CYP2B6 genetic polymorphisms. Efavirenz concentrations were expressed as medians (minimum, maximum).Midpoint concentrations were 1.58 μg/mL (1.36, 6.02) and 3.14 μg/mL (1.74, 7.72) for whites and Latinos, respectively (p < 0.05). Trough concentrations did not vary as a function of ethnicity. Ten percent of Latinos and whites tested positive for homozygous variants of CYP2B6-516 and CYP2B6-785. One white subject tested positive for the homozygous variant of CYP2B6-1459. Trough concentrations for 516TT, 516GT, and 516GG (wild type) were 5.13 μg/mL (4.13, 6.12), 2.13 μg/mL (1.33, 3.37), and 1.44 μg/mL (0.59, 2.92), respectively (p < 0.05). Trough concentrations for 785GG, 785AG, and 785AA (wild type) were 5.12 μg/mL (4.13, 6.12), 1.98 μg/mL (1.33, 3.37), and 1.27 μg/mL (0.59, 2.92), respectively (p < 0.05). None of the patients took concomitant medications that impacted CYP2B6 metabolism.Trough efavirenz concentrations were significantly higher in patients with the 785 (A to G) and 516 (G to T) variants. Midpoint efavirenz concentrations in Latinos were significantly higher than those of whites.

    View details for DOI 10.1345/aph.1P141

    View details for Web of Science ID 000282675100006

    View details for PubMedID 20841522

  • Gross Hematuria in a Young Iraqi Man - Diagnosis: infection due to Schistosoma haematobium CLINICAL INFECTIOUS DISEASES Van Horn, G. T., Goodrich, A., Winslow, D. L. 2010; 50 (8): 1144-?

    View details for DOI 10.1086/651270

    View details for Web of Science ID 000275645900017

    View details for PubMedID 20233043

  • Replication Capacity of HIV-1 in the Presence of Resistance-Associated Substitutions in Protease CLINICAL INFECTIOUS DISEASES Winslow, D. L. 2009; 49 (1): 165–66

    View details for DOI 10.1086/599619

    View details for Web of Science ID 000266766500024

    View details for PubMedID 19500032

  • Efavirenz-induced hypersensitivity reaction manifesting in rash and hepatitis in a Latino male ANNALS OF PHARMACOTHERAPY Leung, J. M., O'Brien, J. G., Wong, H. K., Winslow, D. L. 2008; 42 (3): 425-429


    To report a case of hypersensitivity manifesting in a rash, fever, and life-threatening hepatitis in a patient initiated on efavirenz therapy.A 30-year-old Latino male newly diagnosed with HIV was started on efavirenz-based highly active antiretroviral therapy (HAART) using tenofovir 300 mg, emtricitabine 200 mg, and efavirenz 600 mg once daily. Eleven days after beginning therapy, he developed a hypersensitivity reaction manifesting in rash and fever preceding severe drug-induced hepatitis. Liver enzyme peak values were aspartate transaminase 3410 U/L and alanine transaminase 2132 U/L. Hepatitis resolved with discontinuation of the HAART. The patient was rechallenged with tenofovir and emtricitabine one year later; no adverse reactions occurred.The Naranjo probability scale demonstrated a probable relationship between this adverse reaction and efavirenz. A MEDLINE search (2004 to September 2007) revealed 2 cases of rash preceding hepatitis with the initiation of efavirenz. Both cases were in women; there were no prior reported cases of efavirenz hypersensitivity in men. Although the mechanism of this reaction is unknown, a few factors may have contributed to this reaction. The half-life and the auto-induction of efavirenz may explain the continued rise in liver enzymes and severe hepatitis that continued to occur once the drug was discontinued. Another cause that may have contributed is the metabolism of the medication. CYP2B6 is responsible for almost 90% of the clearance of efavirenz. Data from a recent pharmacokinetic study showed that efavirenz concentrations were higher in both black and Latino patients when compared with those of white patients. In addition, it is highly probable that this patient's liver function was impaired when transaminase levels peaked, resulting in decreased clearance of efavirenz.Although such a hypersensitivity reaction is rare, efavirenz is the most probable cause of the erythematous maculopapular rash and acute hepatitis in this patient. Monitoring of liver function in patients who present with a rash following initiation of efavirenz-based HAART is recommended. In addition, clinicians should exercise caution in patients presenting with rash, fever, and increased liver enzymes (> 3 times the upper limit of normal or patient baseline). It is strongly recommended that efavirenz therapy be withheld in such cases and reevaluated once liver enzyme levels stabilize.

    View details for DOI 10.1345/aph.1K574

    View details for Web of Science ID 000254000200017

    View details for PubMedID 18252833

  • Treating the enemy. Annals of internal medicine Winslow, D. L. 2007; 147 (4): 278-279

    View details for PubMedID 17709761

  • Wind, rain, flooding, and fear: Coordinating military public health in the aftermath of Hurricane Katrina CLINICAL INFECTIOUS DISEASES Winslow, D. L. 2005; 41 (12): 1759-1763


    On 29 August 2005, a category 4 hurricane struck the Gulf Coast of Mississippi and southeast Louisiana, resulting in widespread destruction caused by winds in excess of 190 km/h (120 miles/h), heavy rain, and flooding. Communication, electricity, and fresh water supplies were disrupted throughout the region, rendering much of the area uninhabitable. Despite tremendous obstacles, the US military spearheaded the eventually successful rescue, recovery, and relief operations. This article describes the challenges of protecting the health and safety of these personnel in the immediate aftermath of Hurricane Katrina.

    View details for Web of Science ID 000233698300012

    View details for PubMedID 16288401

  • HIV-1 protease and reverse transcriptase mutation patterns responsible for discordances between genotypic drug resistance interpretation algorithms JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES Ravela, J., Betts, B. J., Brun-Vezinet, F., Vandamme, A. M., Descamps, T., Van Laethem, K., Smith, K., Schapiro, J. M., Winslow, D. L., Reid, C., Shafer, R. W. 2003; 33 (1): 8-14


    Several rules-based algorithms have been developed to interpret results of HIV-1 genotypic resistance tests. To assess the concordance of these algorithms and to identify sequences causing interalgorithm discordances, we applied four publicly available algorithms to the sequences of isolates from 2,045 individuals in northern California. Drug resistance interpretations were classified as S for susceptible, I for intermediate, and R for resistant. Of 30,675 interpretations (2,045 sequences x 15 drugs), 4.4% were completely discordant, with at least one algorithm assigning an S and another an R; 29.2% were partially discordant, with at least one algorithm assigning an S and another an I, or at least one algorithm assigning an I and another an R; and 66.4% displayed complete concordance, with all four algorithms assigning the same interpretation. Discordances between nucleoside reverse transcriptase inhibitor interpretations usually resulted from several simple, frequently occurring mutational patterns. Discordances between protease inhibitor interpretations resulted from a larger number of more complex mutation patterns. Discordances between nonnucleoside reverse transcriptase inhibitor interpretations were uncommon and resulted from a small number of individual drug resistance mutations. Determining the clinical significance of these mutation patterns responsible for interalgorithm discordances will improve interalgorithm concordance and the accuracy of genotypic resistance interpretation.

    View details for Web of Science ID 000182805400002

    View details for PubMedID 12792349

  • Accuracy of the TRUGENE HIV-1 genotyping kit JOURNAL OF CLINICAL MICROBIOLOGY Grant, R. M., Kuritzkes, D. R., JOHNSON, V. A., Mellors, J. W., Sullivan, J. L., Swanstrom, R., D'Aquila, R. T., van Gorder, M., Holodniy, M., Lloyd, R. M., Reid, C., Morgan, G. F., Winslow, D. L. 2003; 41 (4): 1586-1593


    Drug resistance and poor virological responses are associated with well-characterized mutations in the viral reading frames that encode the proteins that are targeted by currently available antiretroviral drugs. An integrated system was developed that includes target gene amplification, DNA sequencing chemistry (TRUGENE HIV-1 Genotyping Kit), and hardware and interpretative software (the OpenGene DNA Sequencing System) for detection of mutations in the human immunodeficiency virus type 1 (HIV-1) protease and reverse transcriptase sequences. The integrated system incorporates reverse transcription-PCR from extracted HIV-1 RNA, a coupled amplification and sequencing step (CLIP), polyacrylamide gel electrophoresis, semiautomated analysis of data, and generation of an interpretative report. To assess the accuracy and robustness of the assay system, 270 coded plasma specimens derived from nine patients were sent to six laboratories for blinded analysis. All specimens contained HIV-1 subtype B viruses. Results of 270 independent assays were compared to "gold standard" consensus sequences of the virus populations determined by sequence analysis of 16 to 20 clones of viral DNA amplicons derived from two independent PCRs using primers not used in the kit. The accuracy of the integrated system for nucleotide base identification was 98.7%, and the accuracy for codon identification at 54 sites associated with drug resistance was 97.6%. In a separate analysis of plasma spiked with infectious molecular clones, the assay reproducibly detected all 72 different drug resistance mutations that were evaluated. There were no significant differences in accuracy between laboratories, between technologists, between kit lots, or between days. This integrated assay system for the detection of HIV-1 drug resistance mutations has a high degree of accuracy and reproducibility in several laboratories.

    View details for DOI 10.1128/JCM.41.4.1586-1593.2003

    View details for Web of Science ID 000182179900037

    View details for PubMedID 12682149